久效磷和林丹对细小色矛线虫种群动态的影响及其机制初探
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摘要
久效磷农药作为一种高毒的有机磷农药,不仅对水生生物具有较强的急性毒性,还会影响生物个体的生殖和发育。实验室前期工作发现久效磷农药作为一种潜在的环境雌激素,具有生殖毒性、神经毒性和遗传毒性。而林丹具有半衰期长,历史用量大,是我国地表水检出率最高的有机氯农药,与有机磷农药共同造成水域环境的农药复合污染,对水生生物的种群动态产生联合影响。研究农药对水生生物种群动态的影响,关键在于选择生活史较短的模式生物。细小色矛线虫具有分布范围广、易于培养、世代周期短等特点,适合作为研究农药对种群动态影响的模式生物,可在较短时间内观察农药对其多世代种群动态的影响。
因此,本文以细小色矛线虫为实验材料,选择水域环境中半衰期较短的有机磷农药——久效磷和半衰期较长有机氯农药——林丹两种农药纯品为研究对象,从个体水平和种群水平,研究两种农药纯品单独暴露、联合暴露对细小色矛线虫子一代和子二代的生殖、生长发育、内禀增长率、种群增长率和性比等种群动态指标的影响;同时采用RAPD方法和尼罗红脂肪活体染色及荧光定量技术,分别检测久效磷和林丹纯品对细小色矛线虫子代基因组DNA多态性和消化管脂肪含量的影响。确定两种农药纯品的联合作用方式,并初步探讨了久效磷和林丹影响种群动态的机制,为进一步阐明农药对水生生态系统的影响机制提供基础数据。研究结果如下:
(1)久效磷改变了细小色矛线虫子一代和子二代的种群动态。0.1、1.0、10.0、100.0、1000.0μg/L久效磷极显著降低了细小色矛线虫亲代和子代的总产卵量,降低了子一代和子二代卵的受精率和胚胎孵化率,延长了子一代和子二代的胚胎发育持续时间,增加了L1幼虫的畸形率,降低了成虫数量,抑制了内禀增长率和种群增长率,导致子代种群偏雌性化,其中1000.0μg/L久效磷导致细小色矛线虫子二代种群消失。
(2)久效磷导致细小色矛线虫子代基因组DNA变化。通过RAPD以及相关的扩增图谱分析发现久效磷暴露导致细小色矛线虫子代基因组DNA的多态性变化,与对照相比,0.1、1.0、10.0和100.0μg/L久效磷暴露组细小色矛线虫子代基因组DNA多态性变化的百分比分别为:26.7%、19.8%、19.8%和24.4%。
(3)久效磷影响细小色矛线虫子代消化管内脂肪含量和分布。尼罗红脂肪活体染色以及荧光定量分析发现久效磷导致细小色矛线虫子代消化管的前、后段的脂肪含量升高,却降低了消化管中段脂肪含量;100.0、1000.0μg/L久效磷暴露组整个消化管的脂肪含量与对照相比显著升高。
(4)林丹改变了细小色矛线虫子一代和子二代的种群动态,导致细小色矛线虫子代基因组DNA的变化,影响细小色矛线虫子代消化管内脂肪含量和分布。0.005、0.05、0.5、5.0和50.0μg/L林丹极显著抑制了细小色矛线虫亲代和子代的生殖力,降低卵的受精率,0.5、5.0和50.0μg/L林丹降低了子一代胚胎孵化率,增加子一代L1幼虫畸形率,5.0和50.0μg/L林丹延长子一代胚胎发育时间,0.005、0.05、0.5、5.0和50.0μg/L林丹极显著降低子二代胚胎孵化率,延长子二代胚胎发育持续时间,增加子二代L1幼虫的畸形率,降低细小色矛线虫子一代和子二代成虫数量、内禀增长率和种群增长率,使子代种群偏雌性化;0.005、0.05、0.5、5.0和50.0μg/L林丹暴露组细小色矛线虫子代基因组DNA多态性变化的百分比分别为:20.9%、20.9%、22.1%、18.6%和17.4%;林丹导致细小色矛线虫子代消化管前、后段脂肪含量的增加,中段脂肪含量的降低,0.5、5.0和50.0μg/L林丹暴露组整个消化管的脂肪含量极显著升高。
(5)久效磷和林丹对细小色矛线虫子代种群动态、基因组DNA多态性和消化管脂肪含量的联合作用方式为相加作用。与用久效磷、林丹分别单独暴露细小色矛线虫相比,久效磷和林丹对细小色矛线虫子一代和子二代的个体发育和种群动态指标的抑制作用更大,其中最高浓度联合暴露组(V)的细小色矛线虫子一代种群消失,联合暴露组IV子二代种群消失;I、II、III、IV联合暴露组细小色矛线虫子代基因组DNA多态性变化的百分比分别为:40. 9%、38.2%、41.8%和41.8%;久效磷和林丹联合暴露导致细小色矛线虫子代消化管整体脂肪含量的极显著增加,I、II、III、IV联合暴露组整个消化管的脂肪含量与对照相比分别增加了26.59%、24.25 %、35.22%、27.43%,联合暴露导致细小色矛线虫子代消化管前、后段脂肪含量的增加,中段脂肪含量的降低。
Monocrotophos is a highly toxic organic phosphorus pesticide, not only having high acute toxicity and neurotoxicity to aquatic organisms, but aslo having impact on the reproductive and development of individual. Pre-job of our aboratory had proved that monocrotophos was found as a potential environmental estrogens, having reproductive toxicity, causing ultrastructure damage of goldfish testis, also affecting multi-generations breeding of zebrafish, it is suggested that the monocrotophos may have a negative impact to population dynamics of aquatic organisms. Lindane has a long half-life, history of usage, the one of the organochlorine pesticides with the highest detection rate in surface water in China, together with the organic phosphorus pesticide caused combined pollution in aquatic ecosystem, having a joint impact on population dynamics of aquatic organisms. To study the impact of pesticides on population dynamics of aquatic organisms, the key is to selection an experimental organism with short generation time, Chromadorina germanica with worldwide distribution, easy to cultivate, and a short generation time. Used as an organism to study the impact of pesticides on population dynamics, and many generations can be observed in a relatively short time.
Therefore, using C. germanica as an experimental organism, Choosing monocrotophos, an organophosphorus pesticides with shorter half-life, and lindane, a organochlorine pesticides with longer half-life, to study the population dynamics changes, using individual endpoints such as fecundity, growth and development, and population endpoints such as intrinsic growth rate, population growth rate and sex ratio, under separate and combined exposure of the two pesticides pure. Meanwhile, using RAPD method and Nile Red fat staining in vivo with fluorescence quantificationm, the changes of genomic DNA polymorphism and intestinal fat storage of C. germanica were detected, caused by monocrotophos and lindane. Joint effects of monocrotophos and lindane on population dynamics, genome DNA polymorphism and intestinal fat storage of C. germanica were determined. The mechanism that population dynamics changes of C. germanica caused by monocrotophos and lindane was primary studied. The results could supply the experimental data to answer the effects of pesticides on aquatic ecosystems. Results showed:
(1) The population dynamics of the first and second offspring of C. germanica were changed by monocrotophos. After exposed to 0.1, 1.0, 10.0, 100.0, 1000.0μg/L monocrotophos, the total fecundity of the parental and offspring were significant reduced, of the first and second offspring, egg fertilization rate and embryo hatchability reduced, embryonic development were delayed, deformity rate of L1 larvae was increased, the number of adults was reducing and the intrinsic growth rate and population growth were suppressed, sex ratio deviated from the one and more female. of which, after exposed to 1000.0μg/L monocrotophos, no second offsprings was observed.
(2) The RAPD profiles of offsprings of C. germanica was changed by monocrotophos; value of polymorphisms of offspring C. germanica genomic DNA are as follows: 26.7%, 19.8%, 19.8% and 24.4% for 0.1, 1.0, 10.0 and 100.0μg/L monocrotophos.
(3) Nile red fluorescence of intestine of C. germanica offsprings was changed by monocrotophos, fat storage of front and post part of intestine increased, but the middle part of intestine reduced; the fat storage of the whole intestine increased, treated by 100.0, 1000.0μg/L monocrotophos
(4) The population dynamics, genomic DNA polymorphisms and fat storage of intestine of the first and second offspring of C. germanica were also changed by lindane. The total fecundity of the parental and offspring was decreased andegg fertilization rate was decreased, the number of adults was reduced, the intrinsic growth rate and population growth were suppressed, in the first and second offspring treated by 0.005, 0.05, 0.5, 5.0 and 50.0μg/L lindane; the embryonic development of first offspring was delayed in 0.5, 5.0 and 50.0μg/L lindane treatment, deformity rate of L1 larvae of first offspring was increased in 5.0 and 50.0μg/L lindane treatment. The value of polymorphisms of offspring C. germanica genomic DNA are as follows: 20.9%, 20.9%, 22.1%, 18.6% and 17.4% for 0.005, 0.05, 0.5, 5.0 and 50.0μg/L lindane. Fat storage of front and post part of intestine was increased, of middle part was decreased for 0.005, 0.05, 0.5, 5.0 and 50.0μg/L lindane. The fat storage of the whole intestine was significantly increased for 0.5, 5.0 and 50.0μg/L lindane.
(5) The population dynamics, genomic DNA polymorphisms and fat storage of intestine of the first and second offspring of C. germanica were strongly changed for joint of monocrotophos and lindane. No first offsprings of C. germanica was observed in the highest joint treatment V. The value of polymorphisms of offspring C. germanica genomic DNA are as follows: 40.9%, 38.2%, 41.8% and 41.8% for joint treatment I, II, III, IV of monocrotophos and lindane. By comparing the results of monocrotophos, lindane separate treatment to the joint treatment, additive effects on the population dynamics, genomic DNA polymorphism and intestinal fat storage of C. germanica were found, after joint treated by monocrotophos and lindane.
