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首页> 外文期刊>Cell biology international. >Mechanisms of the induction of apoptosis in human hepatoma cells by tumour necrosis factor-alpha.
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Mechanisms of the induction of apoptosis in human hepatoma cells by tumour necrosis factor-alpha.

机译：肿瘤坏死因子-α诱导人肝癌细胞凋亡的机制。

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Tumour necrosis factor alpha (TNF-alpha) at 20 ng/ml induced apoptosis in human hepatoma cells in vitro. The effect of TNF-alpha-induced apoptosis was exacerbated by the hypoxanthine-xanthine oxidase (HX/XO) system and cycloheximide (CHX), but alleviated by superoxide dismutase (SOD), suggesting that TNF-alpha-induced apoptosis may be due to oxidative stress, and independent of protein synthesis. TNF-alpha elevated free Ca(2+)concentration, triggered lipid peroxidation and decreased the expression of bcl-2 protein. The findings suggest that TNF-alpha-induced apoptosis may be involved in stimulating Ca(2+)-dependent endonuclease activity and increasing membrane lipid peroxidation. Bcl-2 may play a pivotal role in serving as a Ca(2+)regulator or antioxidant, preventing lipid peroxidation in the process. Copyright 2001 Academic Press.
机译：20 ng / ml的肿瘤坏死因子α（TNF-alpha）在体外诱导人肝癌细胞的凋亡。次黄嘌呤-黄嘌呤氧化酶（HX / XO）系统和环己酰亚胺（CHX）加剧了TNF-α诱导的细胞凋亡的作用，但超氧化物歧化酶（SOD）减轻了TNF-α诱导的细胞凋亡，提示TNF-α诱导的细胞凋亡可能是由于氧化应激，并独立于蛋白质合成。 TNF-alpha升高游离Ca（2+）浓度，触发脂质过氧化并降低bcl-2蛋白的表达。这些发现表明，TNF-α诱导的细胞凋亡可能与刺激Ca（2+）依赖性核酸内切酶活性和增加膜脂质过氧化有关。 Bcl-2可能在起Ca（2+）调节剂或抗氧化剂的作用中起关键作用，防止脂质过氧化过程中。版权所有2001学术出版社。

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