The possible genotoxicity of BPA still remains controversial, even though this compound has received particular attention because of its widespread distribution and concerns for human health. A recent screening of the genotoxic potential of different EDCs in vitro found a low level of DNA breakage after BPA treatments in human cells [6]. Previous studies have reported genotoxic effects of BPA in vitro in human HeLa cells, and in vivo exposures in two aquatic sentinel species, Daphnia and C. tentans [9]. Genotoxic activity was also found in rats, as shown by cytogenetic endpoints (micronucleus, chromosomal aberrations) and the increase of DNA strand breaks in alkaline comet assays [11]. In our study, the genotoxic potential of BPA in C. riparius has been confirmed, showing a differential behavior under short or extended exposures. The extent of DNA damage at the lower concentration decreased with exposure time, possibly due to DNA repair activity. This is one of the first reports supporting the activation of DNA repairing mechanisms under prolonged exposure to BPA, which is in agreement with increased expression of genes involved in DNA repair in human breast epithelial cells [43]. Recent results indicate that BPA may induce DNA damage accumulation in rat germ cells via oxidative stress, concomitant with SOD activity depletion, which can be counteracted by a potent antioxidant such as melatonin [44].