Sarkar S, Yadav P, Bhatnagar D
Centre for Reproductive Biology and Molecular Endocrinology, Indian Institute of Science, Bangalore, India.
J Trace Elem Med Biol. 1997 Apr;11(1):8-13. doi: 10.1016/S0946-672X(97)80002-8.
Cadmium (Cd)-induced oxidative damage in erythrocytes causes loss of membrane function by enhancing lipid peroxidation (LPO) and altering the erythrocyte antioxidant system. Vitamin E and/or selenium (Se) was administered to rats, prior to Cd intoxication, in order to prepare the animals to withstand oxidative assault. The treatment with Cd increased LPO in erythrocytes while animals pretreated with vitamin E and/or Se prior to Cd treatment showed decreased LPO as compared with animals given Cd alone. The erythrocyte SOD and CAT activities decreased significantly with Cd treatment. The pretreatment with vitamin E and/or Se prior to Cd administration partially reversed such changes. The erythrocytes showed a marked depletion in glutathione (GSH) content with Cd treatment. The antioxidant treatments before Cd administration helped to maintain the erythrocyte GSH content. The erythrocyte glutathione reductase (GSH-R) activity increased markedly when treatments with vitamin E and Se were applied. The GSH-R activity was not observed to decrease in animals treated with antioxidant prior to Cd intoxication, which may mean that the replenishment of erythrocyte GSH content is via GSH-R. The glutathione-S-transferase (GST) activity increased significantly with Cd intoxication; however, treatment with antioxidants prior to Cd treatment decreased erythrocyte GST activity. The results show that Cd-induced LPO decreased the antioxidant capability of the erythrocytes, causing erythrocyte membrane damage.
镉(Cd)诱导的红细胞氧化损伤通过增强脂质过氧化(LPO)和改变红细胞抗氧化系统导致膜功能丧失。在镉中毒前给大鼠施用维生素E和/或硒(Se),以使动物能够承受氧化攻击。镉处理会增加红细胞中的LPO,而在镉处理前用维生素E和/或硒预处理的动物与仅给予镉的动物相比,LPO降低。镉处理后红细胞超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性显著降低。镉给药前用维生素E和/或硒预处理可部分逆转这些变化。镉处理使红细胞中的谷胱甘肽(GSH)含量显著减少。镉给药前的抗氧化处理有助于维持红细胞GSH含量。应用维生素E和硒处理时,红细胞谷胱甘肽还原酶(GSH-R)活性显著增加。在镉中毒前用抗氧化剂处理的动物中未观察到GSH-R活性降低,这可能意味着红细胞GSH含量的补充是通过GSH-R进行的。镉中毒时谷胱甘肽-S-转移酶(GST)活性显著增加;然而,镉处理前用抗氧化剂处理可降低红细胞GST活性。结果表明,镉诱导的LPO降低了红细胞的抗氧化能力,导致红细胞膜损伤。