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Arsenic (Ar) is known to exert its toxicity through the generation of ROS and inflammation. The current study investigates the protective effects of sulforaphane (SFN) against arsenic-induced renal damage via PI3K\/Akt-mediated Nrf2 pathway signaling. Thirty-two male albino Wistar rats were randomly divided into four groups of eight animals each, designated as control, arsenic (Ar), sulforaphane plus Ar (SFN+Ar), and sulforaphane alone (SFN), with oral administration of Ar (5\u00a0mg\/kg BW) and SFN (80\u00a0mg\/kg BW) daily for 28\u00a0days. Ar administration significantly (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05) increased the levels of ROS, OHdG, Ar accumulation, and lipid peroxidation, and decreased levels of enzymatic and nonenzymatic antioxidants. Notably, a significant (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05) increase was observed in markers of apoptosis, DNA damage, TUNEL-positive cells, and dark staining of ICAM-1 in renal tissue with decreased PI3K\/Akt\/Nrf2 gene expression. The biochemical findings were supported by histopathological and electron microscopy evaluation, which showed severe renal damage in rats treated with Ar. Pretreatment with SFN significantly (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05) attenuated renal ROS, OHdG, lipid peroxidation, and DNA damage, and increased phase II antioxidants via PI3K\/Akt-mediated Nrf2 activation in renal tissue. These results show that dietary supplementation with SFN protects against Ar-induced nephrotoxicity via the PI3K\/Akt-mediated Nrf2 signaling pathway in the rat kidney.<\/jats:p>","DOI":"10.1007\/s11356-019-04502-w","type":"journal-article","created":{"date-parts":[[2019,3,5]],"date-time":"2019-03-05T10:54:08Z","timestamp":1551783248000},"page":"12247-12263","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":53,"title":["RETRACTED ARTICLE: Sulforaphane potentially attenuates arsenic-induced nephrotoxicity via the PI3K\/Akt\/Nrf2 pathway in albino Wistar rats"],"prefix":"10.1007","volume":"26","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3958-9169","authenticated-orcid":false,"given":"Shanmugam","family":"Thangapandiyan","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mathan","family":"Ramesh","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Selvaraj","family":"Miltonprabu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tamilselvan","family":"Hema","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gunasekaran Bavithra","family":"Jothi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Venkatesan","family":"Nandhini","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2019,3,5]]},"reference":[{"key":"4502_CR1","doi-asserted-by":"publisher","first-page":"753","DOI":"10.1289\/ehp.02110s5753","volume":"110","author":"DT Bau","year":"2002","unstructured":"Bau DT, Wang TS, Chung CH et al (2002) Oxidative DNA adducts and DNA-protein cross-links are the major DNA lesions induced by arsenite. 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