Zinc takes part in several of cellular signaling pathways, containing defense against free radicals, apoptosis, and inflammation. However, interaction between zinc and prostate cancer progression is poorly understood. Therefore, zinc treatment in DU-145 human prostate cancer cells was investigated. First, zinc sulfate (ZnSO4) concentrations with antiproliferative effect were determined using MTT assay. Then, ZnSO4-induced oxidative damage was evaluated by malondialdehyde (MDA) levels, glutathione (GSH) levels, total oxidant status (TOS) levels, and total antioxidant status (TAS) levels. Apoptotic effects of ZnSO4 were determined by measuring biochemical and immunohistochemical parameters including caspase 3 (CASP3), cytochrome C (CYC), Bcl-2-associated X protein (Bax), and B cell CLL/lymphoma 2 (Bcl-2) levels. Inflammatory effects of ZnSO4 were investigated by measuring interleukin-6 (IL-6) levels and tumor necrosis factor-alpha (TNF-α) levels. Finally, morphological analysis was performed using hematoxylin-eosin staining. We found that ZnSO4 caused a concentration-dependent increase in oxidative stress, apoptosis, and inflammation pathways. Moreover, there were a number of morphological alterations in treated cells depending on the ZnSO4 concentration. Consequently, our data showed that zinc acts as a regulator of increased oxidative damage and apoptosis through the upregulation of TNF-α and IL-6.

中文翻译：

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硫酸锌对DU-145人前列腺癌细胞系的浓度依赖性影响：氧化，凋亡，炎症和形态分析。

锌参与多种细胞信号传导途径，其中包括针对自由基，细胞凋亡和炎症的防御作用。然而，人们对锌与前列腺癌进展之间的相互作用了解甚少。因此，研究了锌在DU-145人前列腺癌细胞中的治疗。首先，使用MTT法测定具有抗增殖作用的硫酸锌（ZnSO4）浓度。然后，通过丙二醛（MDA）水平，谷胱甘肽（GSH）水平，总氧化剂状态（TOS）水平和总抗氧化剂状态（TAS）水平评估ZnSO4诱导的氧化损伤。通过测量生化和免疫组化参数，包括胱天蛋白酶3（CASP3），细胞色素C（CYC），Bcl-2相关X蛋白（Bax）和B细胞CLL /淋巴瘤2（Bcl-2）水平，确定ZnSO4的凋亡作用。通过测量白介素6（IL-6）水平和肿瘤坏死因子-α（TNF-α）水平来研究ZnSO4的炎症作用。最后，使用苏木精-伊红染色进行形态分析。我们发现ZnSO4引起氧化应激，细胞凋亡和炎症途径的浓度依赖性增加。此外，根据ZnSO4的浓度，处理过的细胞中存在许多形态学改变。因此，我们的数据表明锌可通过上调TNF-α和IL-6来调节氧化损伤和细胞凋亡。我们发现ZnSO4引起氧化应激，细胞凋亡和炎症途径的浓度依赖性增加。此外，根据ZnSO4的浓度，处理过的细胞中存在许多形态学改变。因此，我们的数据表明锌可通过上调TNF-α和IL-6来调节氧化损伤和细胞凋亡。我们发现ZnSO4引起氧化应激，细胞凋亡和炎症途径的浓度依赖性增加。此外，根据ZnSO4的浓度，处理过的细胞中存在许多形态学改变。因此，我们的数据表明锌可通过上调TNF-α和IL-6来调节氧化损伤和细胞凋亡。