{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T17:51:11Z","timestamp":1792173071780,"version":"4.4.0"},"reference-count":46,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T00:00:00Z","timestamp":1791504000000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Di(2\u2010ethylhexyl) phthalate (DEHP) is a plasticizer used in various plastic items and is hazardous for the environment with significant nephrotoxic potential. Edaravone is a potent anti\u2010oxidant that strongly scavenges the free radicals and protects the cells against oxidative stress. The objective of the present study was to examine the ameliorative potential of edaravone against DEHP\u2010induced nephrotoxicity via targeting oxidative stress and ER stress\u2010related proteins. Twenty\u2010four male albino Wistar rats were randomly divided into four groups. The control group received corn oil orally for 28 days. The DEHP group received DEHP (500\u2009mg\/kg, p.o.) for 28 days. Additionally, two treatment groups received 500\u2009mg\/kg DEHP for 28 days and edaravone (5 and 10\u2009mg\/kg) for the last 14 days (Days 15 to 28). On the 29th day, animals were euthanized, and blood and kidney samples were collected. The renal function test, oxido\u2010nitrosative stress parameters, and histopathology analysis were performed along with the western blotting test. Findings revealed that DEHP significantly increased levels of BUN, creatinine, and urea along with a substantial reduction in GSH levels and an increase in MDA and nitrite levels. The DEHP group also showed upregulated protein levels of GRP78, CHOP, and caspase\u201012. These alterations were accompanied by histological damage. Edaravone treatment alleviated DEHP\u2010induced renal injury by modulation of oxidative stress and ER stress\u2010related markers. These findings give us a mechanistic insight on how edaravone can regulate ER stress\u2010related proteins in DEHP\u2010induced nephrotoxicity and provide its ameliorative effect.<\/jats:p>","DOI":"10.1002\/jbt.71125","type":"journal-article","created":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T09:17:05Z","timestamp":1791537425000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Edaravone Mitigates Di(2\u2010ethylhexyl) Phthalate\u2010Induced Nephrotoxicity Through Attenuation of Oxidative Stress and Endoplasmic Reticulum Stress"],"prefix":"10.1002","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8775-9084","authenticated-orcid":false,"given":"Mohammed Nazish","family":"Quasmi","sequence":"first","affiliation":[{"name":"Department of Pharmaceutical Sciences School of Interdisciplinary Sciences, Central University of Haryana Mahendergarh Haryana 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