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镉诱导的大鼠组织脂质过氧化及抗氧化系统状态

Cadmium-induced lipid peroxidation and the status of the antioxidant system in rat tissues.

作者信息

Sarkar S, Yadav P, Trivedi R, Bansal A K, Bhatnagar D

机构信息

Department of Biochemistry, D.A. University, Indore, India.

出版信息

J Trace Elem Med Biol. 1995 Oct;9(3):144-9. doi: 10.1016/S0946-672X(11)80038-6.

DOI:10.1016/S0946-672X(11)80038-6
PMID:8605602
Abstract

Cadmium may induce oxidative damage in different tissues by enhancing peroxidation of membrane lipids and altering the antioxidant system of the cells. The peroxidative damage to the cell membrane may cause injury to cellular components due to the interaction of metal ions with the cell organelles. The treatment with Cd (0.4 mg/kg body wt, ip) significantly increased lipid peroxidation (LPO) in heart within 3 h of the Cd injection, while the increase in kidney and liver followed 6 to 12 h after Cd intoxication. The antioxidant enzymes and other antioxidants provide protection to the cells against oxidative damage. The superoxide dismutase (SOD) activity increased in heart, kidney and liver within 24 h of Cd intoxication. The CAT activity increased significantly in heart 9 h after Cd injection; however, no significant change in CAT activity was observed in kidney and liver tissues. The GSH content and the activity of GR decreased in heart, kidney and liver 72 h after Cd administration, which has been suggested to be the cause for increased LPO in the tissues. The hexose monophosphate (HMP) shunt enzymes generate NADPH required for the activity of GR which may affect the GSH content in the tissues. The generalised decrease in glucose 6-phosphate dehydrogenase (G6PDH) and 6 phospho gluconate dehydrogenase (6PGDH) at 9 h followed by an increase in these enzymes in tissues 72 h after Cd intoxication suggest that the production of NADPH by the HMP shunt is required to reduce the oxidative damage. The results show that Cd induced LPO in the tissues and the condition was partially counteracted by the antioxidant system.

摘要

镉可通过增强膜脂质过氧化和改变细胞的抗氧化系统,在不同组织中诱导氧化损伤。细胞膜的过氧化损伤可能由于金属离子与细胞器的相互作用而导致细胞成分受损。腹腔注射镉(0.4毫克/千克体重)后3小时内,心脏中的脂质过氧化(LPO)显著增加,而肾脏和肝脏中的脂质过氧化增加则在镉中毒后6至12小时出现。抗氧化酶和其他抗氧化剂为细胞提供保护,使其免受氧化损伤。镉中毒24小时内心脏、肾脏和肝脏中的超氧化物歧化酶(SOD)活性增加。注射镉9小时后,心脏中的过氧化氢酶(CAT)活性显著增加;然而,在肾脏和肝脏组织中未观察到CAT活性有显著变化。镉给药72小时后,心脏、肾脏和肝脏中的谷胱甘肽(GSH)含量和谷胱甘肽还原酶(GR)活性降低,这被认为是组织中LPO增加的原因。磷酸己糖(HMP)支路酶产生GR活性所需的NADPH,这可能会影响组织中的GSH含量。镉中毒9小时后,葡萄糖6-磷酸脱氢酶(G6PDH)和6-磷酸葡萄糖酸脱氢酶(6PGDH)普遍下降,随后在中毒后72小时组织中这些酶增加,这表明HMP支路产生NADPH对于减少氧化损伤是必需的。结果表明,镉诱导组织中的LPO,而抗氧化系统可部分抵消这种情况。

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