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微囊藻毒素-LR 对大鼠睾丸支持细胞产生细胞毒性作用。

Microcystin-LR causes cytotoxicity effects in rat testicular Sertoli cells.

机构信息

Life Science School, Nanjing University, Nanjing, Jiangsu 210093, PR China.

出版信息

Environ Toxicol Pharmacol. 2012 Mar;33(2):318-26. doi: 10.1016/j.etap.2011.12.015. Epub 2011 Dec 29.

DOI:10.1016/j.etap.2011.12.015
PMID:22301162
Abstract

Microcystins (MCs) are produced by cyanobacteria. The most toxic and widely distributed MC is microcystin-LR (MC-LR). The aim of this study was to investigate whether exposure to MC-LR could induce oxidative stress, leading the further toxicity effects on Sertoli cells in vitro. Sertoli cells obtained from rats were cultured with a medium containing 0, 0.5, 5, 50 or 500 nM/l MC-LR. We examined the decrease of mitochondrial membrane potential (MMP), the increase of reactive oxygen species (ROS) production, the increase of lipid peroxidation and decrease of superoxide dismutase (SOD) activity in Sertoli cells after treatment with MC-LR in vitro, and higher expression of caspase-9 and caspase-3, the increase of apoptosis rate. Therefore, we deduced that direct exposure to microcystin-LR could induce oxidative stress generation in Sertoli cells, and subsequently depressed cellular viability and caused cells to undergo apoptosis, resulting in the reproductive toxicity in male rats.

摘要

微囊藻毒素(MCs)由蓝藻产生。毒性最强且分布最广的 MC 是微囊藻毒素-LR(MC-LR)。本研究旨在探讨 MC-LR 暴露是否会诱导氧化应激,从而对体外培养的支持细胞产生进一步的毒性作用。从大鼠中分离的支持细胞在含有 0、0.5、5、50 或 500 nM/L MC-LR 的培养基中进行培养。我们检测了 MC-LR 处理后支持细胞中线粒体膜电位(MMP)的降低、活性氧(ROS)生成的增加、脂质过氧化的增加和超氧化物歧化酶(SOD)活性的降低,以及 caspase-9 和 caspase-3 的高表达、凋亡率的增加。因此,我们推断直接暴露于微囊藻毒素-LR 可诱导支持细胞中氧化应激的产生,进而抑制细胞活力并导致细胞凋亡,从而导致雄性大鼠的生殖毒性。

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