因此,本文以细小色矛线虫为实验材料,选择水域环境中半衰期较短的有机磷农药——久效磷和半衰期较长有机氯农药——林丹两种农药纯品为研究对象,从个体水平和种群水平,研究两种农药纯品单独暴露、联合暴露对细小色矛线虫子一代和子二代的生殖、生长发育、内禀增长率、种群增长率和性比等种群动态指标的影响;同时采用RAPD方法和尼罗红脂肪活体染色及荧光定量技术,分别检测久效磷和林丹纯品对细小色矛线虫子代基因组DNA多态性和消化管脂肪含量的影响。确定两种农药纯品的联合作用方式,并初步探讨了久效磷和林丹影响种群动态的机制,为进一步阐明农药对水生生态系统的影响机制提供基础数据。研究结果如下:
(1)久效磷改变了细小色矛线虫子一代和子二代的种群动态。0.1、1.0、10.0、100.0、1000.0μg/L久效磷极显著降低了细小色矛线虫亲代和子代的总产卵量,降低了子一代和子二代卵的受精率和胚胎孵化率,延长了子一代和子二代的胚胎发育持续时间,增加了L1幼虫的畸形率,降低了成虫数量,抑制了内禀增长率和种群增长率,导致子代种群偏雌性化,其中1000.0μg/L久效磷导致细小色矛线虫子二代种群消失。
(2)久效磷导致细小色矛线虫子代基因组DNA变化。通过RAPD以及相关的扩增图谱分析发现久效磷暴露导致细小色矛线虫子代基因组DNA的多态性变化,与对照相比,0.1、1.0、10.0和100.0μg/L久效磷暴露组细小色矛线虫子代基因组DNA多态性变化的百分比分别为:26.7%、19.8%、19.8%和24.4%。
(3)久效磷影响细小色矛线虫子代消化管内脂肪含量和分布。尼罗红脂肪活体染色以及荧光定量分析发现久效磷导致细小色矛线虫子代消化管的前、后段的脂肪含量升高,却降低了消化管中段脂肪含量;100.0、1000.0μg/L久效磷暴露组整个消化管的脂肪含量与对照相比显著升高。
(4)林丹改变了细小色矛线虫子一代和子二代的种群动态,导致细小色矛线虫子代基因组DNA的变化,影响细小色矛线虫子代消化管内脂肪含量和分布。0.005、0.05、0.5、5.0和50.0μg/L林丹极显著抑制了细小色矛线虫亲代和子代的生殖力,降低卵的受精率,0.5、5.0和50.0μg/L林丹降低了子一代胚胎孵化率,增加子一代L1幼虫畸形率,5.0和50.0μg/L林丹延长子一代胚胎发育时间,0.005、0.05、0.5、5.0和50.0μg/L林丹极显著降低子二代胚胎孵化率,延长子二代胚胎发育持续时间,增加子二代L1幼虫的畸形率,降低细小色矛线虫子一代和子二代成虫数量、内禀增长率和种群增长率,使子代种群偏雌性化;0.005、0.05、0.5、5.0和50.0μg/L林丹暴露组细小色矛线虫子代基因组DNA多态性变化的百分比分别为:20.9%、20.9%、22.1%、18.6%和17.4%;林丹导致细小色矛线虫子代消化管前、后段脂肪含量的增加,中段脂肪含量的降低,0.5、5.0和50.0μg/L林丹暴露组整个消化管的脂肪含量极显著升高。
(5)久效磷和林丹对细小色矛线虫子代种群动态、基因组DNA多态性和消化管脂肪含量的联合作用方式为相加作用。与用久效磷、林丹分别单独暴露细小色矛线虫相比,久效磷和林丹对细小色矛线虫子一代和子二代的个体发育和种群动态指标的抑制作用更大,其中最高浓度联合暴露组(V)的细小色矛线虫子一代种群消失,联合暴露组IV子二代种群消失;I、II、III、IV联合暴露组细小色矛线虫子代基因组DNA多态性变化的百分比分别为:40. 9%、38.2%、41.8%和41.8%;久效磷和林丹联合暴露导致细小色矛线虫子代消化管整体脂肪含量的极显著增加,I、II、III、IV联合暴露组整个消化管的脂肪含量与对照相比分别增加了26.59%、24.25 %、35.22%、27.43%,联合暴露导致细小色矛线虫子代消化管前、后段脂肪含量的增加,中段脂肪含量的降低。
Monocrotophos is a highly toxic organic phosphorus pesticide, not only having high acute toxicity and neurotoxicity to aquatic organisms, but aslo having impact on the reproductive and development of individual. Pre-job of our aboratory had proved that monocrotophos was found as a potential environmental estrogens, having reproductive toxicity, causing ultrastructure damage of goldfish testis, also affecting multi-generations breeding of zebrafish, it is suggested that the monocrotophos may have a negative impact to population dynamics of aquatic organisms. Lindane has a long half-life, history of usage, the one of the organochlorine pesticides with the highest detection rate in surface water in China, together with the organic phosphorus pesticide caused combined pollution in aquatic ecosystem, having a joint impact on population dynamics of aquatic organisms. To study the impact of pesticides on population dynamics of aquatic organisms, the key is to selection an experimental organism with short generation time, Chromadorina germanica with worldwide distribution, easy to cultivate, and a short generation time. Used as an organism to study the impact of pesticides on population dynamics, and many generations can be observed in a relatively short time.
Therefore, using C. germanica as an experimental organism, Choosing monocrotophos, an organophosphorus pesticides with shorter half-life, and lindane, a organochlorine pesticides with longer half-life, to study the population dynamics changes, using individual endpoints such as fecundity, growth and development, and population endpoints such as intrinsic growth rate, population growth rate and sex ratio, under separate and combined exposure of the two pesticides pure. Meanwhile, using RAPD method and Nile Red fat staining in vivo with fluorescence quantificationm, the changes of genomic DNA polymorphism and intestinal fat storage of C. germanica were detected, caused by monocrotophos and lindane. Joint effects of monocrotophos and lindane on population dynamics, genome DNA polymorphism and intestinal fat storage of C. germanica were determined. The mechanism that population dynamics changes of C. germanica caused by monocrotophos and lindane was primary studied. The results could supply the experimental data to answer the effects of pesticides on aquatic ecosystems. Results showed:
(1) The population dynamics of the first and second offspring of C. germanica were changed by monocrotophos. After exposed to 0.1, 1.0, 10.0, 100.0, 1000.0μg/L monocrotophos, the total fecundity of the parental and offspring were significant reduced, of the first and second offspring, egg fertilization rate and embryo hatchability reduced, embryonic development were delayed, deformity rate of L1 larvae was increased, the number of adults was reducing and the intrinsic growth rate and population growth were suppressed, sex ratio deviated from the one and more female. of which, after exposed to 1000.0μg/L monocrotophos, no second offsprings was observed.
(2) The RAPD profiles of offsprings of C. germanica was changed by monocrotophos; value of polymorphisms of offspring C. germanica genomic DNA are as follows: 26.7%, 19.8%, 19.8% and 24.4% for 0.1, 1.0, 10.0 and 100.0μg/L monocrotophos.
(3) Nile red fluorescence of intestine of C. germanica offsprings was changed by monocrotophos, fat storage of front and post part of intestine increased, but the middle part of intestine reduced; the fat storage of the whole intestine increased, treated by 100.0, 1000.0μg/L monocrotophos
(4) The population dynamics, genomic DNA polymorphisms and fat storage of intestine of the first and second offspring of C. germanica were also changed by lindane. The total fecundity of the parental and offspring was decreased andegg fertilization rate was decreased, the number of adults was reduced, the intrinsic growth rate and population growth were suppressed, in the first and second offspring treated by 0.005, 0.05, 0.5, 5.0 and 50.0μg/L lindane; the embryonic development of first offspring was delayed in 0.5, 5.0 and 50.0μg/L lindane treatment, deformity rate of L1 larvae of first offspring was increased in 5.0 and 50.0μg/L lindane treatment. The value of polymorphisms of offspring C. germanica genomic DNA are as follows: 20.9%, 20.9%, 22.1%, 18.6% and 17.4% for 0.005, 0.05, 0.5, 5.0 and 50.0μg/L lindane. Fat storage of front and post part of intestine was increased, of middle part was decreased for 0.005, 0.05, 0.5, 5.0 and 50.0μg/L lindane. The fat storage of the whole intestine was significantly increased for 0.5, 5.0 and 50.0μg/L lindane.
(5) The population dynamics, genomic DNA polymorphisms and fat storage of intestine of the first and second offspring of C. germanica were strongly changed for joint of monocrotophos and lindane. No first offsprings of C. germanica was observed in the highest joint treatment V. The value of polymorphisms of offspring C. germanica genomic DNA are as follows: 40.9%, 38.2%, 41.8% and 41.8% for joint treatment I, II, III, IV of monocrotophos and lindane. By comparing the results of monocrotophos, lindane separate treatment to the joint treatment, additive effects on the population dynamics, genomic DNA polymorphism and intestinal fat storage of C. germanica were found, after joint treated by monocrotophos and lindane.
引文
[1] Agrahari S, Gopal K. Fluctuations of certain biochemical constituents and markers enzymes as a consequence of monocrotophos toxicity in the edible freshwater fish, Channa punctatus. Pesticide Biochemistry and Physiology, 2009, 241-250.
[2] Amjad S, Gray J S. Use of the nematode-copepod ratio as an index of organic pollution. Mar. Pollut. Bull., 1983, 14:178-181.
