Chuan Liu

TL;DR: Melatonin exerts a hepatoprotective effect on mitochondrial-derived O2•−-stimulated autophagic cell death that is dependent on the SIRT3/SOD2 pathway, and is reported to protect against Cd-induced hepatotoxicity.

TL;DR: The results suggest that ER signaling-mediated meiotic disruption may be a major contributor to the molecular events leading to BPA-related male reproductive disorders, and support the growing association between BPA exposure and the rapid increase in the incidence ofmale reproductive disorders.

TL;DR: Results indicate that BPA exposure may induce DNA damage accumulation in germ cells via oxidative stress and suggest that melatonin may be a promising pharmacological candidate for preventing the potential genotoxicity of BPA following occupational or environmental exposure.

TL;DR: SIRT1 plays an essential role in the ability of moderate melatonin to stimulate PGC-1 alpha and improve mitochondrial biogenesis and function at least partially through melatonin receptors in cadmium-induced hepatotoxicity, which indicates that Sirtinol and SIRT1 siRNA each blocked the melatonin-mediated elevation in mitochondrial function.

TL;DR: Findings may imply the novel possibility that RF-EMR with insufficient energy for the direct induction of DNA strand breaks may produce genotoxicity through oxidative DNA base damage in male germ cells.