Suppressive Effect of Molybdenum on Hepatotoxicity of N-Nitrosodiethylamine in Rats

• Published in: Biological & pharmaceutical bulletin Vol. 18; no. 3; pp. 460 - 462
• Main Authors: KOIZUMI, Toshiaki, TAJIMA, Kenichi, EMI, Nobuo, HARA, Atsushi, SUZUKI, Kazuo
• Format: Journal Article
• Language: English
• Published: Tokyo The Pharmaceutical Society of Japan 1995; Maruzen
• Subjects: Animals; Anticarcinogenic Agents - therapeutic use; Biological and medical sciences; Calcium - metabolism; calcium-dependent endonuclease; Diethylnitrosamine - toxicity; DNA - drug effects; DNA - metabolism; DNA Damage; lipid peroxidation; Lipid Peroxidation - drug effects; Liver - drug effects; Liver - metabolism; Liver Neoplasms, Experimental - chemically induced; Liver Neoplasms, Experimental - metabolism; Liver Neoplasms, Experimental - prevention & control; Male; Medical sciences; Miscellaneous; molybdenum; Molybdenum - therapeutic use; N-nitrosodiethylamine; Pharmacology. Drug treatments; Potassium - metabolism; Rats; Rats, Wistar; Nitroso compound; Vertebrata; Intraperitoneal administration; Mammalia; Rat; Toxicity; Animal; Liver; Rodentia; Pretreatment; Carcinogenesis; Molybdenum
• ISSN: 0918-6158; 1347-5215
• DOI: 10.1248/bpb.18.460

In order to elucidate the mechanism by which molybdenum prevents the carcinogenesis of N-nitroso compounds, the effects of Na2MoO4-pretreatment on N-nitrosodiethylamine (NDEA)-induced DNA strand breaks, fluctuation in cation contents and lipid peroxidation levels in rat liver were examined. Male Wistar rats weighing 170-190g were pretreated with Na2MoO4 (1.24 mmol/kg body weight, i.p., once a day) for 3 d and on day 4, they were exposed to NDEA (50 mg/kg body weight, once, i.p.). Three days after exposure to NDEA, the nitroso compound caused DNA strand breaks and disrupted potassium (K) and calcium (Ca) metabolism in the liver but did not affect lipid peroxidation levels. Na2MoO4-pretreatment prevented both NDEA-induced DNA damage and disruption of the metabolism of those cations but rather enhanced lipid peroxidation. These results suggest that Mo prevented NDEA-induced DNA damage by preventing disruption of intracellular Ca metabolism while stimulating the metabolism of the nitroso compound via a nontoxic pathway.