Our results show low levels of enzymatic antioxidants after the subchronic exposure, which could be due to: 1) the possible regulation of enzymatic antioxidants by secondary mediators, such TGF-β, which down-regulate catalase, glutathione reductase and SOD enzymes in the kidney [61]; 2) the susceptibility of antioxidant proteins to oxidation by oxygen and nitrogen radical molecules [62]; and 3) the loss of Nrf-2 activity due to severe kidney damage without de novo synthesis and the restoring of antioxidant levels [63]. This evidence concerns the gene TGFB1 and Nephropathy.