硒对亚急性砷中毒鸡脑损伤影响的研究
摘要
砷和硒均属于非金属元素。试验研究表明一定剂量的硒具有促使砷从体内排出从而缓解砷中毒导致的损伤,发挥一定的保护作用。本试验在此基础上,观察在饲料中添加砷和不同剂量的硒对雏鸡脑组织氧化损伤和神经传导递质相关指标的影响。
试验选取一日龄艾维茵肉鸡200只,随机分成对照组(基础日粮,含砷0.1 mg/kg.含硒0.2mg/kg),染砷组(日粮含As3mg/kg、含硒0.2mg/kg）、低硒组(日粮含As3mg/kg+Se5mg/kg)、中硒组(日粮含As3mg/kg+Se 1 Omg/kg)、高硒组(日粮含As3mg/kg+Se 15mg/kg)五组。在14、21、28、35、42日龄时,每组随机抽取4只进行脑组织样品采集,检测脑组织谷胱甘肽(GSH)含量及谷胱甘肽过氧化物酶(GSH-Px)活性、一氧化氮(NO)含量及一氧化氮合酶(NOS)活性、谷氨酸(Glu)浓度及谷氨酰胺合成酶(GS)活性、乙酰胆碱酯酶(TchE)活性、脑细胞凋亡率等指标的变化情况。
试验结果表明：(1)在试验期间,各试验组脑组织重均呈现出重量增加的趋势,各试验组之间脑组织的重量比较无显著差异；(2)染砷组(As3mg/kg)和高硒组(Se15mg/kg)呈现脑组织蛋白质含量降低趋势,低硒组(As3 mg/kg+Se5mg/kg)和中硒组(As3mg/kg+Se10mg/kg)对3mg/kg;砷造成的脑组织蛋白质含量降低有一定保护作用；(3)单独添加砷的染砷组可致雏鸡脑组织氧化损伤,神经递质发生紊乱,并且使脑细胞凋亡率增加；(4)低硒组和中硒组的硒添加量在氧化损伤方面可以对砷(As3mg/kg)起到拮抗作用,改善砷对脑组织造成的GSH含量和GSH-Px活性、NO含量和NOS活性降低的状况,进而达到改善雏鸡脑组织的氧化应激；(5)低硒组和中硒组的硒添加量对砷造成神经递质紊乱能起到改善的作用,使Glu含量、GS活力、TchE活力趋向于正常状态,对砷造成的脑组织神经递质的紊乱有保护作用；(6)低硒组和中硒组的硒添加量对砷造成的脑组织细胞凋亡率增高起到了保护作用,使脑细胞凋亡状况趋向于正常水平；(7)高硒组的硒添加的剂量对3mg/kg申造成的损伤不能产生保护作用,试验测得结果呈现中毒状态,对脑组织造成的氧化损伤和神经递质紊乱的情况与染砷组的情况相似或更严重。
综上所述,3.0mg/kg饲料砷,能引起脑组织氧化损伤、神经递质紊乱和脑细胞凋亡率增加,对脑组织造成损伤。在饲料中添加硒(5mg/kg和1Omg/kg)能使砷对脑组织造成的GSH含量和GSH-Px活性、NO含量和NOS活性,Glu浓度和GS活性、TchE活性、脑细胞凋亡率紊乱恢复至接近正常水平,表明硒在该剂量下具有拮抗砷毒性的作用。而添加硒(15mg/kg)无此作用反而表现出中毒特性。
Both arsenic and selenium belong to nonmetal. Early studies indicated that arsenic coude be eliminated from the body by selenium and the injury caused by arsenicthat can be recuperated by eliminated. Based on those studies, the purpose of this study is to surve the effect of oxidative and neurotransmitter metabolic disorders on chick caused by arsenic and the different doses of selenium which were added in the composition of basal diets.
