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目的探讨亚砷酸钠亚慢性暴露对小鼠肝脏和大脑组织脂质过氧化水平及抗氧化作用的影响。方法采用亚慢性毒性实验。方法昆明种小鼠60只,按体重随机分成正常对照组、低剂量组、中剂量组和高剂量组,分别自由饮用蒸馏水、0.6、2.5和10.0 mg/L的亚砷酸钠水溶液,连续染毒90 d,实验结束后测定小鼠肝脏和大脑组织中脂质过氧化产物丙二醛(MDA)的含量,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和谷胱甘肽S-转移酶(GST)的活力。结果随着亚砷酸钠染毒剂量的增加,小鼠肝脏和大脑组织中MDA含量增加(P<0.05),SOD、GSH-Px活力降低(P<0.05);肝脏和大脑组织中GST活力随着砷染毒剂量的增加呈现先升高随后降低的趋势(P<0.05)。结论亚砷酸钠亚慢性暴露可使小鼠肝脏和大脑组织脂质过氧化水平增强,抗氧化能力降低,且氧化(抗氧)化水平的改变存在组织特异性。提示脂质过氧化可能是砷毒性作用的机制之一。
Objective To investigate the effects of subchronic exposure to sodium arsenite on lipid peroxidation and antioxidation in mouse liver and brain. Methods Sub-chronic toxicity test. Methods Sixty Kunming mice were randomly divided into normal control group, low dose group, middle dose group and high dose group with distilled water, 0.6, 2.5 and 10.0 mg / L sodium arsenite solution respectively, After 90 days of treatment, the contents of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in liver and brain of mice were measured. ) And glutathione S-transferase (GST) activity. Results As the dose of sodium arsenite increased, the content of MDA in liver and brain increased (P <0.05) and the activity of SOD and GSH-Px decreased (P <0.05). The activity of GST in liver and brain The dose of arsenic increased first and then decreased (P <0.05). Conclusion Subchronic exposures to sodium arsenite increase the levels of lipid peroxidation and antioxidant capacity in the liver and brain of mice, and there is tissue specificity in the alteration of the oxidative (antioxidant) level. Tip lipid peroxidation may be one of the mechanisms of arsenic toxicity.