Bayram Enas Nihad, Al-Bakri Nahla A, Al-Shmgani Hanady S
Department of Biology, College of Education for Pure Sciences (Ibn Al-Haitham), University of Baghdad, Baghdad, Iraq.
J Toxicol. 2023 Feb 6;2023:2200539. doi: 10.1155/2023/2200539. eCollection 2023.
The heavy metal cadmium is extremely harmful to both humans and animals. Zinc supplementation protects the biological system and reduces cadmium-induced toxicity. This study aimed to determine whether zinc chloride (ZnCl) could protect male mice with the damaged liver induced by cadmium chloride (CdCl). The protective role of zinc chloride and expression of the metallothionein (MT), Ki-67, and Bcl-2 apoptotic proteins in hepatocytes were studied after subchronic exposure of mice to cadmium chloride for 21 days. Thirty male mice were randomly categorized into 6 groups (5 mice/group) as follows: a control group that did not receive any treatment, a group given ZnCl at 10 mg/kg alone, and two groups received ZnCl (10 mg/kg) in combination with CdCl at two concentrations (1.5 and 3 mg/kg), while the last two groups received CdCl alone at 1.5 and 3 mg/kg, respectively. Immunohistochemical examination revealed a decrease in Ki-67 expression in Kupffer and endothelial cells, which reflected cell proliferation downregulation accompanied by MT increased expression. However, the Bcl-2 was ameliorated and reduced to demonstrate an enhanced rate of necrosis rather than apoptosis. Furthermore, histopathological results showed significant alteration such as hepatocytes with a pyknotic nucleus, infiltration of inflammatory cells around the central vein, and the presence of many binucleated hepatocytes. Zinc chloride treatment resulted in histological and morphological improvements that were average in the expression of apoptosis proteins modifications induced by cadmium. Our findings revealed that the positive effects of zinc might be linked to the high metallothionein expression and enhanced cell proliferation. Furthermore, at low-dose exposure, cadmium-induced damage to cells could be more closely related to necrosis rather than apoptosis.
重金属镉对人类和动物都极具危害。补充锌可保护生物系统并降低镉诱导的毒性。本研究旨在确定氯化锌（ZnCl）是否能保护因氯化镉（CdCl）导致肝脏受损的雄性小鼠。在小鼠亚慢性暴露于氯化镉21天后，研究了氯化锌的保护作用以及肝细胞中金属硫蛋白（MT）、Ki-67和Bcl-2凋亡蛋白的表达。30只雄性小鼠被随机分为6组（每组5只），如下：未接受任何处理的对照组；单独给予10 mg/kg ZnCl的组；两组分别接受两种浓度（1.5和3 mg/kg）的ZnCl（10 mg/kg）与CdCl联合处理的组；最后两组分别单独接受1.5和3 mg/kg CdCl的组。免疫组织化学检查显示，库普弗细胞和内皮细胞中Ki-67表达降低，这反映了细胞增殖下调，同时MT表达增加。然而，Bcl-2得到改善并降低，表明坏死率增加而非凋亡。此外，组织病理学结果显示出显著改变，如细胞核固缩的肝细胞、中央静脉周围炎性细胞浸润以及许多双核肝细胞的存在。氯化锌处理导致组织学和形态学改善，在镉诱导的凋亡蛋白修饰表达方面表现为中等程度。我们的研究结果表明，锌的积极作用可能与金属硫蛋白的高表达和细胞增殖增强有关。此外，在低剂量暴露时，镉诱导的细胞损伤可能与坏死而非凋亡更密切相关。
