Mitochondria are highly organized multicomponent systems of endogenous fluorescent molecules, which can be detected by fluorescence spectroscopy. They play a crucial role in energetic metabolism of cells. The dysfunction of mitochondria plays a central role in aging and the pathophysiology of a variety of diseases. Mitochondria have an important function also in oncogenesis and tumor progression, and thus provide promising targets for the development of novel anti-cancer agents as new therapeutic opportunities. This requires the need for further use of various biological samples in research to stimulate the entire field of mitochondrial medicine.
In our study, we investigated the effect of resveratrol (at a dose of 100 mg/kg of body weight on daily basis) and ethanol (10% ethanol administered orally on daily basis), on the chemically induced carcinogenesis process in Sprague-Dawley rats at mitochondrial level. Carcinoma formation was induced using N-nitroso-N-methylurea (NMU, 50 mg/kg of body weight on 43th and 50th postnatal days). Mitochondria were isolated from the breast cancer tissue. The changes between controls, NMU carcinogenesis group, resveratrol or ethanol treated groups were measured by the fluorescence spectroscopy method.
The most significant changes were observed in the protein domain (ex/em 280/350 nm), where a significant increase in the chemically induced carcinogenesis group was observed over the treated groups and control. We also monitored decreased autofluorescence (normalized spectra) in the region specific for NADH+H+ (ex/em 350/440 nm) and FAD (ex/em 440/520 nm) in the group where carcinogenesis was induced compared to other groups.
The results showed, that resveratrol lowered the amount of total proteins in breast cancer tissue, which could indicate decreased tumor volume or halting tumor progression and also redox state in resveratrol treated group is much more similar to control. However, it is important to further elucidate its mechanism of action on molecular level, which could be promising strategy against cancer cells.
Keywords: antioxidant, carcinogenesis, autofluorescence