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|Title:||Critical role of reactive oxygen species formation in microcystin-induced cytoskeleton disruption in primary cultured hepatocytes|
|Citation:||Ding, W.-X., Shen, H.-M., Ong, C.-N. (2001-11-23). Critical role of reactive oxygen species formation in microcystin-induced cytoskeleton disruption in primary cultured hepatocytes. Journal of Toxicology and Environmental Health - Part A 64 (6) : 507-519. ScholarBank@NUS Repository. https://doi.org/10.1080/152873901753215966|
|Abstract:||Cyanobacteria (blue-green algae)-contaminated water is a worldwide public health problem. Microcystins are a group of liver-specific toxins generated by cyanobacteria. It is generally believed that the protein phosphorylation that leads to the disruption of intermediate filaments plays an important role in microcystin-induced hepatotoxicity. However, the mechanisms that contribute to the microcystin-induced alterations of microtubules and microfilaments are not fully understood. In the present study, the effects of microcystin-LR (M-LR), the most common microcystin, were examined on the organization of cellular microtubules and microfilaments in primary cultured rat hepatocytes. Our results indicate that M-LR initiated reactive oxygen species (ROS) formation followed by altering the cytoskeleton structures, which eventually led to significant LDH leakage. These effects were completely prevented by TEMPOL, a superoxide dismutase mimic, and also partially prevented by desferoxamine. These findings provide further evidence that ROS formation, especially superoxide radical, plays a crucial role in M-LR-induced disruption of cytoskeleton organization and consequent hepatotoxicity.|
|Source Title:||Journal of Toxicology and Environmental Health - Part A|
|Appears in Collections:||Staff Publications|
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