Department of Toxicology, Medical University of Bialystok, 15-222 Bialystok, Poland.
Nutrients. 2021 Jan 31;13(2):478. doi: 10.3390/nu13020478.
We examined, in a rat model of moderate environmental human exposure to cadmium (Cd), whether the enhanced intake of zinc (Zn) may protect against Cd-caused destroying the oxidative/antioxidative balance and its consequences in the brain. The intoxication with Cd (5 mg/L, 6 months) weakened the enzymatic (superoxide dismutase, glutathione peroxidase, catalase) and non-enzymatic (total thiol groups, reduced glutathione) antioxidative barrier decreasing the total antioxidative status and increased the concentrations of pro-oxidants (hydrogen peroxide, myeloperoxidase) in this organ and its total oxidative status. These resulted in the development of oxidative stress and oxidative modifications of lipids and proteins. The co-administration of Zn (30 and 60 mg/L enhancing this element intake by 79% and 151%, respectively) importantly protected against Cd accumulation in the brain tissue and this xenobiotic-induced development of oxidative stress and oxidative damage to lipids and proteins. Moreover, this bioelement also prevented Cd-mediated oxidative stress evaluated in the serum. The favorable effect of Zn was caused by its independent action and interaction with Cd. Concluding, the enhancement of Zn intake under oral exposure to Cd may prevent the oxidative/antioxidative imbalance and oxidative stress in the brain and thus protect against injury of cellular macromolecules in the nervous system.
我们在镉（Cd）中等环境人体暴露的大鼠模型中研究了，是否增强锌（Zn）的摄入可以防止 Cd 引起的氧化/抗氧化平衡破坏及其在大脑中的后果。Cd（5mg/L，6 个月）中毒削弱了酶（超氧化物歧化酶、谷胱甘肽过氧化物酶、过氧化氢酶）和非酶（总巯基、还原型谷胱甘肽）抗氧化屏障，降低了总抗氧化状态，增加了该器官和总氧化状态的促氧化剂（过氧化氢、髓过氧化物酶）浓度。这导致了氧化应激和脂质及蛋白质的氧化修饰的发展。Zn（30 和 60mg/L）的共同给药（分别增强了该元素的摄入 79%和 151%），重要地防止了 Cd 在脑组织中的积累，以及这种外源性诱导的氧化应激和脂质及蛋白质的氧化损伤的发展。此外，这种生物元素还可以防止 Cd 介导的血清中的氧化应激。Zn 的有利作用是由其独立作用和与 Cd 的相互作用引起的。总之，口服暴露于 Cd 时增强 Zn 的摄入可以防止大脑中的氧化/抗氧化失衡和氧化应激，从而防止神经细胞内大分子的损伤。
