Zinc (Zn) is a fundamental trace element for cell viability and physiology, and concentrations above the physiological level may lead to cell damage. In order to explore the effect of zinc chloride (ZnCl₂) on murine photoreceptor cells, in this study, we investigated the alterations of murine photoreceptor cell proliferation and cell morphology after exposure to various concentrations of ZnCl₂, determined the levels of hydrogen peroxide, hydroxyl radicals, cytochrome c, and ATP before and after cells exposure to different concentrations of ZnCl₂, monitored the changes of mitochondrial membrane potential, and further explored the expressions of BCL2-associated X (Bax) and B cell CLL/lymphoma (Bcl)-2 at gene and protein levels. The results indicated that appropriate ZnCl₂ levels can enhance the cell proliferation, whereas high levels of ZnCl₂ could apparently inhibit cell growth, exaggerate the generation of both hydrogen peroxide and hydroxyl radicals, collapse the mitochondrial membrane potential, and accelerate cytochrome c release into cytosol, decrease the ATP production, elevate the Bax production, and reduce the Bcl-2 expression, thereby disrupting the mitochondrial homeostasis. Consequently, the disrupted mitochondrial homeostasis initiates the mitochondria-mediated apoptotic signaling pathway, leading to cell death. Taken together, the results suggest that the over generation of reactive oxygen species and the activated mitochondrial signaling pathway play an important role in ZnCl₂-induced murine photoreceptor cell death.

锌（Zn）是细胞活力和生理的基本微量元素，高于生理水平的浓度可能导致细胞损伤。为了探讨氯化锌（ZnCl ₂）对鼠类感光细胞的影响，在这项研究中，我们研究了暴露于各种浓度的ZnCl ₂后鼠类感光细胞增殖和细胞形态的变化，确定了过氧化氢的水平，细胞暴露于不同浓度的ZnCl ₂之前和之后的羟基自由基，细胞色素c和ATP，监测线粒体膜电位的变化，并进一步探讨了BCL2相关X（Bax）和B细胞CLL /淋巴瘤（Bcl）-2在基因和蛋白质水平上的表达。结果表明，适当的ZnCl ₂水平可以促进细胞增殖，而高水平的ZnCl _2则明显抑制细胞生长，夸大过氧化氢和羟​​基自由基的产生，破坏线粒体膜电位，并加速细胞色素c的产生。释放到细胞质中，降低ATP的产生，提高Bax的产生，并降低Bcl-2的表达，从而破坏线粒体的体内平衡。因此，破坏的线粒体体内稳态启动了线粒体介导的凋亡信号通路，从而导致细胞死亡。两者合计，结果表明活性氧的过量产生和激活的线粒体信号通路在ZnCl ₂诱导的鼠感光细胞死亡中起重要作用。