200 one-day-old Avian chickens were divided into five groups randomly. And then we fed on the chickens as the composition of basal diets as the follows:control group(basal diet, As O.1mg/kg+Se 0.2mg/kg), exposed group(basal diet, As3mg/kg), low selenium group(basal diet, As3mg/kg+Se5mg/kg), medium content of selenium group(basal diet,As3mg/kg+Sel0mg/kg), high selenium group (basal diet,As3mg/kg+Sel5mg/kg).4 samples of brain tissue were collected randomly and preserved on at 14,21,28,35,42 days. The samples were also tested for glutathione (GSH) contents and glutathione peroxidase (GSH-Px) activity, nitric oxide (NO) contents and nitric oxide synthase (NOS) activity, glutamic acid (Glu) concentration and glutamine synthetase(GS) activity, acetylcholinesterase (TchE) activity and the percentage of the brain cells apoptosis.
The experimental results showed that (1) the brain weight of tests in each group increased in the experiment period and there was no significant difference between groups; (2) the influence caused by arsenic and selenium about the brain protein contents of groups was not obvious; (3) arsenic added into the exposed group can cause brain oxidative damage, neurotransmitter metabolic disorders and the brain cell apoptosis rate increase; (4) selenium added into the low selenium group and the high selenium group could protect against the effects of arsenic on oxidative damage actively, alleviates the situation that GSH contents, GSH-Px activity, NO contents and NOS activity were reduced by arsenic, and then ameliorates brain oxidative damage; (5) selenium added into the low selenium group and the medium content of selenium group could protect against the effects of arsenic on neurotransmitter metabolic disorders actively, makes Glu contents, GS activity and TchE activity tend to normal condition, and ameliorates neurotransmitter metabolic disorders caused by arsenic; (6) selenium added into the low selenium group and the medium content of selenium group could protect against the effects of arsenic on the brain cells apoptosis actively, and then makes this situation tend to normal condition; (7) Compared to other experimental groups, the high selenium group which added into selenium cannot make protective effectly. The test results showed the measured state of intoxication, the brain tissue caused by oxidative damage and neurotransmitter disorders, the situation was similar, exposed group or even more serious.
In short, oxidative and neurotransmitter metabolic disorders on brain can be caused on the concentration of As3mg/kg and this situation can be changed when selenium was added in on the concentration of Se5mg/kg and SelOmg/kg. The brain can be protected by selenium on that concentration, but it was useless to add in selenium on the concentration of Sel5mg/kg.
试验选取一日龄艾维茵肉鸡200只,随机分成对照组(基础日粮,含砷0.1 mg/kg.含硒0.2mg/kg),染砷组(日粮含As3mg/kg、含硒0.2mg/kg）、低硒组(日粮含As3mg/kg+Se5mg/kg)、中硒组(日粮含As3mg/kg+Se 1 Omg/kg)、高硒组(日粮含As3mg/kg+Se 15mg/kg)五组。在14、21、28、35、42日龄时,每组随机抽取4只进行脑组织样品采集,检测脑组织谷胱甘肽(GSH)含量及谷胱甘肽过氧化物酶(GSH-Px)活性、一氧化氮(NO)含量及一氧化氮合酶(NOS)活性、谷氨酸(Glu)浓度及谷氨酰胺合成酶(GS)活性、乙酰胆碱酯酶(TchE)活性、脑细胞凋亡率等指标的变化情况。
试验结果表明：(1)在试验期间,各试验组脑组织重均呈现出重量增加的趋势,各试验组之间脑组织的重量比较无显著差异；(2)染砷组(As3mg/kg)和高硒组(Se15mg/kg)呈现脑组织蛋白质含量降低趋势,低硒组(As3 mg/kg+Se5mg/kg)和中硒组(As3mg/kg+Se10mg/kg)对3mg/kg;砷造成的脑组织蛋白质含量降低有一定保护作用；(3)单独添加砷的染砷组可致雏鸡脑组织氧化损伤,神经递质发生紊乱,并且使脑细胞凋亡率增加；(4)低硒组和中硒组的硒添加量在氧化损伤方面可以对砷(As3mg/kg)起到拮抗作用,改善砷对脑组织造成的GSH含量和GSH-Px活性、NO含量和NOS活性降低的状况,进而达到改善雏鸡脑组织的氧化应激；(5)低硒组和中硒组的硒添加量对砷造成神经递质紊乱能起到改善的作用,使Glu含量、GS活力、TchE活力趋向于正常状态,对砷造成的脑组织神经递质的紊乱有保护作用；(6)低硒组和中硒组的硒添加量对砷造成的脑组织细胞凋亡率增高起到了保护作用,使脑细胞凋亡状况趋向于正常水平；(7)高硒组的硒添加的剂量对3mg/kg申造成的损伤不能产生保护作用,试验测得结果呈现中毒状态,对脑组织造成的氧化损伤和神经递质紊乱的情况与染砷组的情况相似或更严重。