[3] Anderson P.D., and L.J. Weber. The toxicity to aquatic populations of mixtures containing certain heavy metals. Proceedings, International Conference on Heavy Metals in the Environment, Toronto, ON, Canada, 1975, October 27–31, pp. 933–953.
[4] Anderson S, Sadinski W, Shugart L, et al. Genetic and molecular ecotoxicology: a research framework, Environ. Health Perspect., 1994, 102: 3~8.
[5] Andre P S. Evolution of the control of sexual identity in nematodes. Seminars in Cell & Developmental Biology, 2007, 18: 362~370.
[6] Atienzar F A, Conradi M, Evenden A J, et al. Qualitative assessment of genotoxicity using random amplified polymorphic DNA: comparison of genomic template stability with key fitness parameters in Daphnia magna exposed to benzo[α]pyrene [J]. Environ.Toxicol.Chem., 1999, 18: 2275-2282.
[7] Atienzar F A, Cordi B, Donkin M E, et al. Comparison of ultraviolet-induced genotoxicity detected by random amplified polymorphic DNA with chlorophyll fluorescence and growth in a marine macroalgae, Palmaria palmate [J]. Aquat.Toxicol., 2000, 50:1-12.
[8] Atienzar F A, Jha A N. The random amplified polymorphic DNA (RAPD) assay to determine DNA alterations, repair and transgenerational effects in B(a)P exposed Daphnia magna. Mutation Research, 2004, 552: 125~140.
[9] Atienzar F A, Venier P, Jha A N, et al. Evaluation of the random amplified polymorphic DNA(RAPD) assay for the detection of DNA damage and mutations. Mutation Research, 2002, 521: 151~163.
[10] Atienzar F A, Victoria V C, Awadhesh N J, et al. Fitness parameters and DNA effects are sensitive indicators of copper induced toxicity in Daphnia magna [J]. Toxicol.Sci., 2001, 59: 241~250.
[11] Atkinson A, Siegel V, Pakhomov E, et al. Long-term decline in krill stock and increase in salps within the Southern Ocean. Nature, 2004, 432: 100~103.
[12] Becerril C, Acevedo H, Ferrero M, et al. DNA fingerprint comparison of rainbow trout and RTG-2 cell lineusing random amplified polymorphic DNA. Ecotoxicology, 2001, 10: 115~124.
[13] Becerril C, Ferrero M, Sanz F, et al. Detection of mitomycin C-induced genetic damage in fish cells by use of RAPD. Mutagenesis, 1999, 14: 449~456.
[14] Belfiore N M, Anderson S L. Effects of contaminants on genetic patterns in aquatic organisms: a review. Mutat. Res., 2001, 489: 97~122.
[15] Berenbaum M C. What is synergy? Pharmacol Rev, 1989, 41: 93.
[16] Bernardes A T. Mutation load and the extinction of large populations. Physica A, 1996, 230: 156~173.
[17] Bickham J W, Sandhu S, Hebert P D N, et al. Effects of chemical contaminants on genetic diversity in natural populations: implications for biomonitoring and ecotoxicology. Mutat. Res., 2000, 463: 33~51.
[18] Bliss C I. The toxicity of poisons applied jointly .Ann Appl Biol,1939, 26:585~615.
[19] Bolognesi C, Giada F, Claudia L, et al. Genotoxicity biomarkers in Mytilus galloprovincialis: wild versus caged mussels. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 2004, 552(1-2): 153~162.
[20] Brock T J, Browse J, Watts J L. Fatty acid desaturation and the regulation of adiposity in Caenorhabditis elegans. Genetics, 2007, 176: 865~875.
[21] Bustnes J O, Helberg M, Strann K B, et al. Environmental pollutants in endangered vs. increasing subspecies of the lesser black-backed gull on the Norwegian Coast. Environmental Pollution, 2006, (144)3: 893~901.
[22] Byerly L, Cassada R. C., Russell R. L. The life cycle of the nematode Caenorhabditis elegans I Wild-type growth and reproduction. Developmental Biology, 1976, 51:23~33.
[23] Casta?o A, Becerril C. In vitro assessment of DNA damage after short-and long-term exposure to benzo(a)pyrene using RAPD and the RTG-2 fish cell line. Mutation Research, 2004, 552: 141~151.
[24] Channa K, Nagalakshmi K, Gu Z. Genomic instability in silica and cadmium chloride- transformed BALB/c-3T3 and tumor cell lines by random amplified polymorphic DNA analysis [J]. Mutation Research, 1999, 425:117-123.
[25] Chiang S H, MacDougald O A. Will fatty worms help cure human obesity? Trends in Genetics, 2003, 19(10): 523~525.
[26] Chow Hu H, Pasternak J. Protein changes during maturation of the free-living nematode Panagrellus silusiae. J. Exp. Zool., 1969, 170:77-84.
[27] Clark W C. Hermaphroditism as a reproductive strategy for metazoans some correlated benefits. NZ J Zool, 1978, 5(4):769~80.
[28] Colborn T, Dumanoski D, Myers J P. Our Stolen Future. New York, Duuten, 1996, 1~60.
[29] Cronin M A, Bickham J W. A population genetic analysis of the potential for a crude oil spill to induce heritable mutations and impact natural populations. Ecotoxicology. 1998, 7: 259~278.
[30] Davidson C. Declining downwind : amphibian population declines in california and historical pesticide use. Ecological Applications, 2004, 14(6): 1892~1902.
[31] Diekmann M, Hultsch V, Nagel R. On the relevance of genotoxicity for fish populations I: effects of a model genotoxicant on zebrafish (Danio rerio) in a complete life-cycle test [J]. Aquatic Toxicology, 2004,68:13-26.
[32] Ferrando M D, Janssen C R, Andreu E, et al. Ecotoxicological studies with the freshwater rotifer Brachionus calyciflorus. II. An assessment of the chronic toxicity of lindane and 3,4-dichloroaniline using life tables. Hydrobiologia, 1993, 255~256(1): 33~40.
[33] Fry and Toone. DDT-induced feminization of gull embryos. Science, 1981, 213(4510): 922~924.
[34] Gama-Flores J L, Sarma S S S, Nandini S. Acute and chronic toxicity of the pesticide methyl parathion to the rotifer Brachionus angularis (Rotifera) at different algal (Chlorella vulgaris) food densities. Aquatic Ecology, 2004, 38: 27~36.
[35] Gao J J, Liu L H, Liu X R, et al. Occurrence and distribution of organochlorine pesticides-lindane, p, p’-DDT, and heptachlor epoxide-in surface water of China. Environment International, 2008, 34: 1097~1103.
[36] Ghiselin MT. The evolution of hermaphroditism among animals. Q Rev Biol, 1969, 44(2):189~208.
[37] Gillespie R B, Guttman S I. Chemical-induced changes in the genetic structure of populations: effects on allozymes, in: V. E. Forbes (Ed.), Genetics and Ecotoxicology, Taylor & Francis, Philadelphia, 1999, pp. 55~77.
[38] Goodbell P B, Ferris H. Influence of environmental factors on the hatch and survival of Meloidogyne incognita [J]. Journal of Nematology, 1989,21(3):328~334.
[39] Guillette L J, Jr, Gunderson M P. Alterations in development of reproductive and endocrine systems of wildlife populations exposed to endocrine-disrupting contaminants. Reproduction, 2001, 122: 857~864.
[40] Hans D W, Ronny B, Thierry B. The population genetic of littorea (Mollusca: Gastropoda) along a pollution in the Scheldt estuary (The Netherlands) using RAPD analysis [J]. Science of Total Environment, 2004, 325:59-69.
[41] Harris F A, Chambers H W. Interaction of insecticidal mixtures in Tobacco Budworm. J Econ Entomol, 1973, 66(2): 517~518.
[42] Hartl D L, Clark A G. Principles of Population Genetics, second ed., Sinauer Associates, Inc., Suderland,USA, 1998.
[43] Hebert P D N, Luiker M M. Genetic effects of contaminant exposure—towards an assessment of impacts on animal populations. Sci. Total Environ, 1996, 191: 23~58.
[44] Heip C., Smol N., Absillis V. Influence of temperature on the reproductive potential of Oncholaimus oxyuris. Mar. Biol., 1978, 45: 255~260.
[45] Hellerer T, Axang C, Brackmann C, et al. Monitoring of lipid storage in Caenorhabditis elegans using coherent anti-Stokes Raman scattering (CARS) microscopy, Proc. Natl. Acad. Sci. U. S. A., 2007, 104: 14658~14663.
[46] Howell R. Acute toxicity of heavy metals to two species of marine nematodes Marine Environmental Research, Volume 11, Issue 3, 1984, Pages 153~161.
[47] Huang D J, Chen H C, Wu J P, et al. Reproduction obstacles for the female green neon shrimp (Neocaridina denticulata). Chemosphere, 2006, 64: 11~16.
[48] Huang L, Xi Y L, Zha C W, et al. Effect of Aldrin on Life History Characteristics of Rotifer Brachionus calyciflorus Pallas. Bulletin of Environmental Contamination and Toxicology, 2007, 79: 524~528.
[49] Hunt E G, Bischoff A I. Inimical effects on wildlife of periodic DDD applications to Clear Lake. Calif. Fish Game, 1960, 46: 91~105.
[50] Ide H, Petrullo L A, Hataet Z, etal. Processing of DNA base damage by DNA polymerases dihydrothymine and b-ureidoisobutyric acid as models forinstructive and noninstructive lesions. J. Biol. Chem. 1991, 266: 1469~1477.
[51] Jaensson A, Scott A P, Moore A, et al. Effects of a pyrethroid pesticide on endocrine responses to female odours and reproductive behaviour in male parr of brown trout (Salmo trutta L.). Aquatic Toxicology, 2007, 81: 1~9.
