Cong Zhang

TL;DR: It is demonstrated that the nephrotoxicity of Cd exposure results in oxidative stress and mitochondrial dysfunction by activating the Nrf2 signaling pathway and inhibiting UPRmt in the kidneys.

TL;DR: Resveratrol attenuated Cd-induced excessive mitochondrial fission and promoted mitochondrial fusion, which reversed PINK1/Parkin-mediated mitophagy initiation and explicate the potential protection against C d-induced nephrotoxicity and mitochondria damage.

TL;DR: It is suggested that DEHP-induced hepatotoxicity in quail was associated with activating the NRF2 mediated antioxidant defense and mtUPR, and showed that mitochondrial functions and redox homeostasis were affected by DEHP and resulted in irreversible hepatic injury.

TL;DR: Selenium supplement ameliorated the cytotoxicity of Cd by recovering hepatocyte morphology and function, inhibiting reactive oxygen species (ROS) and malondialdehyde (MDA) production, reducing intracellular LDH release, autophagy and apoptosis, and increasing the major antioxidative activities.

TL;DR: Findings showed a potential protection of Se against Cd-induced hepatotoxicity via suppressing ER stress response, and evidently relieved hepatocytes injury via modulating ER-resident selenoproteins transcription to inhibit ER stress.