Arsenic was an established carcinogen and toxicant, occurring in drinking water and food. Arsenic was increasingly being blamed as a risk factor for diabetes mellitus. Recent studies have found that arsenic could induce the generation of reactive oxygen species (ROS) and mitochondria were the major targets of ROS. Damage mitochondria could be removed by mitophagy and mitophagy played a defensive role against cellular apoptosis. To investigate whether the arsenic could induce the injury in mitochondria, we treated Wistar rat offsprings and INS-1 cells with As2O3 and sodium arsenite, respectively. Our results showed that arsenic induced the generation of ROS in both rat offsprings’ pancreas and INS-1 cells. The generation of ROS induced by arsenic could inhibit the expression of PPARγ. PPARγ is a major impact on mitochondrial function. The inhibition of PPARγ induced the reduction of PINK1 signaling and the upregulation of Bax. PINK1 signaling was one of the classical pathways of mitophagy. The inhibition of mitophagy induced the activation of apoptosis both in rat offsprings’ pancreas and INS-1 cells. After treated with Rosiglitazone (RGS, PPARγ receptor agonist), PPARγ was rescued, the expression of PINK1 significantly increasing and the apoptosis was restrained. We used Taurine (Tau) as the protective agent both in rat offsprings’ pancreas and INS-1 cells, after treated with Tau, the production of ROS was decreased significantly and the downgrade of PPARγ was rescued.