[52] Jensen K M, Korte J J, Kahl M D, et al. Aspects of basic reproductive biology and endocrinology in the fathead minnow (Pimephales promelas) [J]. Comparative Biochemistry and Physiology Part C, 2001,128:127-141.
[53] Jensen P. Food ingestion and growth of the diatom-feeding nematode chromadorita tenuis. Marine Biology, 1984, 81:307-310.
[54] Jones K C, Voogt Pde. Persistent organic pollutant (POPS): state of the science. Environmental Pollution, 1999, 100: 209~221.
[55] Josephine A H, Franck A A, Awadhesh N J. Genotoxic, cytotoxic, developmental and survival effects oftritiated water in the early life stages of the marine mollusc, Mytius edulis [J]. Aquatic Toxicology, 2005, 74:205~217.
[56] Keplinger M L, Deichmann W B. Acute toxicity of combinations of pesticides, Toxicol Appl Phamacol, 1967, 10(3): 586~595.
[57] Kimble J, Sharrock W. J. Tissue-specific synthesis of yolk proteins in Caenorhabditis elegans. Dev. Biol., 1983, 96 (1):189~196.
[58] Kniazeva M, Crawford Q T, Seiber M, et al. Monomethyl branchedchain fatty acids play an essential role in Caenorhabditis elegans development, PLoS Biol. 2004, 2, E257.
[59] Kohra S, Kuwahara K, Takao Y, et al. Effect of Bisphenol A on the Feeding Behavior of Caenorhabditis elegans. Journal of health science, 2002, 48(1): 93~95.
[60] Kulshrestha S K, Arora Neelam. Impairments induced by sublethal doses of two pesticides in the ovaries of a freshwater teleost Channa striatus bloch. Toxicology Letters, 1984, (20)1: 93~98.
[61] Liu W, Li P J, Qi X M, et al. DNA changes in barley (Hordeum vulgare) seedlings induced by cadmium pollution using RAPD analysis. Chemosphere, 2005, 61: 158~167.
[62] Macdonald R W, Barrie L A, Bidleman T F. Contaminants in the Canadian Arctic: 5 years of progress in understanding sources, occurrence and pathways. The Science of the Total Environment, 2000, 264: 93~234.
[63] Macek K J, Buxton K S, Derr S K, et al. Chronic toxicity of lindane to selected aquatic invertebrates and fishes. Environmental Protection Agency, Report EPA-600/3-76-046, 1976: 50.
[64] Mahmoudi E, Essid N, Beyrem H, et al. Individual and combined effects of lead and zinc on a free-living marine nematode community: Results from microcosm experiments. Journal of Experimental Marine Biology and Ecology, 2007, 343 (2): 217~226.
[65] Mckay R M, Mckay J P, Avery L, et al. C.elegans: a model for exploring the genetics of fat storage. Developmental Cell, 2003, 4: 131~142.
[66] Mengoni A, Gonnelli C, GalaMi F. Genetic diversity and heavy metal tolerance in populations of Silecw paradoxa L.(Caryophyllaeeae):a random anaplified polymorphic DNA analysis [J]. Mol.Ecol, 2000, 9: 1319~1324.
[67] Menzel R, Yeo H L, Rienau S, et al. Cytochrome P450s and short-chain dehydrogenases mediate the toxicogenomic response of PCB52 in the nematode Caenorhabditis elegans. J Mol Biol, 2007, 370: 1~13.
[68] Mukhopadhyay A, Deplancke B, Walhout A J M, et al. C.elegans tubby regulates life span and fat storage by two independent mechanisms. Cell Metabolism, 2005, 2: 35~42.
[69] Mullaney B C, Ashrafi K. C.elegans fat storage and metabolic regulation. Biochimica et Biophysica Acta, 2009, unpublished.
[70] Muthanna A. AI-Omar, Nehla H, et al. Residues of organochlorine insecticides in fish from polluted Water. Bull. Environ. Contam. Toxicol. 1986, 36: 109~113.
[71] Neelamegam P, Rajendran A, Maruthanayagam C, et al. Design and development of embedded system for the study of the biochemical variations induced by monocrotophos in Cyprinus carpio. Measurement, 2007, 40: 372~377.
[72] Nelson J R, Lawrence C W, Hinkle D C. Thymine-thymine dimmer bypass by yeast DNA-polymerase-zeta. Science, 1996, 272: 1646~1649.
[73] Pesando D, Robert S, Huitorel P. Effects of methoxychlor, dieldrin and lindane on sea urchin fertilization and early development. Aquatic Toxicology. 2004, 66: 225~239.
[74] Placket R L,Hewiett P S. Journal of the Royal Statistical Soeiety Series,1952, B14: 143~163.
[75] Platt H M, Warwick R M. The significance of free-living nematodes to the littoral ecosystem. The shore environment, 1980, 2:729-759.
[76] Platt H M., Warwick R M. Free-living marine nematodes Part I British Enoplids. Cambridge London New York. New Rochelle Melbourne Sydney. The Linnean Sciety of London and The Estuarine and Brackish-water. Sciences Association Cambridge University Press, 1983:1-8.
[77] Raffaelli D G, Mason C F. Pollution monitoring with meiofauna using the ratio of nematodes to copepods. Mar. Pollut. Bull., 1981, 12:158-163.
[78] Roche H, Buet A, Ramade F. Relationships between persistent organic chemicals residues and biochemical constituents in fish from a protected area: the French National Nature Reserve of Camargue. Comparative Biochemistry and Physiology Part C, 2002, 133: 393~410.
[79] Rothman W. Present at the environmental risk assessment conference. Alexandria V A,1988 Sep 21.
[80] Saleha B B, Danadevi K, Rahman M F, et al. Genotoxic effect of monocrotophos to sentinel species using comet assay. Food and Chemical Toxicology, 2001, 39(4):361~366.
[81] Sarma S S S, Nandini S, Gama-Flores J L. Effects of methyl parathion on the population growth of the rotifer Brachionus patulus (Muller) under different algal food (Chlorella vulgaris) densities. Ecotoxicology and Environm ental Safety, 2001, 48: 190~195.
[82] Semenza J C, Tolbert P E, Rubin C H, et al. Reproductive toxins and alligator abnormalities at Lake Apopka, Florida[J].Environmmental Health Perspectives. 1997, 105(10): 1030~1032.
[83] Silvestroni L, Fiorini R, Palleschi S. Partition of the organochlorine insecticide lindane into the human sperm surface induces membrane depolarization and Ca2+ influx. Biochem. J., 1997, 321: 691~698.
[84] Simpson V R, Bain M S, Brown R, et al. A long-term study of vitamin A and polychlorinated hydrocarbon levels in otters (Lutra lutra) in south west England. Environmental Pollution, Volume 110, Issue 2, November 2000, Pages 267~275.
[85] Singh P B, Sahu V, Singh V, et al. Sperm motility in the fishes of pesticide exposed and from polluted rivers of Gomti and Ganga of north India. Food and Chemical Toxicology, 2008, 46: 3764~3769.
[86] Staton J L, Schizas N V, Chandler G T, et al. Ecotoxicology and population genetics: the emergence of“phylogeographic and evolutionary ecotoxicology”. Ecotoxicology, 2001, 10: 217~222.
[87] Susan G N, Lee K L, Adams S M. Evaluation alterations of genetic diversity in sunfish populations exposed to contaminants using RAPD assay [J]. Aquatic Toxicology, 1998, 43:163-178.
[88] Theodorakis C W, Shugart L R. Genetic ecotoxicology II: population genetic structure in mosquitofish exposed in situ to radionuclides. Ecotoxicology, 1997, 6: 335~354.
[89] Theodorakis C W. Integration of genotoxic and population genetic endpoints in biomonitoring and risk assessment. Ecotoxcicology, 2001, 10: 245~256.
[90] Tietjen J H, Lee J J. The use of free-living nematodes as a bioassay for estuarine sediments. Marine Environmental Research, 1984, 11: 233~251.
[91] Tominaga N, Kazuhiro U, Masato K, et al. Caenorhabditis elegans Responses to Specific Steroid Hormones. Journal of Health Science, 2003, 49(1):28-33.
[92] Tominaga N, Mineko T, Shiya K, et al. A Convenient Sublethal Assay of Alkylphenol and Organotin Compounds Using the Nematode Caenorhabditis elegans. Journal of Health Science, 2002, 48(6):555-559.
[93] Tominaga N, Shiya K, Taisen I, et al. Effects of Perfluoro Organic Compound Toxicity on Nematode Caenorhabditis elegans Fecundity. Journal of Health Science, 2004, 50(5):545-550.
[94] Tominaga N, Shiya K, Taisen I, et el. A Multi-Generation Sulblethal Assay of Phenols Using the nematode Caenorhabditis elegans. Journal of Health Science, 2003, 49(6):459~463.
[95] Ura K, Toshinori K, Sachiko S, et al. Aquatic Acute Toxicity Testing Using the Nematode Caenorhabditis elegans. Journal of Health Science, 2002, 48(6) 583-586.
[96] Van Gilst M R, Hadjivassiliou H, Yamamoto K R. A Caenorhabditis elegans nutrient response system partially dependent on nuclear receptor NHR-49, Proc. Natl. Acad. Sci. U. S. A. 2005, 102: 13496~13501.
[97] Vonier P M, Crain D A, McLachlan J A, et al. Interaction of environmental chemicals with the estrogen andprogesterone receptors from the oviduct of the American alligator. Environmental Health Perspectives, 1996, 104 1318–1322.
[98] Vrank G., Heip C. Calculation of the intrinsic rate of natural increase rm with Rhabditis marina. Nematologica, 1983, 29: 468~477.
