Protective role of sulforaphane against oxidative stress mediated mitochondrial dysfunction induced by benzo(a)pyrene in female Swiss albino mice.

Recent focus of cancer chemoprevention is on intermediate biomarkers capable of detecting early changes that can be correlated with inhibition of carcinogenic initiation and progression. The present study aimed to delineate in vivo anti-initiating mechanisms of orally administered sulforaphane (SFN) with special reference to mitochondrial dysfunction in target (lungs) and non-target (liver) tissues employing benzo(a)pyrene [B(a)P] as the model carcinogen. The recent revival of interest in the study of mitochondria has been stimulated by the evidence that genetic and/or metabolic alterations in this organelle lead to a variety of human diseases including cancer. These alterations could be either causative or contributing factors. Hence the activities of mitochondrial specific enzymes of TCA cycle and the electron transport complexes were analyzed in the experimental groups to assess the ATP production. Short-term tests such as the assessment of antioxidant status and reactive oxygen species (ROS)-induced lipid peroxidation, are widely used in the detection and evaluation of anticarcinogens. The assessment of mitochondrial lipid peroxidation along with the antioxidant status proved worthy for the correlation to the degree of damage. The induction of cancer was confirmed by the immunohistochemistry for Bcl-2. The results prove sulforaphane to be very successful in combating the oxidative stress mediated mitochondrial dysfunction in experimental lung carcinogenesis induced by benzo(a)pyrene.