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Chronic exposures to arsenic had been associated with metabolism diseases. Peroxisome proliferator-activated receptor gamma (PPARγ) was found in the liver, regulated metabolism. Here, we found that the expression of PPARγ was decreased, the generation of reactive oxygen species (ROS) and autophagy were increased after treatment with As 2 O 3  in offsprings’ livers. Taurine (Tau), a sulfur-containing β–amino acid could reverse As 2 O 3 -inhibited PPARγ. Tau also inhibit the generation of ROS and autophagy. We also found that As 2 O 3  caused autophagic cell death and ROS accelerated in HepG2 cells. Before incubation with As 2 O 3 , the cells were pretreated with PPARγ activator Rosiglitazone (RGS), we found that autophagy and ROS was inhibited in HepG2 cells, suggesting that inhibition of PPARγ contributed to As 2 O 3 -induced autophagy and the generation of ROS. After pretreatment with Tau, the level of PPARγ was improved and the autophagy and ROS was inhibited in As 2 O 3 -treated cells, suggesting that Tau could protect hepatocytes against As 2 O 3  through modulating PPARγ pathway.

Taurine protects against As2O3-induced autophagy in livers of rat offsprings through PPARγ pathway