Inhibition by an extract of Ocimum sanctum of DNA-binding activity of 7,12-dimethylbenz[ a]anthracene in rat hepatocytes in vitro

• Published in: Cancer letters 1998-06, Vol.128 (2), p.155-160
• Main Authors: Prashar, Ritu, Kumar, Ashok, Hewer, Alan, Cole, Kathleen J, Davis, Warren, Phillips, David H
• Format: Article
• Language: English
• Subjects: 32P-Postlabelling; 9,10-Dimethyl-1,2-benzanthracene - analogs & derivatives; 9,10-Dimethyl-1,2-benzanthracene - metabolism; 9,10-Dimethyl-1,2-benzanthracene - toxicity; Animals; Anticarcinogenic Agents - pharmacology; Biological and medical sciences; Carcinogenesis, carcinogens and anticarcinogens; Carcinogens - metabolism; Carcinogens - toxicity; Cells, Cultured; Chemical agents; Chemoprevention; DNA - metabolism; DNA adducts; DNA Adducts - metabolism; Female; Liver - drug effects; Liver - metabolism; Medical sciences; Ocimun sanctum; Plant Extracts - pharmacology; Plant Leaves - chemistry; Plants, Medicinal - chemistry; Rats; Rats, Inbred F344; Tumors
• ISSN: 0304-3835; 1872-7980
• DOI: 10.1016/S0304-3835(98)00068-8

Ocimum sanctum is a traditional medicinal plant. Previous studies have shown that extracts of O. sanctum inhibit the induction of skin papillomas in mice by 7,12-dimethylbenz[ a]anthracene (DMBA). In the present study, primary cultures of rat hepatocytes were treated with 0–500 μg of O. sanctum extract for 24 h and then with DMBA (10 or 50 μg) for 18 h. Cells were then harvested and their DNA was isolated and analyzed by 32P-postlabelling. A significant reduction in the levels of DMBA–DNA adducts was observed in all cultures pretreated with O. sanctum extract. This effect was more pronounced at the lower dose of DMBA (10 μg). Hepatocytes which were treated with the highest dose of extract (500 μg) showed a maximum reduction of 93% in the mean values of DMBA–DNA adducts. The viability of the cells was not adversely affected by pretreatment with extract. Our findings suggest that O. sanctum leaf extract blocks or suppresses the events associated with chemical carcinogenesis by inhibiting metabolic activation of the carcinogen.