{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T19:56:14Z","timestamp":1789934174888,"version":"4.0.1"},"reference-count":44,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2016,3,17]],"date-time":"2016-03-17T00:00:00Z","timestamp":1458172800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81071005"],"award-info":[{"award-number":["81071005"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environmental Toxicology"],"published-print":{"date-parts":[[2017,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>As an endogenous gaseous mediator, H<jats:sub>2<\/jats:sub>S exerts antioxidative, antiapoptotic, and cytoprotective effects in livers. This study was designed to investigate the protective role of H<jats:sub>2<\/jats:sub>S against uranium\u2010induced hepatotoxicity in adult SD male rats after <jats:italic>in vivo<\/jats:italic> effect of uranium on endogenous H<jats:sub>2<\/jats:sub>S production was determined in livers. The levels of endogenous H<jats:sub>2<\/jats:sub>S and H<jats:sub>2<\/jats:sub>S\u2010producing enzymes (CBS and CSE) were measured in liver homogenates from uranium \u2010intoxicated rats. In rats injected intraperitoneally (i.p.) with uranyl acetate or NaHS (an H<jats:sub>2<\/jats:sub>S donor) alone or in combination, we examined biochemical parameters to assess liver function, revealed hepatic histopathological alteration, investigated oxidative stress markers, and explored apoptotic signaling in liver homogenates. The results suggest that uranium\u2010intoxication in rats decreased CBS and CSE protein expression, H<jats:sub>2<\/jats:sub>S synthesis capacity, and endogenous H<jats:sub>2<\/jats:sub>S generation. NaHS administration in uranium\u2010intoxicated rats produced amelioration in liver biochemical indices and histopathological effects, decreased MDA content, and increased GSH level and antioxidative enzymes activities like SOD, CAT, GPx, and GST. NaHS administration in uranium\u2010intoxicated rats attenuated uranium\u2010activated phosphorylation state of JNK. NaHS treatment in uranium\u2010intoxicated rats increased antiapoptotic Bcl\u20102 but decreased pro\u2010apoptotic Bax, resulting in the rise of Bcl\u20102\/Bax ratio. NaHS treatment in uranium\u2010intoxicated rats reduced the apoptosis mediator caspase\u20103 and cytochrome c release and elevated ATP contents. Taken together, these data implicate that H<jats:sub>2<\/jats:sub>S can afford protection to rat livers against uranium\u2010induced adverse effects mediated by up\u2010regulation of antioxidant and antiapoptotic signaling. The anti\u2010apoptotic property of H<jats:sub>2<\/jats:sub>S may be involved, at least in part, in inhibiting JNK signaling. \u00a9 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 581\u2013593, 2017.<\/jats:p>","DOI":"10.1002\/tox.22261","type":"journal-article","created":{"date-parts":[[2016,3,19]],"date-time":"2016-03-19T07:09:38Z","timestamp":1458371378000},"page":"581-593","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Hydrogen sulfide alleviates uranium\u2010induced acute hepatotoxicity in rats: Role of antioxidant and antiapoptotic signaling"],"prefix":"10.1002","volume":"32","author":[{"given":"Yan","family":"Yuan","sequence":"first","affiliation":[{"name":"Department of Biology, Institute of Biology, School of Pharmaceutical and Biological Science, University of South China Changsheng West Road 28 Hengyang City Hunan Province 421001 People's Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jifang","family":"Zheng","sequence":"additional","affiliation":[{"name":"Department of Biology, Institute of Biology, School of 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