Research Article Damaging Effects of Bisphenol A on the Kidney and the Protection by Melatonin: Emerging Evidences from In Vivo and In Vitro Studies Anongporn Kobroob , 1 Wachirasek Peerapanyasut, 1 Nipon Chattipakorn , 2 and Orawan Wongmekiat 1 1 Department of Physiology, Faculty of Medicine, Renal Physiology Unit, Chiang Mai University, Chiang Mai 50200, Thailand 2 Department of Physiology, Faculty of Medicine, Cardiac Electrophysiology Research and Training Center, Chiang Mai University, Chiang Mai 50200, Thailand Correspondence should be addressed to Orawan Wongmekiat; wongmekiat_o@yahoo.co.uk Received 21 July 2017; Revised 11 December 2017; Accepted 31 December 2017; Published 18 February 2018 Academic Editor: Serafina Perrone Copyright © 2018 Anongporn Kobroob et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This study investigates the effects of bisphenol A (BPA) contamination on the kidney and the possible protection by melatonin in experimental rats and isolated mitochondrial models. Rats exposed to BPA (50, 100, and 150 mg/kg, i.p.) for 5 weeks demonstrated renal damages as evident by increased serum urea and creatinine and decreased creatinine clearance, together with the presence of proteinuria and glomerular injuries in a dose-dependent manner. These changes were associated with increased lipid peroxidation and decreased antioxidant glutathione and superoxide dismutase. Mitochondrial dysfunction was also evident as indicated by increased reactive oxygen species production, decreased membrane potential change, and mitochondrial swelling. Coadministration of melatonin resulted in the reversal of all the changes caused by BPA. Studies using isolated mitochondria showed that BPA incubation produced dose-dependent impairment in mitochondrial function. Preincubation with melatonin was able to sustain mitochondrial function and architecture and decreases oxidative stress upon exposure to BPA. The findings indicated that BPA is capable of acting directly on the kidney mitochondria, causing mitochondrial oxidative stress, dysfunction, and subsequently, leading to whole organ damage. Emerging evidence further suggests the protective benefits of melatonin against BPA nephrotoxicity, which may be mediated, in part, by its ability to diminish oxidative stress and maintain redox equilibrium within the mitochondria. 1. Introduction Bisphenol A (BPA) is one of the oldest synthetic compounds known for its endocrine activity, although it is subsequently replaced by the stronger estrogenic activity of diethylstilbes- trol. BPA is now used extensively as a starting material for epoxy resins lining food and beverage containers and as a monomer in polycarbonate and polysulfone-based plastics in a multitude of consumer products, including medical and dental devices [1]. Epidemiological studies have shown that over 90% of individuals tested had detectable levels of BPA, providing important evidence of ubiquitous and con- tinual BPA exposure even in the general population [2]. Although published data regarding occupational exposure to BPA are limited and the potential for BPA-related health effects among the workers is unknown, recent study has shown the increased urinary total BPA concentrations in the group of manufacturing workers [3]. These data have raised concerns about the possible implication of BPA in the etiology of various human diseases [4]. Experiments using cultured cells and laboratory animals demonstrated that BPA is able to accumulate and affect several vital organ functions, including the testis [5], brain [6], heart [7], liver [8], and pancreas [9]. The findings also indicate an involve- ment of oxidative stress and mitochondrial dysfunction to the damaging effect of BPA [10–13]. Hindawi Oxidative Medicine and Cellular Longevity Volume 2018, Article ID 3082438, 15 pages https://doi.org/10.1155/2018/3082438