Fig. 3.

In testes, Microcystin-LR (MC-LR) crosses the blood–testis barrier and induces mitochondrial dependent apoptotic pathway in response to DNA damage and/or oxidative stress in spermatogenic cells, Sertoli cells and Leydig cells, resulting in disruption of cytoskeleton and testicular atrophy. At the hormonal level this results in decrease of testosterone level and overall decline in male reproductive potential. MC-LR also acts as a possible human carcinogen due to its potential carcinogenic activity via inhibition of protein phosphatases, which leads to the hyper-phosphorylation of cellular proteins.