不同特性纳米银致ICR小鼠氧化损伤效应
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摘要
目的探究暴露20 nm无包被和聚乙烯吡咯烷酮(PVP)包被纳米银(Ag NPs和Ag NPs-PVP)的亚急性毒性效应和对主要脏器的氧化损伤。方法通过ICR小鼠经口暴露Ag NPs和Ag NPs-PVP(10、50、250 mg/kg)28 d,计算脏器系数并检测生化指标及各脏器的氧化应激指标。结果与对照组相比,硝酸银(Ag NO3)组和纳米银各剂量组小鼠体增重降低3.6%~86.3%,Ag NPs和Ag NPs-PVP高剂量组总蛋白(TP)、白蛋白(ALB)、球蛋白(GLO)、谷丙转氨酶(ALT)、谷草转氨酶(AST)指标升高17.8%、19.8%、15.1%、6.5%、59.1%和46.9%、32.1%、66.5%、10.9%、69.7%,肝脏脏器系数降低5.5%~27.9%,肺脏、肾脏的脏器系数明显升高8.5%~43.1%、8.0%~34.1%(P<0.05)。肝脏中2种纳米银的丙二醛(MDA)含量和超氧化物歧化酶(SOD)活力呈剂量依赖性升高24.5%~157.8%和10.6%~153.21%,谷胱甘肽(GSH)含量呈现先升高再降低的趋势。肺脏中2种纳米银的MDA含量呈剂量依赖性升高4.1%~111.6%,Ag NPs和Ag NPs-PVP中、高剂量组SOD活力和GSH含量均降低(P<0.05)。肾脏中2种纳米银的MDA含量明显升高14.7%~83.3%、SOD活力先升高再降低、GSH含量降低6.7%~31.3%,Ag NPs-PVP中剂量组SOD活力升高36.7%有统计学意义(P<0.05)结论因此经口暴露纳米银对ICR小鼠可产生亚急性毒性,对肝脏、肺脏、肾脏可产生氧化损伤,且PVP包被纳米银的毒性高于无包被纳米银。
Objective To assess subacute toxic effects and oxidative damage of major organs induced by uncoated silver nanoparticles(Ag NPs) and polyvinyl pyrrolidone(PVP) coated Ag NPs(Ag NPs-PVP) in ICR mice. Methods ICR mice were orally administered with 20 nm Ag NPs or Ag NPs-PVP at dosages of 10, 50, and 250 mg/kg/day once a day for 28 days.Then, organ coefficients of the mice were determined; liver function indicies, contents of malondialdehyde(MDA) and glutathione(GSH) and the activity of superoxide dismutase(SOD) in liver, lung, and kidney tissues of the mice were detected. Results Compared with those of the control group, the mice exposed to silver nitrate(Ag NO3) and various dosages of Ag NPs or Ag NPs-PVP had significantly decreased body weight gain(3.6% – 86.3 %) and organ coefficient of liver(5.5% – 27.9%) but increased organ coefficient of lung(8.5% – 43.1%) and kidney(8.0% – 34.1%)(P < 0.05 for all); the mice exposed to high dosage of Ag NPs and Ag NPs-PVP had significantly increased serum total protein(TP)(17.8% increase for Ag NPs group and 46.9% for Ag NPs-PVP group), albumin(ALB)(19.8% and 32.1%), globulin(GLO)(15.1% and 66.5%),alanine aminotransferase(ALT)(6.5% and 10.9%), and aspartate aminotransferase(AST)(59.1% and 69.7%)(P < 0.05 for all). For the mice treated with various dosages of Ag NPs or Ag NPs-PVP, the content of MDA increased by24.5% to 157.8% and that of SOD by 10.6% to 153.21% in a significant dose-dependent manner, but the content of GSH increased first and then decreased in liver tissues; in lung tissues, the content of MDA increased significantly by 4.1% to111.6% with the increment of the dosage, while the activity of SOD and content of GSH reduced significantly in moderate and high Ag NPs or Ag NPs-PVP dose groups(P < 0.05 for all); in kidney tissues, the content of MDA increased by 14.7% to83.3% and the activity of SOD increased firstly and then decreased but increased significantly by 36.7% in moderate Ag NPsPVP group(P < 0.05), while the content of GSH decreased by 6.7% to 31.3%. Conclusion Oral administration of silver nanoparticles results in subacute toxicity and oxidative damage on lung, liver, kidney in ICR mice and the effects of PVP coated Ag NPs are stronger than those of uncoated Ag NPs.