综上所述,3.0mg/kg饲料砷,能引起脑组织氧化损伤、神经递质紊乱和脑细胞凋亡率增加,对脑组织造成损伤。在饲料中添加硒(5mg/kg和1Omg/kg)能使砷对脑组织造成的GSH含量和GSH-Px活性、NO含量和NOS活性,Glu浓度和GS活性、TchE活性、脑细胞凋亡率紊乱恢复至接近正常水平,表明硒在该剂量下具有拮抗砷毒性的作用。而添加硒(15mg/kg)无此作用反而表现出中毒特性。
Both arsenic and selenium belong to nonmetal. Early studies indicated that arsenic coude be eliminated from the body by selenium and the injury caused by arsenicthat can be recuperated by eliminated. Based on those studies, the purpose of this study is to surve the effect of oxidative and neurotransmitter metabolic disorders on chick caused by arsenic and the different doses of selenium which were added in the composition of basal diets.
200 one-day-old Avian chickens were divided into five groups randomly. And then we fed on the chickens as the composition of basal diets as the follows:control group(basal diet, As O.1mg/kg+Se 0.2mg/kg), exposed group(basal diet, As3mg/kg), low selenium group(basal diet, As3mg/kg+Se5mg/kg), medium content of selenium group(basal diet,As3mg/kg+Sel0mg/kg), high selenium group (basal diet,As3mg/kg+Sel5mg/kg).4 samples of brain tissue were collected randomly and preserved on at 14,21,28,35,42 days. The samples were also tested for glutathione (GSH) contents and glutathione peroxidase (GSH-Px) activity, nitric oxide (NO) contents and nitric oxide synthase (NOS) activity, glutamic acid (Glu) concentration and glutamine synthetase(GS) activity, acetylcholinesterase (TchE) activity and the percentage of the brain cells apoptosis.
The experimental results showed that (1) the brain weight of tests in each group increased in the experiment period and there was no significant difference between groups; (2) the influence caused by arsenic and selenium about the brain protein contents of groups was not obvious; (3) arsenic added into the exposed group can cause brain oxidative damage, neurotransmitter metabolic disorders and the brain cell apoptosis rate increase; (4) selenium added into the low selenium group and the high selenium group could protect against the effects of arsenic on oxidative damage actively, alleviates the situation that GSH contents, GSH-Px activity, NO contents and NOS activity were reduced by arsenic, and then ameliorates brain oxidative damage; (5) selenium added into the low selenium group and the medium content of selenium group could protect against the effects of arsenic on neurotransmitter metabolic disorders actively, makes Glu contents, GS activity and TchE activity tend to normal condition, and ameliorates neurotransmitter metabolic disorders caused by arsenic; (6) selenium added into the low selenium group and the medium content of selenium group could protect against the effects of arsenic on the brain cells apoptosis actively, and then makes this situation tend to normal condition; (7) Compared to other experimental groups, the high selenium group which added into selenium cannot make protective effectly. The test results showed the measured state of intoxication, the brain tissue caused by oxidative damage and neurotransmitter disorders, the situation was similar, exposed group or even more serious.
In short, oxidative and neurotransmitter metabolic disorders on brain can be caused on the concentration of As3mg/kg and this situation can be changed when selenium was added in on the concentration of Se5mg/kg and SelOmg/kg. The brain can be protected by selenium on that concentration, but it was useless to add in selenium on the concentration of Sel5mg/kg.
引文
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