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Protective effect of manganese in cadmium-induced hepatic oxidative damage changes in cadmium distribution and trace elements level in mice

机译:锰对镉引起的肝氧化损伤镉分布变化和微量元素水平的保护作用

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摘要

Oxidative tissue damage is considered an early sign of cadmium (Cd) toxicity and has been linked with carcinogenesis. Manganese(II)-at low doses, was found to act as a potent antioxidant against oxidative stress in different in vitro systems producing lipid peroxidation conditions. The present study investigates in vivo antioxidant effects of Mn2+ pretreatment in acute Cd intoxication with regard to lipid peroxidation, antioxidant defense system and cadmium distribution in the tissues of mice. Four groups of male mice (n=7–8) were used: Cd group was injected sc a single dose of CdCl2 · 2½ H2O · (7 mg/kg b.w.); Cd+Mn group was treated ip with MnCl2 · 4H2O (20 mg/kg b.w.) 24 hours before Cd intoxication; Mn group received manganese treatment only; Control group received saline only. Twenty-four hours after Cd intoxication an increased lipid peroxidation (p<0.05), depleted GSH level (p<0.01), increased activity of GSH-Px (p<0.05) and inhibited CAT activity (p<0.01) were found in Cd-treated group compared to controls. Manganese(II) pre-treatment either completely prevented (LP, GSH, GSH-Px) or significantly attenuated (CAT) these changes. Manganese(II) treatment alone decreased LP, enhanced hepatic GSH level and had no effect on antioxidant enzymes compared to control group. A significant increase of Cd concentration in the liver and decreased Cd concentration in the kidneys and testes were found in Cd+Mn treated mice compared to Cd-only treated group. The effect of manganese may result from a different metallothionein induction in particular organs. Manganese(II) pretreatment attenuated the interference of cadmium with Ca homeostasis, the alteration in Zn and Cu levels remained mostly unaffected.
机译:氧化性组织损伤被认为是镉(Cd)毒性的早期迹象,并与致癌作用有关。低剂量的锰(II)被发现在产生脂质过氧化条件的不同体外系统中作为有效的抗氧化应激抗氧化剂。本研究从脂质过氧化,抗氧化防御系统和镉在小鼠组织中的分布方面研究了Mn 2 + 预处理在急性Cd中毒中的体内抗氧化作用。使用四组雄性小鼠(n = 7-8):镉组皮下注射单剂量的CdCl2·2½H2O·(7 mg / kg b.w.);镉中毒前24小时,用MnCl2·4H2O(20 mg / kg b.w.)腹膜内处理Cd + Mn组。锰组仅接受锰处理;对照组仅接受生理盐水。镉中毒后二十四小时,发现镉中脂质过氧化增加(p <0.05),GSH耗竭(p <0.01),GSH-Px活性增加(p <0.05)和CAT活性受到抑制(p <0.01)。治疗组与对照组比较。锰(II)预处理可以完全防止(LP,GSH,GSH-Px)或显着减弱(CAT)这些变化。与对照组相比,单独使用锰(II)处理可降低LP,提高肝脏GSH水平,并且对抗氧化酶没有影响。与仅使用Cd的治疗组相比,在Cd + Mn处理的小鼠中发现肝脏中Cd浓度显着增加,而肾脏和睾丸中Cd浓度降低。锰的作用可能是由特定器官中不同的金属硫蛋白诱导引起的。锰(II)预处理减弱了镉对钙稳态的干扰,锌和铜水平的变化大部分未受影响。

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