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Renal ischemia\u2013reperfusion (RIR) is the major cause of acute kidney injury with high prevalence and increased long\u2010term risks for multiple comorbidities and mortality. As the kidney is susceptible to these conditions, we explored whether the outcomes following the RIR episode could be influenced by BPA exposure, and investigated the therapeutic possibility by N\u2010acetylcysteine (NAC) including the mechanisms involved. Three groups of male Wistar rats were fed with vehicle, BPA 5, and 50\u2009mg\/kg, respectively, for five consecutive weeks then underwent the sham operation. Three other groups with identical treatment underwent bilateral renal IR induction (45\u2010min ischemia followed by 24\u2010hr reperfusion). An additional RIR group was treated with BPA 50 plus NAC 100\u2009mg\/kg. BPA\u2010exposed rats that encountered RIR episode showed dose\u2010dependent worsening of RIR injury as evidenced by augmentations of renal dysfunction and histopathological abnormalities, oxidative stress, apoptosis, mitochondrial functional impairment, mitochondrial dynamic, and mitophagy disproportion compared with the vehicle\u2010exposed RIR group. The NAC therapy considerably attenuated the exacerbated effects of BPA, which was associated with increased AMP\u2010activated protein kinase (AMPK), PGC\u20101\u03b1, silent information regulator 3 or sirtuin 3 (SIRT3), and mitofusin 2 (MFN2) expressions but decreased Phosphorylated dynamin\u2010related protein 1 (p\u2010DRP1)\/Dynamin\u2010related protein 1 (DRP1), PTEN\u2010induced putative kinase (PINK), and PARKIN expressions. These findings reveal the detrimental effect of repeated BPA exposure on the renal outcomes following the IR episode, and further demonstrate the protective efficacy of NAC by maintaining mitochondrial homeostasis, which is, partly, mediated through the AMPK\u2010PGC\u20101\u03b1\u2010SIRT3 axis.<\/jats:p>","DOI":"10.1002\/iub.2175","type":"journal-article","created":{"date-parts":[[2019,10,6]],"date-time":"2019-10-06T09:08:13Z","timestamp":1570352893000},"page":"758-770","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["Bisphenol A aggravates renal ischemia\u2013reperfusion injury by disrupting mitochondrial homeostasis and N\u2010acetylcysteine mitigates the injurious outcomes"],"prefix":"10.1002","volume":"72","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7741-308X","authenticated-orcid":false,"given":"Wachirasek","family":"Peerapanyasut","sequence":"first","affiliation":[{"name":"Renal Physiology Unit, Department of Physiology, Faculty of Medicine Chiang Mai University  Chiang Mai Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anongporn","family":"Kobroob","sequence":"additional","affiliation":[{"name":"Division of Physiology, School of Medical Science University of Phayao  Phayao Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Siripong","family":"Palee","sequence":"additional","affiliation":[{"name":"Cardiac Electrophysiology Research and Training Center, Department of Physiology, Faculty of Medicine Chiang Mai University  Chiang Mai Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nipon","family":"Chattipakorn","sequence":"additional","affiliation":[{"name":"Cardiac Electrophysiology Research and Training Center, Department of Physiology, Faculty of Medicine Chiang Mai University  Chiang Mai Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8535-3870","authenticated-orcid":false,"given":"Orawan","family":"Wongmekiat","sequence":"additional","affiliation":[{"name":"Renal Physiology Unit, Department of Physiology, Faculty of Medicine Chiang Mai University  Chiang Mai Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2019,10,6]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/em.22072"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.422"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1155\/2018\/3082438"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.envint.2013.12.007"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-med-050214-013407"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.107"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI37829"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI77632"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017060659"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1002\/tox.22193"},{"key":"e_1_2_8_12_1","doi-asserted-by":"publisher","DOI":"10.3109\/0886022X.2014.949768"},{"key":"e_1_2_8_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.transproceed.2015.09.035"},{"key":"e_1_2_8_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2018.11.005"},{"key":"e_1_2_8_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.fct.2011.03.032"},{"key":"e_1_2_8_16_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0159414"},{"key":"e_1_2_8_17_1","doi-asserted-by":"publisher","DOI":"10.1093\/toxsci\/68.1.121"},{"key":"e_1_2_8_18_1","doi-asserted-by":"publisher","DOI":"10.1002\/iub.2066"},{"key":"e_1_2_8_19_1","doi-asserted-by":"publisher","DOI":"10.1093\/annweh\/wxw021"},{"key":"e_1_2_8_20_1","doi-asserted-by":"publisher","DOI":"10.3109\/10715762.2013.858148"},{"key":"e_1_2_8_21_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cbi.2012.08.026"},{"key":"e_1_2_8_22_1","doi-asserted-by":"crossref","first-page":"13424","DOI":"10.1016\/S0021-9258(17)38738-0","article-title":"Swelling and contraction of the mitochondrial matrix. 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