[99] Vranken G, Brussel V D. Vanderheaghen R. Research on the development of a standardized ecotoxicological test on marine nematodes I culture conditions and critearia for two Monhysterids Monhystera disjuncta and Monhystera microphthalma. Ecotoxicological Testing For The Marine Environment, 1984, 2(588):159~184.
[100] Vranken G, Heip C. Toxicity of copper, mercury and lead to a marine nematode Marine Pollution Bulletin, 1986, 17(10): 453~457.
[101] Vranken G, TiréC, Heip C. Effect of temperature and food on hexavalent chromium toxicity to the marine nematode Monhystera disjuncta Marine Environmental Research, 1989, 27(2): 127~136.
[102] Wadsworth W G, Riddle D L. Developmental regulation of energy metabolism in Caenorhabditis elegans. Dev. Biol., 1989, 132: 167~173.
[103] Warwick R M. Survival strategies of meiofauna In feeding and surviva strategies of estuarine organisms. Plenum, New York. N. V. Jones and W. J. Wolff. 1981b:39-52.
[104] Warwick R M. The influence of temperature and salinity on energy partitioning in the marine nematode Diplolaimelloides bruciei. Oecologia, 1981a, 51:318-325.
[105] Wester P W. Histopathological effects of environmental pollutantsβ-HCH and methyl mercury on reproductive organs in freshwater fish. Comparative Biochemistry and Physiology Part C: Comparative Pharmacology, 1991, (100)1-2: 237-239.
[106] White J. The anatomy in the Nematode Caenorhabditis elegans. W. W. Wood, editor. Cold Spring Harbor Laboratory Press. Cold Spring Harbor N.Y., 1988:81~122.
[107] WHO. Combination Effectsin Chemical carcinogenesis. Newyork: VCH Publishers. 1988: 5~20.
[108] WHO. Technic Report Seris. 1981, 662: 8~9.
[109] Wiemeyer S M , Bunck C M, Stafford C J.Environmental contaminants in bald eagles eggs--1980-84--and further interpretations of relationships to productivity and shell thickness. Arch. Environ. Contam. Toxicol. 1993.24, 213~227.
[110] Winter M J, Norman D, Ruth A H, et al. DNA strand breaks and adducts determined in feral and caged chub (Leuciscus cephalus) exposed to rivers exhibiting variable water quality around Birmingham, UK. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 2004, 552 (1-2): 163~175.
[111] Wolf H De, Blust R, Bacekljau T. The population genetic structure of Littorina littorea (Mollusca: Gastropoda) along a pollution gradient in the Scheldt estuary (The Netherlands) using RAPD analysis. Science of the Total Environment, 2004, 325: 59~69.
[112] Wright S. Evolution in Mendelian populations. Genetics, 1931, 16: 97~159.
[113] Zha C W, Xi Y L, Huang L, et al. Effect of Sublethal Exposure to Chlordecone on Life History Characteristics of Freshwater Rotifer Brachionus calyciflorus Pallas. Bulletin of Environmental Contamination and Toxicology, 2007, 78: 71~75.
[114] Zhang P, Song J M, Yuan H M. Persistent organic pollutant residues in the sediments and mollusks from the Bohai Sea coastal areas, North China: An overview. Environment Internationla, 2008,(2009) : 632~646.
[115]邴欣,汝少国,姜明.久效磷对金鱼的环境雌激素效应的研究.高技术通讯, 2006, 16(11): 1195~1199.
[116]查金苗,王子健.利用日本青鳉早期发育阶段暴露评估排水的急、慢性毒性和内分泌干扰效应[J].环境科学学报, 2005, 25(12):1682-1686.
[117]程晓洁.久效磷对金鱼(Carassius Auratus)的遗传毒性研究.青岛:中国海洋大学, 2008.
[118]房燕,汝少国,邴欣等.久效磷对金鱼精巢超显微结构和特征性酶活性的影响.水产学报, 2007, 31(5): 568~574.
[119]冯静仪.关于农药的联合毒性.江苏农药, 1995, 2: 2-4, 34.
[120]谷艳芳,柳爱莲,丁圣彦,等.农药胁迫对草履虫个体生长和种群动态的影响.生态学杂志, 2007, 26 (5): 678~681.
[121]郭玉清,张志南,慕芳红,等.渤海海洋线虫与底栖桡足类数量之比的应用研究.海洋科学, 2002, 26 (12): 27~31.
[122]胡璟,张梦妮,邓惠文,等.不同性质天然水中铜在虹鳟(Oncorhynchus mykiss)鳃表的形态及对虹鳟的毒性[J].应用与环境生物学报, 2005,11(6):714-716.
[123]康跃惠,张干,盛国英,等.固相萃取法测定水源地中的有机磷农药[J].中国环境科学, 2000,20(1): 1~4.
[124]柯丽霞,席贻龙,査春旺,等.甲胺磷和17β-雌二醇对萼花臂尾轮虫实验种群动态的影响.应用生态学报, 2008, 19 (1): 157~162.
[125]李永波,胡先奇,向红琼.三种防治因子对南方根结线虫胚胎发育及二龄幼虫作用的比较.黔南民族师范学院学报, 2004, 24(3): 36~39.
[126]李永玉洪华生王新红等.厦门海域有机磷农药污染现状与来源分析.环境科学学报, 2005, 25(8): 1071~1077.
[127]刘学,李贤相,江隆久等.μ-cell法测定农药对男性精子机能影响的分析.疾病控制杂志, 1999, 3(2): 84~87.
[128]陆秀红,刘志明,刘纪霜等.白花曼陀罗叶总碱提取物杀线活性及其作用机理研究.中国农学通报, 2006, 22(12): 331~334.
[129]汝少国,李永祺.有机磷农药对扁藻的联合毒性研究.青岛海洋大学学报:自然科学版, 1996, 26 (2): 197~202.
[130]史清毅,汝少国,邴欣.久效磷对雄性孔雀鱼生殖毒性研究.安全与环境学报, 2007, 7(3): 4~9.
[131]史清毅.久效磷对斑马鱼(Danio rerio)2世代繁殖的影响.青岛:中国海洋大学, 2007.
[132]孙金秀,陈波,姚佩佩.农药混剂联合毒性评价.卫生研究, 2000, 29 (2): 65~68.
[133]谭福杰,沈晋良,陈进.杀虫剂混合应用的研究.南京农业大学学报, 1987, 4(增刊): 146~149.
[134]王摆,汝少国,王蔚.久效磷对细小色矛线虫胚胎发育和繁殖的影响.中国环境科学2009, 29(5): 362~367.
[135]王摆,汝少国,于子山等.自由生活海洋线虫Chromadorina sp.的生活史研究.水生生物学报, 2007, 31(5): 751~754.
[136]王摆.以海洋线虫Chromadorina sp.为模型动物的环境激素活体筛选的初步研究.青岛:中国海洋大学,2006.
[137]王凌,黎先春,殷月芬等.莱州湾水体中有机磷农药的残留监测与风险影响评价.安全与环境学报,2007,7(3): 83~85.
[138]王硕治.久效磷对自由生活海洋线虫Chromadorina sp.的亚致死毒性效应研究.青岛:中国海洋大学,2007.
[139]王悠,唐学玺,李永祺.蒽与有机磷农药对海洋微藻的联合毒性.海洋科学, 2000, 24(4): 5~7.
[140]王毓秀,张利民,邹敏.化学农药与环境激素.农村生态环境, 1999, 15 (4): 37~41.
[141]魏渲辉,汝少国,姜明,等.久效磷对美国红鱼鳃Na+/K+-ATP酶活性和超显微结构的影响.应用生态学报, 2003, 14(12): 2289~2294.
[142]魏子昌.湖北省水资源开发利用现状及保护问题浅论.水资源保护, 1988, 4: 96~101.
[143]文艳华,冯志新,陈立等.三尖杉枝叶粉末防治花生根结线虫病.植物保护学报, 2004, 31(2): 161~165.
[144]徐炜.高效液相色谱法测定环境水体中8种农药残留量.环境与健康杂志, 2000, 17(6): 362~363.
[145]闫建国,汝少国,邴欣等.久效磷对黄鳝过氧化氢酶和Na+/K+-ATP酶活性的影响.环境科学研究, 2006b, 19(3): 96~100.
[146]闫建国,汝少国,王蔚.久效磷对黄鳝乙酰胆碱酯酶、羧酸酯酶和磷酸酶活性的影响[J].安全与环境学报, 2006a, 6(3): 61~63.
[147]杨超,佟延功,崔国权,等.西泉眼水库及周围地区林丹环境污染调查.中国公共卫生, 2005, 21 (2): 236.
[148]杨家新,王笑,周宁.三种农药对萼花臂尾轮虫种群变动的影响初探.淡水渔业, 2004, 34 (2): 02~22.
[149]杨景辉.土壤污染与防治.北京:科学出版社, 1995, 290~291.
[150]尹明泉.农药对地下水污染评价方法的探讨.山东地质情报, 1992, 4: 19~23.
[151]张波,李鹏.食品中有机磷杀虫剂残留对人体健康的损害作用.中国食品学报, 2004,4(4): 98~102.
[152]张秋菊,程晓华,魏昭荣,等.新疆地下水中农药污染水平调查.干旱环境监测, 2001, 15 (3): 159~161.
[153]张一宾,孙晶.国外有机磷农药的概况及对我国有机磷农药发展的看法.农药, 1999, 38: 1~3.
[154]张志南,党宏月,于子山.青岛湾有机质污染带小型底栖生物群落的研究.青岛海洋大学学报:自然科学版, 1993, 23(1): 83~91.
[155]朱琳,史淑洁.斑马鱼胚胎发育技术在毒性评价中的应用[J].应用生态学报, 2002,13(2): 252~254.
[2] Amjad S, Gray J S. Use of the nematode-copepod ratio as an index of organic pollution. Mar. Pollut. Bull., 1983, 14:178-181.
