Protective effects of N-acetylcysteine against cadmium-induced damage in cultured rat normal liver cells.

Protective effects of N-acetylcysteine against cadmium-induced damage in cultured rat normal liver cells.
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DOI:
10.3892/ijmm.2010.564
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发表时间:
2011-02
影响因子:
5.4
通讯作者:
Darling-Reed SF
Darling-Reed SF
中科院分区:
医学3区
文献类型:
--
作者:
Odewumi CO;Badisa VL;Le UT;Latinwo LM;Ikediobi CO;Badisa RB;Darling-Reed SF

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本研究通过测定镉(Cd)处理大鼠肝细胞的活力、抗氧化酶水平和细胞周期,研究还原性谷胱甘肽前体n -乙酰半胱氨酸(NAC)的保护作用。150 μM CdCl2单独处理和150 μM CdCl2与5 mM NAC(处理前2 h、同时处理和处理后2 h)共处理24 h后,150 μM CdCl2单独处理的细胞活力下降至40.1%,而5 mM NAC(处理前、同时处理和处理后)共处理的细胞活力分别显著提高至83.7%、86.2和83.7%,高于对照组(100%)。单用CdCl2处理的细胞过氧化氢酶水平下降到检测不到的水平,而在共处理的细胞(处理前、同时和后)过氧化氢酶水平分别显著增加到40.1%、34.3%和13.2%。在CdCl2单独处理的细胞中,谷胱甘肽过氧化物酶水平下降到78.3%,而在共处理的细胞(处理前、同时处理和处理后)中,谷胱甘肽过氧化物酶水平分别上升到84.5%、83.3%和87.9%。单独镉处理的细胞谷胱甘肽还原酶水平降至56.1%,而NAC(预处理、同时处理和后处理)处理的细胞谷胱甘肽还原酶水平分别显著升高至79.5%、78.5%和78.2%。Cd在S期和G2/M期引起细胞周期阻滞。与NAC共处理通过将细胞转移到G1期来抑制细胞周期阻滞。这些结果清楚地表明NAC对cd诱导的大鼠肝细胞损伤具有保护作用。
In this study, the protective effects of N-acetylcysteine (NAC), a precursor of reduced glutathione, were studied by measuring the viability, the levels of antioxidant enzymes, and by analyzing the cell cycle in cadmium (Cd)-treated rat liver cells. The cells were treated with 150 μM CdCl2 alone or co-treated with 150 μM CdCl2 and 5 mM NAC (2 h pre-, simultaneous or 2 h post-treatment) for 24 h. The viability of the cells treated with 150 μM CdCl2 alone decreased to 40.1%, while that of the cells co-treated with 5 mM NAC (pre-, simultaneous and post-treatment) significantly increased to 83.7, 86.2 and 83.7%, respectively in comparison to the control cells (100%). The catalase enzyme level decreased to undetectable level in the cells treated with CdCl2 alone, while it significantly increased in the co-treated cells (pre-, simultaneous and post-treatment) to 40.1, 34.3 and 13.2%, respectively. In the cells treated with CdCl2 alone, the glutathione peroxidase enzyme level decreased to 78.3%, while it increased in the co-treated cells (pre-, simultaneous, and post-treatment) to 84.5, 83.3 and 87.9%, respectively. The glutathione reductase enzyme level decreased to 56.1% in the cells treated with cadmium alone, but significantly increased in the cells co treated with NAC (pre-, simultaneous and post-treatment) to 79.5, 78.5 and 78.2%, respectively. Cd caused cell cycle arrest at the S and G2/M phases. The co-treatment with NAC inhibited cell cycle arrest by shifting the cells to the G1 phase. These results clearly show the protective effects of NAC against Cd-induced damage in rat liver cells.
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