title: Inhibition of altered liver cell foci and persistent nodule growth by vanadium during diethylnitrosamine-induced hepatocarcinogenesis in rats.
abstract: The effect of vanadium, a recently established trace element, on diethylnitrosamine (DENA)-induced hepatocarcinogenesis was examined in male Sprague-Dawley rats. Rats were divided into four groups (Groups 1-4). While Group 1 served as normal group, initiation of hepatocarcinogenesis was performed in all other groups (Groups 2-4) by a single intraperitoneal injection of DENA (200 mg/kg body weight). Supplementary vanadium at the level of 0.2 and 0.5 ppm (as ammonium monovanadate) added to the drinking water was given to Groups 3 and 4 respectively ad libitum four weeks before DENA administration and continued for 8 or 16 weeks after the carcinogenic insult. Rats were sacrificed at the 12th or 20th week after the experiment began. No significant differences were observed in food and water intakes or in growth rates among the groups. Supplementation with vanadium (in Groups 3 and 4) for 12 or 20 weeks dose-dependently reduced the incidence, total number, multiplicity and altered the size distribution of visible persistent (neoplastic) hepatocyte nodules as compared to DENA control (Group 2). Mean nodular volume and nodular volume as percentage of liver volume were also inhibited upon vanadium supplementations. The morphometric analysis of preneoplastic focal lesions observed in hematoxylin and eosin-stained liver sections revealed the occurrence of a decreased number of altered liver cell foci/cm2 and the average focal area, coupled with a decrement in the percentage area of liver parenchyma occupied by foci in vanadium-supplemented groups (Groups 3 and 4). All these results were found to be more pronounced at the 20th week as compared to the 12th week of the study. However, the results with 0.5 ppm vanadium at the 20th week were mostly at a statistically significant level. The findings of the study suggest that vanadium at a dose of 0.5 ppm may have a potential anticarcinogenic property against chemically induced hepatic neoplasia without any apparent sign of toxicity. This attribute could open new vistas in cancer chemotherapy.
authors.affiliation: Department of Pharmaceutical Technology, Jadavpur University, Calcutta, India.
authors.forename: A
authors.initials: A
authors.lastname: Bishayee
authors.forename: M
authors.initials: M
authors.lastname: Chatterjee
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects; D056486:Chemical and Drug Induced Liver Injury; D004052:Diethylnitrosamine; D018450:Disease Progression; D006965:Hyperplasia; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008107:Liver Diseases / Q000188:drug therapy* / Q000473:pathology; D008114:Liver Neoplasms, Experimental / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D009929:Organ Size / Q000187:drug effects; D011230:Precancerous Conditions / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014638:Vanadates / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D004052:Diethylnitrosamine; D014638:Vanadates