“…Several types of indirect DNA damage are caused by estrogeninduced oxidants, such as oxidized DNA bases, DNA strand breakage, and adduct formation by reactive aldehydes derived from lipid hydroperoxides (Cavlieri et al, 2000). On the other hand, enzymes, such as glutathione, a major endogenous antioxidant, which plays a crucial role in protecting cells from exogenous and endogenous toxins, and which exists in the glutathione reduced (GSH) and glutathione disulphide (GSSG), was reported by Lv et al (2016) an increased dose dependent, specifically the activity of GSSG of P. aibuhitensis exposed to E2; in addition to this, Guti errez-G omez et al (2016) also found a significant increase in the activity of the antioxidant enzymes superoxide dismutase, the first defense and the main enzyme responsible for the conversion of superoxide anion to hydrogen peroxide, and glutathione peroxidase in blood of C. carpio exposed to concentration of 1 mg L À1 E2 at 96 h; the increase of these enzymes could explain the results in the comet assay that demonstrated less damage to concentration of 1 mg L À1 , evidencing a greater activity as a mechanism to counteract oxidative DNA damage induced by E2. However, occasionally, such damage is not effectively repaired or is erroneously repaired, eliciting changes in the original DNA sequence (Cavalieri and Rogan, 2014), for this reason, and to evidence the damage, the comet assay is often applied in conjunction with the MNi test, that due to its simplicity, is one of the most applicable techniques to identify genomic alterations in environmental animals.…”