Bisdemethoxycurcumin chemoprevents 7,12-dimethylbenz(a)anthracene-induced mammary toxicity via modulation of oxidative processes.

Bisdemethoxycurcumin (BDMC) is a naturally occurring compound having anti-cancer properties. We investigated the effect of BDMC on DMBA-induced mammary toxicity in female Wistar rats. Forty-eight virgin female rats were divided into six groups at random. Group 1 received corn oil, group 2 received DMBA (50 mg/kg), groups 3 and 4 received DMBA and BDMC (25 mg/kg and 50 mg/kg), group 5 received BDMC (50 mg/kg), and group 6 received DMBA and vincristine. A single dosage of DMBA was administered (i.p.) at six weeks, followed by BDMC (orally) and vincristine (i.p.) three times a week for thirteen weeks. The DMBA significantly increased lactate dehydrogenase activity by 1.3 folds. Similarly, DMBA increased nitric oxide, malondialdehyde, and myeloperoxidase activities by 12, 204, and 6.3%, respectively. DMBA-rats decreases glutathione-S-transferase, superoxide dismutase, and glutathione peroxidase activities. Immunohistochemistry analysis revealed that B-cell lymphoma-2, estrogen receptor, and human epidermal receptor-2 were strongly expressed in DMBA-rats, but progesterone receptor and Bcl-2 associated protein were weakly expressed. In DMBA rats, histology revealed mammary glands with moderate proliferating ducts and fibrosis. Co-treatment with BDMC reduces hormone receptors activities, improved antioxidant and apoptotic status. BDMC protected the mammary gland from DMBA toxicity by targeting cellular pathways involved in oxidative stress and apoptosis.