Involvement of oxidative stress and cytoskeletal disruption in microcystin-induced apoptosis in CIK cells

摘要: The outbreak of cyanobacterial blooms induces the production and release microcystins (MCs) into water, representing a health hazard to aquatic organisms even humans. Some recent studies have suggested that kidney is another important target organ MCs except liver, however, potential toxicity mechanisms are still unclear. In this study, we first investigated collaborative effect oxidative stress cytoskeletal disruption in microcystin-induced apoptosis CIK (Ctenopharyngodon idellus kidney) cells vitro. were treated with 0, 1, 10, 100 mu g/L microcystin-LR (MC-LR) for 24 48 h. Cell viability was increased by MC-LR 1 group, while decreased group at cycle assay showed 10 induced cell through G(1) S G(2)/M phases, reduced G2/M phase population. markedly groups. Elevated reactive oxygen species (ROS) production, malondialdehyde (MDA) contents, glutathione (GSH) levels, modulated antioxidant enzymes including catalase (CAT) superoxide dismutase (SOD) observed exposed MC-LR. These alterations more pronounced higher doses (10 g/L), indicating Laser scanning confocal microscope observation aggregation collapse microfilaments (MFs) microtubules (MTs) cells, loss some cytoskeleton structure. Moreover, transcriptional changes genes (beta-actin, Ic3a, keratin) also determined, which high probability structure damage. Our data suggest may interact each other jointly lead renal MCs. (C) 2015 Elsevier B.V. All rights reserved.