Cancer oxidant stress

Xenobiotic-Sensing Nuclear Receptors in Cancer, Oxidative Stress and Pollution... 

Riso P, del Bo C. Preventive effects of broccoli bioactives role on oxidative stress and cancer risk. In Preedy VR, editor. Cancer Oxidative Stress and Dietary Antioxidants. Elsevier Inc 2014. p. 115-125. 

The protective effects of carotenoids against chronic diseases appear to be correlated to their antioxidant capacities. Indeed, oxidative stress and reactive oxygen species (ROS) formation are at the basis of oxidative processes occurring in cardiovascular incidents, cancers, and ocular diseases. Carotenoids are then able to scavenge free radicals such as singlet molecular oxygen ( O2) and peroxyl radicals particularly, and protect cellular systems from oxidation. 

Betalains have shown strong antioxidant activities in biological environments such as membranes and LDLs," -" suggesting that the consumption of betalain-colored foods may exert protective effects against certain oxidative stress-related diseases (i.e., cancers) in humans. Beetroot has been used as a treatment for cancer in Europe for several centuries. The high content of betanin in red beetroot (300 to 600 mg/kg) may be the explanation for the purported cancer chemopreventive effects of beets. 

Oxidative stress, DNA repair, and cancer susceptibility. Cancer Detect. Prev. 14, 555-561. 

Umemura, T., Sai, K., Takagi, A., Hasegawa, R. and Kurokawa, Y. (1991). The effects of exogenous glutathione and cysteine on oxidative stress induced by ferric nitrilo-triacetate. Cancer Lett. 58, 49-56. 

Phagocyte-derived ROMs have been implicated in the pathogenesis of a number of pulmonary diseases, including emphysema, acute respiratory distress syndrome, and various environmental diseases such as asbestos-related fibrosis and cancer (Mossman and Marsh, 1985). The relatively high oxygen tension in pulmonary tissue renders the lung prone to oxidative stress (Edwards and Lloyd, 1988). 

Evans, P.H., Campbell, A.K., Yano, E. and Morgan, L.G. (1989a). Environmental cancer, phagocytic oxidant stress and nutritional interactions. In Nutritional Impact of Food Processing (eds. J.C. Somogyi and H.R. Muller) pp. 313-326. Karger, Basel. 

Another peculiarity of the study is that the use of a biological system has allowed the authors to hypothesize a possible mechanism of action of the leachate as a mixture, hypothesis that could have been drafted on the basis of the only knowledge derived by chemical analysis. Researchers suggest that leachate inhibits cell proliferation at low doses probably inducing a reversible cell cycle arrest that becomes irreversible at high doses, probably due to leachate-induced oxidative stress. This activity is mainly due to the chemical compounds extracted in the aqueous phase. Similar effects were noticed by previous investigations on other human cells (human peripheral blood lymphocytes and a human breast cancer cell line, MCF-7) [31, 32], supporting the hypothesis that cells that survive the initial insult from leachate constituents maintains the potential to proliferate until the effects on cell metabolism lead to death. 

Numerous excellent reviews on the possible role of oxygen radicals in cancer and carcinogenesis have been published 10-20 years ago [147-153], Earliest studies have been much concerned with the role of SOD in tumor cells. Despite some contradictory results, it is general conclusion that tumor cells are usually characterized by lowered CuZnSOD activity and always by lowered MnSOD activity [147]. The origin of SOD declining in cancer cells is unknown. It has been suggested that MnSOD is not induced in cancer immortalized cells in response to oxidative stress, but the reason of this is uncertain [154],... 

In agreement with the above consideration of the role of oxidative stress in cancer development, it was found that tumor cells (thymocytes) are more sensitive to oxidative stress than normal thymocytes [178], There are apparently the other free radical-mediated damaging processes, which can be more intensive in tumors. For example, it has been found that metHb formation was significantly elevated in cancer patients [179]. 

It has been suggested that tamoxifen, one of the most effective therapeutic and chemopreventive agent for breast cancer, modulates protein kinase C through oxidative stress in breast cancer cells [194], Unfortunately, most breast cancers initially responsive to tamoxifen treatment later become resistant. Schiff et al. [195] suggested that the conversion of breast tumors to a tamoxifen-resistant phenotype is associated with oxidative stress and depends on significantly enhanced SOD activity in tumors. 

Gupta, S. et al., Arsenic trioxide induces apoptosis in peripheral blood T lymphocyte subsets by inducing oxidative stress A role of Bcl-2, Mol. Cancer Then, 2,711, 2003. 

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