[3] Anderson P.D., and L.J. Weber. The toxicity to aquatic populations of mixtures containing certain heavy metals. Proceedings, International Conference on Heavy Metals in the Environment, Toronto, ON, Canada, 1975, October 27–31, pp. 933–953.
[4] Anderson S, Sadinski W, Shugart L, et al. Genetic and molecular ecotoxicology: a research framework, Environ. Health Perspect., 1994, 102: 3~8.
[5] Andre P S. Evolution of the control of sexual identity in nematodes. Seminars in Cell & Developmental Biology, 2007, 18: 362~370.
[6] Atienzar F A, Conradi M, Evenden A J, et al. Qualitative assessment of genotoxicity using random amplified polymorphic DNA: comparison of genomic template stability with key fitness parameters in Daphnia magna exposed to benzo[α]pyrene [J]. Environ.Toxicol.Chem., 1999, 18: 2275-2282.
[7] Atienzar F A, Cordi B, Donkin M E, et al. Comparison of ultraviolet-induced genotoxicity detected by random amplified polymorphic DNA with chlorophyll fluorescence and growth in a marine macroalgae, Palmaria palmate [J]. Aquat.Toxicol., 2000, 50:1-12.
[8] Atienzar F A, Jha A N. The random amplified polymorphic DNA (RAPD) assay to determine DNA alterations, repair and transgenerational effects in B(a)P exposed Daphnia magna. Mutation Research, 2004, 552: 125~140.
[9] Atienzar F A, Venier P, Jha A N, et al. Evaluation of the random amplified polymorphic DNA(RAPD) assay for the detection of DNA damage and mutations. Mutation Research, 2002, 521: 151~163.
[10] Atienzar F A, Victoria V C, Awadhesh N J, et al. Fitness parameters and DNA effects are sensitive indicators of copper induced toxicity in Daphnia magna [J]. Toxicol.Sci., 2001, 59: 241~250.
[11] Atkinson A, Siegel V, Pakhomov E, et al. Long-term decline in krill stock and increase in salps within the Southern Ocean. Nature, 2004, 432: 100~103.
[12] Becerril C, Acevedo H, Ferrero M, et al. DNA fingerprint comparison of rainbow trout and RTG-2 cell lineusing random amplified polymorphic DNA. Ecotoxicology, 2001, 10: 115~124.
[13] Becerril C, Ferrero M, Sanz F, et al. Detection of mitomycin C-induced genetic damage in fish cells by use of RAPD. Mutagenesis, 1999, 14: 449~456.
[14] Belfiore N M, Anderson S L. Effects of contaminants on genetic patterns in aquatic organisms: a review. Mutat. Res., 2001, 489: 97~122.
[15] Berenbaum M C. What is synergy? Pharmacol Rev, 1989, 41: 93.
[16] Bernardes A T. Mutation load and the extinction of large populations. Physica A, 1996, 230: 156~173.
[17] Bickham J W, Sandhu S, Hebert P D N, et al. Effects of chemical contaminants on genetic diversity in natural populations: implications for biomonitoring and ecotoxicology. Mutat. Res., 2000, 463: 33~51.
[18] Bliss C I. The toxicity of poisons applied jointly .Ann Appl Biol,1939, 26:585~615.
[19] Bolognesi C, Giada F, Claudia L, et al. Genotoxicity biomarkers in Mytilus galloprovincialis: wild versus caged mussels. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 2004, 552(1-2): 153~162.
[20] Brock T J, Browse J, Watts J L. Fatty acid desaturation and the regulation of adiposity in Caenorhabditis elegans. Genetics, 2007, 176: 865~875.
[21] Bustnes J O, Helberg M, Strann K B, et al. Environmental pollutants in endangered vs. increasing subspecies of the lesser black-backed gull on the Norwegian Coast. Environmental Pollution, 2006, (144)3: 893~901.
[22] Byerly L, Cassada R. C., Russell R. L. The life cycle of the nematode Caenorhabditis elegans I Wild-type growth and reproduction. Developmental Biology, 1976, 51:23~33.
[23] Casta?o A, Becerril C. In vitro assessment of DNA damage after short-and long-term exposure to benzo(a)pyrene using RAPD and the RTG-2 fish cell line. Mutation Research, 2004, 552: 141~151.
[24] Channa K, Nagalakshmi K, Gu Z. Genomic instability in silica and cadmium chloride- transformed BALB/c-3T3 and tumor cell lines by random amplified polymorphic DNA analysis [J]. Mutation Research, 1999, 425:117-123.
[25] Chiang S H, MacDougald O A. Will fatty worms help cure human obesity? Trends in Genetics, 2003, 19(10): 523~525.
[26] Chow Hu H, Pasternak J. Protein changes during maturation of the free-living nematode Panagrellus silusiae. J. Exp. Zool., 1969, 170:77-84.
[27] Clark W C. Hermaphroditism as a reproductive strategy for metazoans some correlated benefits. NZ J Zool, 1978, 5(4):769~80.
[28] Colborn T, Dumanoski D, Myers J P. Our Stolen Future. New York, Duuten, 1996, 1~60.
[29] Cronin M A, Bickham J W. A population genetic analysis of the potential for a crude oil spill to induce heritable mutations and impact natural populations. Ecotoxicology. 1998, 7: 259~278.
[30] Davidson C. Declining downwind : amphibian population declines in california and historical pesticide use. Ecological Applications, 2004, 14(6): 1892~1902.
[31] Diekmann M, Hultsch V, Nagel R. On the relevance of genotoxicity for fish populations I: effects of a model genotoxicant on zebrafish (Danio rerio) in a complete life-cycle test [J]. Aquatic Toxicology, 2004,68:13-26.
[32] Ferrando M D, Janssen C R, Andreu E, et al. Ecotoxicological studies with the freshwater rotifer Brachionus calyciflorus. II. An assessment of the chronic toxicity of lindane and 3,4-dichloroaniline using life tables. Hydrobiologia, 1993, 255~256(1): 33~40.
[33] Fry and Toone. DDT-induced feminization of gull embryos. Science, 1981, 213(4510): 922~924.
[34] Gama-Flores J L, Sarma S S S, Nandini S. Acute and chronic toxicity of the pesticide methyl parathion to the rotifer Brachionus angularis (Rotifera) at different algal (Chlorella vulgaris) food densities. Aquatic Ecology, 2004, 38: 27~36.
[35] Gao J J, Liu L H, Liu X R, et al. Occurrence and distribution of organochlorine pesticides-lindane, p, p’-DDT, and heptachlor epoxide-in surface water of China. Environment International, 2008, 34: 1097~1103.
[36] Ghiselin MT. The evolution of hermaphroditism among animals. Q Rev Biol, 1969, 44(2):189~208.
[37] Gillespie R B, Guttman S I. Chemical-induced changes in the genetic structure of populations: effects on allozymes, in: V. E. Forbes (Ed.), Genetics and Ecotoxicology, Taylor & Francis, Philadelphia, 1999, pp. 55~77.
[38] Goodbell P B, Ferris H. Influence of environmental factors on the hatch and survival of Meloidogyne incognita [J]. Journal of Nematology, 1989,21(3):328~334.
[39] Guillette L J, Jr, Gunderson M P. Alterations in development of reproductive and endocrine systems of wildlife populations exposed to endocrine-disrupting contaminants. Reproduction, 2001, 122: 857~864.
[40] Hans D W, Ronny B, Thierry B. The population genetic of littorea (Mollusca: Gastropoda) along a pollution in the Scheldt estuary (The Netherlands) using RAPD analysis [J]. Science of Total Environment, 2004, 325:59-69.
[41] Harris F A, Chambers H W. Interaction of insecticidal mixtures in Tobacco Budworm. J Econ Entomol, 1973, 66(2): 517~518.
[42] Hartl D L, Clark A G. Principles of Population Genetics, second ed., Sinauer Associates, Inc., Suderland,USA, 1998.
[43] Hebert P D N, Luiker M M. Genetic effects of contaminant exposure—towards an assessment of impacts on animal populations. Sci. Total Environ, 1996, 191: 23~58.
[44] Heip C., Smol N., Absillis V. Influence of temperature on the reproductive potential of Oncholaimus oxyuris. Mar. Biol., 1978, 45: 255~260.
[45] Hellerer T, Axang C, Brackmann C, et al. Monitoring of lipid storage in Caenorhabditis elegans using coherent anti-Stokes Raman scattering (CARS) microscopy, Proc. Natl. Acad. Sci. U. S. A., 2007, 104: 14658~14663.
[46] Howell R. Acute toxicity of heavy metals to two species of marine nematodes Marine Environmental Research, Volume 11, Issue 3, 1984, Pages 153~161.
[47] Huang D J, Chen H C, Wu J P, et al. Reproduction obstacles for the female green neon shrimp (Neocaridina denticulata). Chemosphere, 2006, 64: 11~16.
[48] Huang L, Xi Y L, Zha C W, et al. Effect of Aldrin on Life History Characteristics of Rotifer Brachionus calyciflorus Pallas. Bulletin of Environmental Contamination and Toxicology, 2007, 79: 524~528.
[49] Hunt E G, Bischoff A I. Inimical effects on wildlife of periodic DDD applications to Clear Lake. Calif. Fish Game, 1960, 46: 91~105.
[50] Ide H, Petrullo L A, Hataet Z, etal. Processing of DNA base damage by DNA polymerases dihydrothymine and b-ureidoisobutyric acid as models forinstructive and noninstructive lesions. J. Biol. Chem. 1991, 266: 1469~1477.
[51] Jaensson A, Scott A P, Moore A, et al. Effects of a pyrethroid pesticide on endocrine responses to female odours and reproductive behaviour in male parr of brown trout (Salmo trutta L.). Aquatic Toxicology, 2007, 81: 1~9.
