Department of Toxicology, Medical University of Bialystok, Poland.
Chem Biol Interact. 2011 Sep 30;193(3):191-203. doi: 10.1016/j.cbi.2011.05.008. Epub 2011 May 24.
It was estimated, in a rat model of moderate and relatively high chronic human exposure to cadmium (Cd), whether enhanced zinc (Zn) consumption may prevent Cd-induced liver injury and if the possible protective effect of this bioelement depends on its intake. For this purpose, the structure and function of the liver of the rats that received Zn (30 and 60mg/l) or/and Cd (5 and 50mg/l) for 6months were evaluated. The treatment with Cd led to, dependent on the exposure level, pathological changes in the liver, including enhanced apoptosis and induction of inflammatory and necrotic processes. Moreover, the serum activities of hepatic marker enzymes (alanine transaminase and aspartate transaminase) and the concentration of proinflammatory cytokine - tumor necrosis factor α were increased. The supplementation with 30 and 60mg Zn/l (enhancing daily Zn intake by 79% and 151%, respectively) partially or totally prevented from some of the Cd-induced changes in the liver structure and function; however, it provided no protection from necrosis, and the administration of 60mg Zn/l during the higher Cd exposure even intensified this process. At both levels of Cd treatment, the use of 30mg Zn/l was more effective in preventing liver injury than that of 60mg Zn/l. The hepatoprotective impact of Zn may be explained, at least partly, by its antioxidative, antiapoptotic and anti-inflammatory action, ability to stimulate regenerative processes in the liver tissue, and indirect action resulting in a decrease in the liver pool of the non-metallothionein-bound Cd(2+) ions able to exert toxic action. The results provide strong evidence that enhanced Zn consumption may be beneficial in protection from Cd hepatotoxicity; however, its excessive intake at relatively high exposure to Cd may intensify liver injury.
在一个中等程度和相对较高的慢性人类暴露于镉（Cd）的大鼠模型中，评估了增强锌（Zn）消耗是否可以预防 Cd 诱导的肝损伤，以及这种生物元素的可能保护作用是否取决于其摄入量。为此，评估了接受 Zn（30 和 60mg/L）和/或 Cd（5 和 50mg/L）6 个月的大鼠的肝脏结构和功能。用 Cd 处理导致，取决于暴露水平，肝脏的病理变化，包括增强的细胞凋亡和诱导的炎症和坏死过程。此外，血清中肝标志物酶（丙氨酸转氨酶和天冬氨酸转氨酶）的活性和促炎细胞因子 - 肿瘤坏死因子 α 的浓度增加。补充 30 和 60mg Zn/L（分别增强每日 Zn 摄入量的 79%和 151%）部分或完全防止了一些 Cd 诱导的肝脏结构和功能变化；然而，它不能防止坏死，并且在较高 Cd 暴露期间给予 60mg Zn/L 甚至加剧了这一过程。在 Cd 处理的两个水平上，使用 30mg Zn/L 预防肝损伤比使用 60mg Zn/L 更有效。Zn 的肝保护作用可能至少部分解释为其抗氧化、抗凋亡和抗炎作用、刺激肝组织再生过程的能力以及间接作用，导致肝脏中非金属硫蛋白结合的 Cd(2+)离子池减少，从而发挥毒性作用。结果提供了强有力的证据，表明增强 Zn 消耗可能有益于预防 Cd 肝毒性；然而，在相对较高的 Cd 暴露下，其过量摄入可能会加剧肝损伤。
