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六氯苯对大鼠的毒性及氧化应激作用

[Toxicity and oxidative stress on rats by hexachlorobenzene].

作者信息

Li Yuan-feng, Shi Nian, Li Huang-yuan, Liu Ying-sheng, Sun Min, Hu Fu-yong

机构信息

Department of Health Toxicology, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

出版信息

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2006 Oct;24(10):601-4.

Abstract

OBJECTIVE

To study the toxicity on rats by hexachlorobenzene (HCB), and to explore the role of oxidative stress in the mechanism of HCB intoxication.

METHODS

SD female rats were fed on a powdered diet containing 0.25 per thousand or 2.00 per thousand HCB for 14 days. The content of malondialdehyde (MDA) and the activity of total-superoxide dismutase (T-SOD), catalase (CAT) and glutathione peroxidase (GSH-PX) in cerebral cortex, hippocampus, liver tissue and serum were determined. Eleven biochemical indicators including alkaline phosphatase (ALP) were surveyed.

RESULTS

(1) MDA levels in cerebral cortex, hippocampus, liver and serum of the high dosage group rats and that in hippocampus and serum of the low dosage group were significantly higher than that of the control group. (2) The activity of T-SOD was increased in cerebral cortex and hippocampus of the rats in both groups (P < 0.01), but decreased in the serum of the high dosage group (P < 0.01). (3) The activity of CAT was also increased in the hippocampus of rats in the high dosage group. (4) In cerebral cortex and hippocampus of the rats in the high dosage group and in the hippocampus of the rats in the low dosage group, the activity of GSH-PX was significantly higher compared with the control group. However, in liver of both dosage groups, the activity of GSH-PX was decreased (P < 0.01). (5) The activity of serum alkaline phosphatase of both dosage groups was also decreased, but the contents of both serum albumin and total cholesterol were significantly higher than those of the control group (P < 0.01).

CONCLUSION

HCB can induce enhanced lipid peroxidation on SD rats, and the oxidative stress plays an important role in the mechanism of neurotoxicity and hepatotoxicity.

摘要

目的

研究六氯苯(HCB)对大鼠的毒性作用,并探讨氧化应激在HCB中毒机制中的作用。

方法

将雌性SD大鼠喂饲含0.25‰或2.00‰HCB的粉状饲料14天。测定大脑皮质、海马、肝组织及血清中丙二醛(MDA)含量以及总超氧化物歧化酶(T-SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-PX)活性。检测包括碱性磷酸酶(ALP)在内的11项生化指标。

结果

(1)高剂量组大鼠大脑皮质、海马、肝脏及血清中MDA水平以及低剂量组大鼠海马和血清中MDA水平均显著高于对照组。(2)两组大鼠大脑皮质和海马中T-SOD活性升高(P<0.01),但高剂量组大鼠血清中T-SOD活性降低(P<0.01)。(3)高剂量组大鼠海马中CAT活性也升高。(4)高剂量组大鼠大脑皮质和海马以及低剂量组大鼠海马中GSH-PX活性均显著高于对照组。然而,两个剂量组大鼠肝脏中GSH-PX活性均降低(P<0.01)。(5)两个剂量组大鼠血清碱性磷酸酶活性也降低,但血清白蛋白和总胆固醇含量均显著高于对照组(P<0.01)。

结论

HCB可诱导SD大鼠脂质过氧化增强,氧化应激在神经毒性和肝毒性机制中起重要作用。

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