[52] Jensen K M, Korte J J, Kahl M D, et al. Aspects of basic reproductive biology and endocrinology in the fathead minnow (Pimephales promelas) [J]. Comparative Biochemistry and Physiology Part C, 2001,128:127-141.
[53] Jensen P. Food ingestion and growth of the diatom-feeding nematode chromadorita tenuis. Marine Biology, 1984, 81:307-310.
[54] Jones K C, Voogt Pde. Persistent organic pollutant (POPS): state of the science. Environmental Pollution, 1999, 100: 209~221.
[55] Josephine A H, Franck A A, Awadhesh N J. Genotoxic, cytotoxic, developmental and survival effects oftritiated water in the early life stages of the marine mollusc, Mytius edulis [J]. Aquatic Toxicology, 2005, 74:205~217.
[56] Keplinger M L, Deichmann W B. Acute toxicity of combinations of pesticides, Toxicol Appl Phamacol, 1967, 10(3): 586~595.
[57] Kimble J, Sharrock W. J. Tissue-specific synthesis of yolk proteins in Caenorhabditis elegans. Dev. Biol., 1983, 96 (1):189~196.
[58] Kniazeva M, Crawford Q T, Seiber M, et al. Monomethyl branchedchain fatty acids play an essential role in Caenorhabditis elegans development, PLoS Biol. 2004, 2, E257.
[59] Kohra S, Kuwahara K, Takao Y, et al. Effect of Bisphenol A on the Feeding Behavior of Caenorhabditis elegans. Journal of health science, 2002, 48(1): 93~95.
[60] Kulshrestha S K, Arora Neelam. Impairments induced by sublethal doses of two pesticides in the ovaries of a freshwater teleost Channa striatus bloch. Toxicology Letters, 1984, (20)1: 93~98.
[61] Liu W, Li P J, Qi X M, et al. DNA changes in barley (Hordeum vulgare) seedlings induced by cadmium pollution using RAPD analysis. Chemosphere, 2005, 61: 158~167.
[62] Macdonald R W, Barrie L A, Bidleman T F. Contaminants in the Canadian Arctic: 5 years of progress in understanding sources, occurrence and pathways. The Science of the Total Environment, 2000, 264: 93~234.
[63] Macek K J, Buxton K S, Derr S K, et al. Chronic toxicity of lindane to selected aquatic invertebrates and fishes. Environmental Protection Agency, Report EPA-600/3-76-046, 1976: 50.
[64] Mahmoudi E, Essid N, Beyrem H, et al. Individual and combined effects of lead and zinc on a free-living marine nematode community: Results from microcosm experiments. Journal of Experimental Marine Biology and Ecology, 2007, 343 (2): 217~226.
[65] Mckay R M, Mckay J P, Avery L, et al. C.elegans: a model for exploring the genetics of fat storage. Developmental Cell, 2003, 4: 131~142.
[66] Mengoni A, Gonnelli C, GalaMi F. Genetic diversity and heavy metal tolerance in populations of Silecw paradoxa L.(Caryophyllaeeae):a random anaplified polymorphic DNA analysis [J]. Mol.Ecol, 2000, 9: 1319~1324.
[67] Menzel R, Yeo H L, Rienau S, et al. Cytochrome P450s and short-chain dehydrogenases mediate the toxicogenomic response of PCB52 in the nematode Caenorhabditis elegans. J Mol Biol, 2007, 370: 1~13.
[68] Mukhopadhyay A, Deplancke B, Walhout A J M, et al. C.elegans tubby regulates life span and fat storage by two independent mechanisms. Cell Metabolism, 2005, 2: 35~42.
[69] Mullaney B C, Ashrafi K. C.elegans fat storage and metabolic regulation. Biochimica et Biophysica Acta, 2009, unpublished.
[70] Muthanna A. AI-Omar, Nehla H, et al. Residues of organochlorine insecticides in fish from polluted Water. Bull. Environ. Contam. Toxicol. 1986, 36: 109~113.
[71] Neelamegam P, Rajendran A, Maruthanayagam C, et al. Design and development of embedded system for the study of the biochemical variations induced by monocrotophos in Cyprinus carpio. Measurement, 2007, 40: 372~377.
[72] Nelson J R, Lawrence C W, Hinkle D C. Thymine-thymine dimmer bypass by yeast DNA-polymerase-zeta. Science, 1996, 272: 1646~1649.
[73] Pesando D, Robert S, Huitorel P. Effects of methoxychlor, dieldrin and lindane on sea urchin fertilization and early development. Aquatic Toxicology. 2004, 66: 225~239.
[74] Placket R L,Hewiett P S. Journal of the Royal Statistical Soeiety Series,1952, B14: 143~163.
[75] Platt H M, Warwick R M. The significance of free-living nematodes to the littoral ecosystem. The shore environment, 1980, 2:729-759.
[76] Platt H M., Warwick R M. Free-living marine nematodes Part I British Enoplids. Cambridge London New York. New Rochelle Melbourne Sydney. The Linnean Sciety of London and The Estuarine and Brackish-water. Sciences Association Cambridge University Press, 1983:1-8.
[77] Raffaelli D G, Mason C F. Pollution monitoring with meiofauna using the ratio of nematodes to copepods. Mar. Pollut. Bull., 1981, 12:158-163.
[78] Roche H, Buet A, Ramade F. Relationships between persistent organic chemicals residues and biochemical constituents in fish from a protected area: the French National Nature Reserve of Camargue. Comparative Biochemistry and Physiology Part C, 2002, 133: 393~410.
[79] Rothman W. Present at the environmental risk assessment conference. Alexandria V A,1988 Sep 21.
[80] Saleha B B, Danadevi K, Rahman M F, et al. Genotoxic effect of monocrotophos to sentinel species using comet assay. Food and Chemical Toxicology, 2001, 39(4):361~366.
[81] Sarma S S S, Nandini S, Gama-Flores J L. Effects of methyl parathion on the population growth of the rotifer Brachionus patulus (Muller) under different algal food (Chlorella vulgaris) densities. Ecotoxicology and Environm ental Safety, 2001, 48: 190~195.
[82] Semenza J C, Tolbert P E, Rubin C H, et al. Reproductive toxins and alligator abnormalities at Lake Apopka, Florida[J].Environmmental Health Perspectives. 1997, 105(10): 1030~1032.
[83] Silvestroni L, Fiorini R, Palleschi S. Partition of the organochlorine insecticide lindane into the human sperm surface induces membrane depolarization and Ca2+ influx. Biochem. J., 1997, 321: 691~698.
[84] Simpson V R, Bain M S, Brown R, et al. A long-term study of vitamin A and polychlorinated hydrocarbon levels in otters (Lutra lutra) in south west England. Environmental Pollution, Volume 110, Issue 2, November 2000, Pages 267~275.
[85] Singh P B, Sahu V, Singh V, et al. Sperm motility in the fishes of pesticide exposed and from polluted rivers of Gomti and Ganga of north India. Food and Chemical Toxicology, 2008, 46: 3764~3769.
[86] Staton J L, Schizas N V, Chandler G T, et al. Ecotoxicology and population genetics: the emergence of“phylogeographic and evolutionary ecotoxicology”. Ecotoxicology, 2001, 10: 217~222.
[87] Susan G N, Lee K L, Adams S M. Evaluation alterations of genetic diversity in sunfish populations exposed to contaminants using RAPD assay [J]. Aquatic Toxicology, 1998, 43:163-178.
[88] Theodorakis C W, Shugart L R. Genetic ecotoxicology II: population genetic structure in mosquitofish exposed in situ to radionuclides. Ecotoxicology, 1997, 6: 335~354.
[89] Theodorakis C W. Integration of genotoxic and population genetic endpoints in biomonitoring and risk assessment. Ecotoxcicology, 2001, 10: 245~256.
[90] Tietjen J H, Lee J J. The use of free-living nematodes as a bioassay for estuarine sediments. Marine Environmental Research, 1984, 11: 233~251.
[91] Tominaga N, Kazuhiro U, Masato K, et al. Caenorhabditis elegans Responses to Specific Steroid Hormones. Journal of Health Science, 2003, 49(1):28-33.
[92] Tominaga N, Mineko T, Shiya K, et al. A Convenient Sublethal Assay of Alkylphenol and Organotin Compounds Using the Nematode Caenorhabditis elegans. Journal of Health Science, 2002, 48(6):555-559.
[93] Tominaga N, Shiya K, Taisen I, et al. Effects of Perfluoro Organic Compound Toxicity on Nematode Caenorhabditis elegans Fecundity. Journal of Health Science, 2004, 50(5):545-550.
[94] Tominaga N, Shiya K, Taisen I, et el. A Multi-Generation Sulblethal Assay of Phenols Using the nematode Caenorhabditis elegans. Journal of Health Science, 2003, 49(6):459~463.
[95] Ura K, Toshinori K, Sachiko S, et al. Aquatic Acute Toxicity Testing Using the Nematode Caenorhabditis elegans. Journal of Health Science, 2002, 48(6) 583-586.
[96] Van Gilst M R, Hadjivassiliou H, Yamamoto K R. A Caenorhabditis elegans nutrient response system partially dependent on nuclear receptor NHR-49, Proc. Natl. Acad. Sci. U. S. A. 2005, 102: 13496~13501.
[97] Vonier P M, Crain D A, McLachlan J A, et al. Interaction of environmental chemicals with the estrogen andprogesterone receptors from the oviduct of the American alligator. Environmental Health Perspectives, 1996, 104 1318–1322.
[98] Vrank G., Heip C. Calculation of the intrinsic rate of natural increase rm with Rhabditis marina. Nematologica, 1983, 29: 468~477.
