{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,17]],"date-time":"2026-01-17T01:34:38Z","timestamp":1768613678901,"version":"3.49.0"},"reference-count":61,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2007,1,22]],"date-time":"2007-01-22T00:00:00Z","timestamp":1169424000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2007,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Carcinogen\u2010induced early DNA lesions and metallothionein (MT) over\u2010expression have been implicated in cell proliferation and thereby subsequent expression of premalignant phenotype of the cell. We have therefore investigated the chemopreventive potential of vanadium in a multi\u2010biomarker approach, viz. 8\u2010hydroxy\u20102\u2032\u2010deoxyguanosines (8\u2010OHdGs), DNA single\u2010strand breaks (SSBs), DNA\u2010protein crosslinks (DPCs), chromosomal aberrations (CAs), in situ MT expression, and cell proliferation in rat liver preneoplasia. Hepatocarcinogenesis was induced in male Sprague\u2013Dawley rats with a single, necrogenic, intraperitoneal (i.p.) injection of diethylnitrosamine (DEN) (200 mg\/Kg body weight) at week 4 of the experimental protocol followed by promotion with phenobarbital (PB) (0.05% in basal diet), on and from week 8 and continued till 32 weeks in a long\u2010term regimen. There was a significant and steady elevation of modified DNA bases 8\u2010OHdGs (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.0001; 90.69%) along with substantial increments of the extent of SSBs (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001) and CAs (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001) following DEN exposure. Supplementation of vanadium at a dose of 0.5 ppm abated the formations of 8\u2010OHdGs (80.63%; <jats:italic>P<\/jats:italic>\u2009&lt;\u20090.0001), SS\u2010DNAs (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001) and SSBs\/DNA unit (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.01; 56.39%), DPCs (59.26%; <jats:italic>P<\/jats:italic>\u2009&lt;\u20090.0001) and CAs (71.52%; <jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001) in preneoplastic rat liver studied at various time points. Low dose of vanadium treatment further reduced liver\u2010MT immunoreactivity (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05) and BrdU\u2010labeling index (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.02) and a significant positive correlation (r\u2009=\u20090.92; r<jats:sup>2<\/jats:sup>\u2009=\u20090.85; <jats:italic>P<\/jats:italic>\u2009=\u20090.0001) was noted between them. Continuous vanadium administration also decreased nodular incidence (66.67%) and nodule multiplicity (62.12%; <jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001) along with substantial improvement in the altered hepatocellular phenotype when compared to DEN\u2009+\u2009PB treatment alone. The study indicates that vanadium\u2010mediated suppression of cell proliferation and resulting premalignant expression might be due to the observed reductions in hepatic 8\u2010OHdGs, SSBs, DPCs, CAs, and MT immunoreactivity. Vanadium is chemopreventive for DEN\u2010induced hepatocellular preneoplasia in rats. J. Cell. Biochem. 101: 244\u2013258, 2007. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcb.21169","type":"journal-article","created":{"date-parts":[[2007,1,22]],"date-time":"2007-01-22T18:37:18Z","timestamp":1169491038000},"page":"244-258","source":"Crossref","is-referenced-by-count":13,"title":["Molecular basis of vanadium\u2010mediated inhibition of hepatocellular preneoplasia during experimental hepatocarcinogenesis in rats"],"prefix":"10.1002","volume":"101","author":[{"given":"Tridib","family":"Chakraborty","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.H.M. 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