Biological Species and Environment Study in Microsystins Causing Apotosis in Heart

Abstract:

The occurrence of heavy cyanobacterial blooms in eutrophic freshwater ecosystems has been a worldwide problem. Microcystins, the predominant toxins of cyanobacterial blooms, are associated with mortality and illness in both animals and human. In present study, we monitored the apoptosis of heart from MCs intoxication, and evaluated the roles of main apoptosis-related genes expression in cardiotoxic effects. The results revealed that MCs exposure led to the gradually rise in apoptotic cell number. Meanwhile, Bax, Bcl-2, p53, Caspase-3 and Caspase-9 gene expressions were significantly elevated simultaneously with the extension of the time. It suggested that MCs can cause damage to heart directly.

• Periodical: Advanced Materials Research (Volume 886)
• Pages: 341-344
• DOI: https://doi.org/10.4028/www.scientific.net/AMR.886.341
• Online since: January 2014
• Authors: Tong Qiu*
• Keywords: Apotosis, Heart, Microcystin, Real Time PCR

References

[4] Significance of differences between the treated and control groups was analyzed by Student's t test. Statistical significance was concluded at P < 0. 05 and 0. 01. Results and discussion Cyanobacterial blooms in fresh surface waters occur worldwide with ever increasing incidence. Microcystins, the predominant toxins of cyanobacterial blooms, are associated with mortality and illness in both animals and human. In present study, biological species and environment study in microsystins causing apotosis in heart were carried out. As shown in Fig. 1, only a few apoptotic cells were observed in rats at the beginning of the experiment. In contrast, a remarkable increase in the number of apoptotic cells was observed in the MCs-treated rats (Fig. 1). The percentage of apoptotic cells in MCs-treated rats was significantly elevated as the extension of the exposure time. The level of apoptosis peaked at 6 h after treatment, which was nearly 45%. The TUNEL assay demonstrated the presence of apoptotic cells in the heart of rats treated with MCs. Monitoring of time course changes deduced that MCs exposure induced cell apoptosis in rats' heart gradually. Fig. 1. TUNEL labeling of sections from rats. The Control section shows very few cells positive for TUNEL (brown deposits). And increased number of apoptotic cells is observed as the extension of exposure time. Induction of p.53.

[5] Bax can promote apoptosis by homodimerizing or heterodimerizing with Bcl-2. Therefore, the alteration of Bax to Bcl-2 ratio appears to determine whether some cells live or die.

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[7] The time-dependent up-regulation of mRNA and activation of proteins suggest that the apoptogenic effect of MCs might be mediated via the up-regulation of the activation of caspases. Fig. 2. Time course of p.53.

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