[99] Vranken G, Brussel V D. Vanderheaghen R. Research on the development of a standardized ecotoxicological test on marine nematodes I culture conditions and critearia for two Monhysterids Monhystera disjuncta and Monhystera microphthalma. Ecotoxicological Testing For The Marine Environment, 1984, 2(588):159~184.
[100] Vranken G, Heip C. Toxicity of copper, mercury and lead to a marine nematode Marine Pollution Bulletin, 1986, 17(10): 453~457.
[101] Vranken G, TiréC, Heip C. Effect of temperature and food on hexavalent chromium toxicity to the marine nematode Monhystera disjuncta Marine Environmental Research, 1989, 27(2): 127~136.
[102] Wadsworth W G, Riddle D L. Developmental regulation of energy metabolism in Caenorhabditis elegans. Dev. Biol., 1989, 132: 167~173.
[103] Warwick R M. Survival strategies of meiofauna In feeding and surviva strategies of estuarine organisms. Plenum, New York. N. V. Jones and W. J. Wolff. 1981b:39-52.
[104] Warwick R M. The influence of temperature and salinity on energy partitioning in the marine nematode Diplolaimelloides bruciei. Oecologia, 1981a, 51:318-325.
[105] Wester P W. Histopathological effects of environmental pollutantsβ-HCH and methyl mercury on reproductive organs in freshwater fish. Comparative Biochemistry and Physiology Part C: Comparative Pharmacology, 1991, (100)1-2: 237-239.
[106] White J. The anatomy in the Nematode Caenorhabditis elegans. W. W. Wood, editor. Cold Spring Harbor Laboratory Press. Cold Spring Harbor N.Y., 1988:81~122.
[107] WHO. Combination Effectsin Chemical carcinogenesis. Newyork: VCH Publishers. 1988: 5~20.
[108] WHO. Technic Report Seris. 1981, 662: 8~9.
[109] Wiemeyer S M , Bunck C M, Stafford C J.Environmental contaminants in bald eagles eggs--1980-84--and further interpretations of relationships to productivity and shell thickness. Arch. Environ. Contam. Toxicol. 1993.24, 213~227.
[110] Winter M J, Norman D, Ruth A H, et al. DNA strand breaks and adducts determined in feral and caged chub (Leuciscus cephalus) exposed to rivers exhibiting variable water quality around Birmingham, UK. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 2004, 552 (1-2): 163~175.
[111] Wolf H De, Blust R, Bacekljau T. The population genetic structure of Littorina littorea (Mollusca: Gastropoda) along a pollution gradient in the Scheldt estuary (The Netherlands) using RAPD analysis. Science of the Total Environment, 2004, 325: 59~69.
[112] Wright S. Evolution in Mendelian populations. Genetics, 1931, 16: 97~159.
[113] Zha C W, Xi Y L, Huang L, et al. Effect of Sublethal Exposure to Chlordecone on Life History Characteristics of Freshwater Rotifer Brachionus calyciflorus Pallas. Bulletin of Environmental Contamination and Toxicology, 2007, 78: 71~75.
[114] Zhang P, Song J M, Yuan H M. Persistent organic pollutant residues in the sediments and mollusks from the Bohai Sea coastal areas, North China: An overview. Environment Internationla, 2008,(2009) : 632~646.
[115]邴欣,汝少国,姜明.久效磷对金鱼的环境雌激素效应的研究.高技术通讯, 2006, 16(11): 1195~1199.
[116]查金苗,王子健.利用日本青鳉早期发育阶段暴露评估排水的急、慢性毒性和内分泌干扰效应[J].环境科学学报, 2005, 25(12):1682-1686.
[117]程晓洁.久效磷对金鱼(Carassius Auratus)的遗传毒性研究.青岛:中国海洋大学, 2008.
[118]房燕,汝少国,邴欣等.久效磷对金鱼精巢超显微结构和特征性酶活性的影响.水产学报, 2007, 31(5): 568~574.
[119]冯静仪.关于农药的联合毒性.江苏农药, 1995, 2: 2-4, 34.
[120]谷艳芳,柳爱莲,丁圣彦,等.农药胁迫对草履虫个体生长和种群动态的影响.生态学杂志, 2007, 26 (5): 678~681.
[121]郭玉清,张志南,慕芳红,等.渤海海洋线虫与底栖桡足类数量之比的应用研究.海洋科学, 2002, 26 (12): 27~31.
[122]胡璟,张梦妮,邓惠文,等.不同性质天然水中铜在虹鳟(Oncorhynchus mykiss)鳃表的形态及对虹鳟的毒性[J].应用与环境生物学报, 2005,11(6):714-716.
[123]康跃惠,张干,盛国英,等.固相萃取法测定水源地中的有机磷农药[J].中国环境科学, 2000,20(1): 1~4.
[124]柯丽霞,席贻龙,査春旺,等.甲胺磷和17β-雌二醇对萼花臂尾轮虫实验种群动态的影响.应用生态学报, 2008, 19 (1): 157~162.
[125]李永波,胡先奇,向红琼.三种防治因子对南方根结线虫胚胎发育及二龄幼虫作用的比较.黔南民族师范学院学报, 2004, 24(3): 36~39.
[126]李永玉洪华生王新红等.厦门海域有机磷农药污染现状与来源分析.环境科学学报, 2005, 25(8): 1071~1077.
[127]刘学,李贤相,江隆久等.μ-cell法测定农药对男性精子机能影响的分析.疾病控制杂志, 1999, 3(2): 84~87.
[128]陆秀红,刘志明,刘纪霜等.白花曼陀罗叶总碱提取物杀线活性及其作用机理研究.中国农学通报, 2006, 22(12): 331~334.
[129]汝少国,李永祺.有机磷农药对扁藻的联合毒性研究.青岛海洋大学学报:自然科学版, 1996, 26 (2): 197~202.
[130]史清毅,汝少国,邴欣.久效磷对雄性孔雀鱼生殖毒性研究.安全与环境学报, 2007, 7(3): 4~9.
[131]史清毅.久效磷对斑马鱼(Danio rerio)2世代繁殖的影响.青岛:中国海洋大学, 2007.
[132]孙金秀,陈波,姚佩佩.农药混剂联合毒性评价.卫生研究, 2000, 29 (2): 65~68.
[133]谭福杰,沈晋良,陈进.杀虫剂混合应用的研究.南京农业大学学报, 1987, 4(增刊): 146~149.
[134]王摆,汝少国,王蔚.久效磷对细小色矛线虫胚胎发育和繁殖的影响.中国环境科学2009, 29(5): 362~367.
[135]王摆,汝少国,于子山等.自由生活海洋线虫Chromadorina sp.的生活史研究.水生生物学报, 2007, 31(5): 751~754.
[136]王摆.以海洋线虫Chromadorina sp.为模型动物的环境激素活体筛选的初步研究.青岛:中国海洋大学,2006.
[137]王凌,黎先春,殷月芬等.莱州湾水体中有机磷农药的残留监测与风险影响评价.安全与环境学报,2007,7(3): 83~85.
[138]王硕治.久效磷对自由生活海洋线虫Chromadorina sp.的亚致死毒性效应研究.青岛:中国海洋大学,2007.
[139]王悠,唐学玺,李永祺.蒽与有机磷农药对海洋微藻的联合毒性.海洋科学, 2000, 24(4): 5~7.
[140]王毓秀,张利民,邹敏.化学农药与环境激素.农村生态环境, 1999, 15 (4): 37~41.
[141]魏渲辉,汝少国,姜明,等.久效磷对美国红鱼鳃Na+/K+-ATP酶活性和超显微结构的影响.应用生态学报, 2003, 14(12): 2289~2294.
[142]魏子昌.湖北省水资源开发利用现状及保护问题浅论.水资源保护, 1988, 4: 96~101.
[143]文艳华,冯志新,陈立等.三尖杉枝叶粉末防治花生根结线虫病.植物保护学报, 2004, 31(2): 161~165.
[144]徐炜.高效液相色谱法测定环境水体中8种农药残留量.环境与健康杂志, 2000, 17(6): 362~363.
[145]闫建国,汝少国,邴欣等.久效磷对黄鳝过氧化氢酶和Na+/K+-ATP酶活性的影响.环境科学研究, 2006b, 19(3): 96~100.
[146]闫建国,汝少国,王蔚.久效磷对黄鳝乙酰胆碱酯酶、羧酸酯酶和磷酸酶活性的影响[J].安全与环境学报, 2006a, 6(3): 61~63.
[147]杨超,佟延功,崔国权,等.西泉眼水库及周围地区林丹环境污染调查.中国公共卫生, 2005, 21 (2): 236.
[148]杨家新,王笑,周宁.三种农药对萼花臂尾轮虫种群变动的影响初探.淡水渔业, 2004, 34 (2): 02~22.
[149]杨景辉.土壤污染与防治.北京:科学出版社, 1995, 290~291.
[150]尹明泉.农药对地下水污染评价方法的探讨.山东地质情报, 1992, 4: 19~23.
[151]张波,李鹏.食品中有机磷杀虫剂残留对人体健康的损害作用.中国食品学报, 2004,4(4): 98~102.
[152]张秋菊,程晓华,魏昭荣,等.新疆地下水中农药污染水平调查.干旱环境监测, 2001, 15 (3): 159~161.
[153]张一宾,孙晶.国外有机磷农药的概况及对我国有机磷农药发展的看法.农药, 1999, 38: 1~3.
[154]张志南,党宏月,于子山.青岛湾有机质污染带小型底栖生物群落的研究.青岛海洋大学学报:自然科学版, 1993, 23(1): 83~91.
[155]朱琳,史淑洁.斑马鱼胚胎发育技术在毒性评价中的应用[J].应用生态学报, 2002,13(2): 252~254.