Perfluorohexane sulfonate (PFHxS) induces liver cytotoxicity by activating autophagy and endoplasmic reticulum stress-regulated mitochondrial pathway apoptosis.

Perfluorohexane sulfonate (PFHxS), a common alternative to perfluorootane sulfonate, is extensively used in various industrial products. As PFHxS contamination becomes more prevalent, it has been detected in human umbilical cord blood, serum, and breast milk, among other samples. In humans, the elimination half-life of PFHxS is at least 8.

Ochratoxin A-induced mitochondrial pathway apoptosis and ferroptosis by promoting glycolysis.

Ochratoxin A (OTA), a toxic secondary metabolite recognized for its harmful effects on the kidneys, and it is commonly present in various foods and animal feeds. Although there have been few reports on the involvement of metabolic enzymes in OTA-induced nephrotoxicity and metabolic reprogramming in OTA-induced digestive tract toxicity, it remains unclear whether OTA's primary nephrotoxic effects are mediated through metabolic reprogramming. In this study, we examined the effects of OTA and/or 2-deoxy-D-glucose (2-DG) on cell viability, levels of reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and lactic acid (LA), as well as protein levels in human proximal tubule epithelial (HK-2) cells.

Central role of Sigma-1 receptor in ochratoxin A-induced ferroptosis.

Ochratoxin A (OTA), a secondary fungal metabolite known for its nephrotoxic effects, is prevalent in various feeds and food items. Our recent study suggests that OTA-induced nephrotoxicity is linked to the Sigma-1 receptor (Sig-1R)-mediated mitochondrial pathway apoptosis in human proximal tubule epithelial-originated kidney-2 (HK-2) cells. However, the contribution of Sig-1R to OTA-induced nephrotoxicity involving other forms of regulated cell death, such as ferroptosis, remains unexplored.