The latest advances in the reproductive toxicity of microcystin-LR

Microcystin-LR (MC-LR) is an emerging environmental pollutant produced by cyanobacteria that poses a threat to wild life and human health. In recent years, the reproductive toxicity of MC-LR has gained widespread attention, a large number of toxicological studies have filled the gaps in past research and more molecular mechanisms have been elucidated. Hence, this paper reviews the latest research advances on MC-LR-induced reproductive toxicity. MC-LR can damage the structure and function of the testis, ovary, prostate, placenta and other organs of animals and then reduce their fertility. Meanwhile, MC-LR can also be transmitted through the placenta to the offspring causing trans-generational and developmental toxicity including death, malformation, growth retardation, and organ dysfunction in embryos and juveniles. The mechanisms of MC-LR-induced reproductive toxicity mainly include the inhibition of protein phosphatase 1/2 A (PP1/2 A) activity and the induction of oxidative stress. On the one hand, MC-LR triggers the hyperphosphorylation of certain proteins by inhibiting intracellular PP1/2 A activity, thereby activating multiple signaling pathways that cause inflammation and blood-testis barrier destruction, etc. On the other hand, MC-LR-induced oxidative stress can result in cell programmed death via the mitochondrial and endoplasmic reticulum pathways. It is worth noting that epigenetic modifications are also involved in reproductive cell apoptosis, which may be an important direction for future research. Furthermore, this paper proposes for the first time that MC-LR can produce estrogenic effects in animals as an environmental estrogen. New findings and suggestions in this review could be areas of interest for future research.

Automated summary

MC-LR is an emerging environmental pollutant produced by cyanobacteria that poses a threat to wildlife and human health by damaging reproductive organs and causing trans-generational and developmental toxicity. The mechanisms of MC-LR-induced reproductive toxicity mainly include the inhibition of protein phosphatase activity and the induction of oxidative stress, with potential involvement of epigenetic modifications. Additional research is needed to further understand the estrogenic effects of MC-LR and its impact on reproductive health.