Objective To assess subacute toxic effects and oxidative damage of major organs induced by uncoated silver nanoparticles(Ag NPs) and polyvinyl pyrrolidone(PVP) coated Ag NPs(Ag NPs-PVP) in ICR mice. Methods ICR mice were orally administered with 20 nm Ag NPs or Ag NPs-PVP at dosages of 10, 50, and 250 mg/kg/day once a day for 28 days.Then, organ coefficients of the mice were determined; liver function indicies, contents of malondialdehyde(MDA) and glutathione(GSH) and the activity of superoxide dismutase(SOD) in liver, lung, and kidney tissues of the mice were detected. Results Compared with those of the control group, the mice exposed to silver nitrate(Ag NO3) and various dosages of Ag NPs or Ag NPs-PVP had significantly decreased body weight gain(3.6% – 86.3 %) and organ coefficient of liver(5.5% – 27.9%) but increased organ coefficient of lung(8.5% – 43.1%) and kidney(8.0% – 34.1%)(P < 0.05 for all); the mice exposed to high dosage of Ag NPs and Ag NPs-PVP had significantly increased serum total protein(TP)(17.8% increase for Ag NPs group and 46.9% for Ag NPs-PVP group), albumin(ALB)(19.8% and 32.1%), globulin(GLO)(15.1% and 66.5%),alanine aminotransferase(ALT)(6.5% and 10.9%), and aspartate aminotransferase(AST)(59.1% and 69.7%)(P < 0.05 for all). For the mice treated with various dosages of Ag NPs or Ag NPs-PVP, the content of MDA increased by24.5% to 157.8% and that of SOD by 10.6% to 153.21% in a significant dose-dependent manner, but the content of GSH increased first and then decreased in liver tissues; in lung tissues, the content of MDA increased significantly by 4.1% to111.6% with the increment of the dosage, while the activity of SOD and content of GSH reduced significantly in moderate and high Ag NPs or Ag NPs-PVP dose groups(P < 0.05 for all); in kidney tissues, the content of MDA increased by 14.7% to83.3% and the activity of SOD increased firstly and then decreased but increased significantly by 36.7% in moderate Ag NPsPVP group(P < 0.05), while the content of GSH decreased by 6.7% to 31.3%. Conclusion Oral administration of silver nanoparticles results in subacute toxicity and oxidative damage on lung, liver, kidney in ICR mice and the effects of PVP coated Ag NPs are stronger than those of uncoated Ag NPs.
引文
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[3]Saura CS,Joyce N,Steven MB,et al.Flow cytometric evaluation of the contribution of ionic silver to genotoxic potential of nanosilver in human liver Hep G2 and colon Caco2 cells[J].J Appl Toxicol,2016,36(4):521-531.
[4]Ahn JM,Eom HJ,Yang X,et al.Comparative toxicity of silver nanoparticles on oxidative stress and DNA damage in the nematode,Caenorhabditis elegans[J].Chemosphere,2014,108:343-352.
[5]Ellegaard-Jensen L,Jensen KA,Johansen A.Nano-silver induces dose-response effects on the nematode Caenorhabditis elegans[J].Ecotoxicol Environ Saf,2012,80:216-223.
[6]Sankar R,Karthik A,Prabu A,et al.Origanum vulgare mediated biosynthesis of silver nanoparticles for its antibacterial and anticancer activity[J].Colloid Surf B,2013,108(8):80-84.
[7]Hadrup N,Lam HR.Oral toxicity of silver ions,silver nanoparticles and colloidal silver-a review[J].Regul Toxicol Pharmacol,2014,68(1):1-7.
[8]Kim YS,Song MY,Park JD,et al.Subchronic oral toxicity of silver nanoparticles[J].Part Fibre Toxicol,2012,7(20):1-11.
[9]Garcia T,Lafuente D,Blanco J,et al.Oral subchronic exposure to silver nanoparticles in rats[J].Food Chem Toxicol,2016,92:177-187.
[10]Park EJ,Bae E,Yi J,et al.Repeated-dose toxicity and inflammatory responses in mice by oral administration of silver nanoparticles[J].Environ Toxicol Pharmacol,2010,30(2):162-168.
[11]Ebabe Elle R,Gaillet S,VidéJ,et al.Dietary exposure to silver nanoparticles in Sprague-Dawley rats:effects on oxidative stress and inflammation[J].Food Chem Toxicol,2013,60(10):297-301.
[12]Li L,Jiao Y,Jin T,et al.Phenolic alkaloid oleracein E attenuates oxidative stress and neurotoxicity in Al Cl3-treated mice[J].Life Sciences,2017,191:211-218.
[13]Bulle S,Reddy VD,Padmavathi P,et al.Modulatory role of Pterocarpus santalinus against alcohol-induced liver oxidative/nitrosative damage in rats[J].Biomed Pharmacother,2016,83:1057-1063.
[14]Alarifi S,Ali D,Gurabi MAAl,et al.Determination of nephrotoxicity and genotoxic potential of silver nanoparticles in Swiss albino mice[J].Toxico Enviro Chem,2017,99(2):294-301.
[15]Martins ADC Jr,Azevedo LF,de Souza Rocha CC,et al.Evaluation of distribution,redox parameters,and genotoxicity in Wistar rats co-exposed to silver and titanium dioxide nanoparticles[J].J Toxicol Environ Health A,2017,80(19-21):1156-1165.