Environmental Toxicology · 2009 · 66 citations · 34 references
Life SciencesCell BiologyToxicologyApoptosisMitochondrial BiologyReproductive ToxicologyApoptosis RegulationApoptotic SignalingBcl-2 Family ProteinsTesticular PhysiologyTesticular ToxicologyApoptosis In TestisBcl-2 Protein ExpressionBcl-2 Protein RegulationMitochondria-dependent Cell DeathP53-mediated ApoptosisP53-mediated Cell DeathPro-apoptotic Bax ActivationSublethal Toxic Effects
It has been reported that microcystins (MCs) could accumulate in the gonads of mammals and MCs exposure exerts obvious toxic effects on male reproductive system of mammals. We have comfirmedthat MCs could accumulate and induce apoptosis in rat testis. The p53, Bax, and Bcl-2 protein play important roles in mitochondria-dependent apoptotic pathway, and this study aimed to investigate whether the p53, Bax, and Bcl-2 pathway is involved in microcystins-induced apoptosis in rat testis and discussed the possible mechanisms. Our results show that MCs led to persistent increase of transcriptional and protein level of P53 and Bax expression but led to decrease of Bcl-2 expression, resulting in an increased ratio of Bax to Bcl-2, which might contribute to apoptotic cell death of rat testis following MCs treatment. The increased ratio of expression of Bax to that of Bcl-2 induced by MCs suggests their important role in MCs-induced apoptosis in rat testis tissue.
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