Recent studies indicate the role of the micronutrient vanadium in chemoprevention in many animal models, human cancer cell lines, and also in xenografted human carcinomas of the lung, breast, and gastrointestinal tract. The present studies were undertaken to ascertain the antineoplastic potential of vanadium in a defined model of mammary carcinogenesis. Female Sprague-Dawley rats, at 50 days of age, were treated with 7,12-dimethylbenz() anthracene (DMBA) (0.5 mg/100 g body weight) by a tail vein injection in oil emulsion. Vanadium (ammonium metavanadate) at a concentration of 0.5 ppm (4.27 μmol/l) was supplemented in drinking water and given ad libitum to the experimental group after the carcinogen treatment, and it continued until the termination of the study. In vivo studies of DNA chain breaks demonstrated that vanadium offered significant (61%, P < 0.005) protection against generation of single-strand breaks when compared with the DMBA control group. Supplementation of vanadium normalizes the level of zinc, iron, and copper as revealed by proton-induced X-ray emission analysis to a substantial extent (P < 0.01). In vitro study of chromosomal aberrations (CAs) revealed that vanadium triggered a protective effect (62.9%) on induction of CAs, which was maximum on structural aberrations followed by numerical and physiological types. Histopathological and morphological analyses were done as end-point biomarkers. We conclude herein that vanadium has the potential to reduce genomic instability in mammary carcinoma in rats.