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氯化锰对人脑胶质瘤 T98G 细胞株诱导氧化应激和炎症细胞因子的作用。

Induction of oxidative stress and inflammatory cytokines by manganese chloride in cultured T98G cells, human brain glioblastoma cell line.

机构信息

College of Pharmacy, Dongduk Women's University, 23-1, Wolgok-dong, Seongbuk-gu, Seoul 136-714, Republic of Korea.

出版信息

Toxicol In Vitro. 2010 Mar;24(2):472-9. doi: 10.1016/j.tiv.2009.09.022. Epub 2009 Oct 6.

Abstract

Manganese, an essential trace nutrient in human beings, has been widely used in the steel industry to improve hardness, stiffness, and strength. With the increased applications of manganese compounds, discharge into the environment has rapidly increased and may exert adverse effects on human health. In this study, manganese toxicity was investigated using cultured T98G cells, which are derived from human glioblasts with the ability to differentiate into several different types of neuroglia. Cytotoxicity was shown in manganese-treated groups (100, 200, 400, and 800microM of MnCl(2)), and cell viability was decreased to 58.8% of the control group at 2days after treatment with 800microM of MnCl(2). When cells were treated with manganese for 24h, ROS dose-dependently increased while antioxidant intracellular GSH decreased. With the generation of ROS, the increased activity of caspase-3 was shown, and was followed by chromatin condensation and breakage, which is an indication of the cellular apoptotic process. ROS also triggered pro-inflammatory responses in cultured T98G cells, which were demonstrated by the increased gene expression and protein levels of IL-6 and IL-8.

摘要

锰是人体必需的痕量营养元素,在钢铁工业中被广泛用于提高硬度、刚度和强度。随着锰化合物应用的增加,其向环境中的排放迅速增加,可能对人类健康产生不良影响。在这项研究中,使用 T98G 细胞(源自人成胶质细胞瘤,能够分化为多种神经胶质细胞)来研究锰的毒性。在锰处理组(100、200、400 和 800μM 的 MnCl2)中观察到细胞毒性,用 800μM 的 MnCl2 处理 2 天后,细胞活力下降至对照组的 58.8%。当细胞用锰处理 24 小时时,ROS 呈剂量依赖性增加,而抗氧化细胞内 GSH 减少。随着 ROS 的产生,显示 caspase-3 的活性增加,随后是染色质浓缩和断裂,这是细胞凋亡过程的一个迹象。ROS 还引发了培养的 T98G 细胞的促炎反应,这表现在 IL-6 和 IL-8 的基因表达和蛋白水平增加。

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