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These data indicate that fish oil feeding downregulated the endogenous PPAR-activation system and increased antioxidant gene expressions to protect against ROS excess Fish oil feeding alters liver gene expressions to defend against PPARalpha activation and ROS production. Takahashi M, Tsuboyama-Kasaoka N, Nakatani T, Ishii M, Tsutsumi S, Aburatani H, Ezaki O. Am J Physiol Gastrointest Liver Physiol. 2002 Feb;282(2):G338-48. PMID: 11804856

Waamika Enterprises Is the Best RO Service Provider In Dehardun and Also Provides their Services in Haridwar, Rishikesh, Vikasnagar, Selaqui, Doiwala, JollyGrant and Mussoriee Uttrakhand.

A new study showing a reduction in the toxic side effects of ROS-generating chemotherapies with concurrent antioxidant supplementation will be presented at the 43rd Annual Meeting of the American Society of Clinical Oncology (ASCO) that takes place June 1-5 at McCormick Place in Chicago. According to the study's authors, mitigating chemotherapy toxicity by supplementing with antioxidants may improve survival rates and tumor response by helping patients complete their prescribed treatment cycles.

Dietary cis-monounsaturated fatty acids and metabolic control in type 2 diabetes. Ros E. Am J Clin Nutr. 2003 Sep;78(3 Suppl):617S-625S. Review. PMID: 12936956

Neuroprotective effects of berberine on stroke models in vitro and in vivo. Zhou XQ, Zeng XN, Kong H, Sun XL. Neurosci Lett. 2008 Dec 5;447(1):31-6. Epub 2008 Sep 30. PMID: 18838103 doi:10.1016/j.neulet.2008.09.064 Findings of this study suggest that berberine protects against ischemic brain injury by decreasing the intracellular ROS level and subsequently inhibiting mitochondrial apoptotic pathway.

Fatty fish and fish omega-3 fatty acid intakes decrease the breast cancer risk: a case-control study. Kim J, Lim SY, Shin A, Sung MK, Ro J, Kang HS, Lee KS, Kim SW, Lee ES. BMC Cancer. 2009 Jun 30;9:216. PMID: 19566923 doi: 10.1186/1471-2407-9-216 Conclusion These results suggest that high consumption of fatty fish is associated with a reduced risk for breast cancer, and that the intake of omega-3 fatty acids from fish is inversely associated with postmenopausal breast cancer risk

Vitamin C antagonizes the cytotoxic effects of antineoplastic drugs.\nHeaney ML, Gardner JR, Karasavvas N, Golde DW, Scheinberg DA, Smith EA, O'Connor OA.\nCancer Res. 2008 Oct 1;68(19):8031-8.\nPMID: 18829561

Reports that vitamins C and E may blunt the positive effects of exercise are misleading, according to an antioxidant expert. German researchers have reported that antioxidant vitamins C and E may blunt the positive effects of exercise, with respect to insulin sensitivity. Findings were published in the Proceedings of the National Academy of Sciences. Reacting to the study , Alexander Schauss, PhD, from AIBMR Life Sciences, a nutraceutical products consultancy, told NutraIngredients.com that the title of the study (Antioxidants prevent health-promoting effects of physical exercise in humans) was misleading. "The primary objective of this study was to study the effect of a 4-week intensive 5-days a week exercise program on insulin sensitivity. Yet the title of the paper leads one to believe otherwise," he said. "This is a small gender-biased study of 40 male subjects, 25 to 35 years of age. When I read through the study for the first time I had to wonder how could the authors have come up with such a title for their paper?" he asked.

Supplements of antioxidant vitamins after exercise may decrease the benefits of the workout by blocking the positive effects of reactive oxygen, says a new study. Researchers from Germany and the US report in the Proceedings of the National Academy of Sciences that a combination of 1,000 mg per day of vitamin C and 400 IU per day of vitamin E adversely affected insulin sensitivity, and thereby increase the risk of type 2 diabetes. Participants, both trained and untrained, underwent 85 minutes of exercise five days per week for four weeks.

Antioxidants prevent health-promoting effects of physical exercise in humans. Ristow M, Zarse K, Oberbach A, Klöting N, Birringer M, Kiehntopf M, Stumvoll M, Kahn CR, Blüher M. Proc Natl Acad Sci U S A. 2009 May 26;106(21):8665-70. Epub 2009 May 11. PMID: 19433800 DOI: 10.1073/pnas.0903485106

Fatty Acid Peroxidation & Free Radicals

Aspirin-triggered lipoxin A4 blocks reactive oxygen species generation in endothelial cells: a novel antioxidative mechanism. Nascimento-Silva V, Arruda MA, Barja-Fidalgo C, Fierro IM. Thromb Haemost. 2007 Jan;97(1):88-98. PMID: 17200775 DOI: 10.1160/TH06-06-0315

Antioxidative and anti-inflammatory actions of docosahexaenoic acid and eicosapentaenoic acid in renal epithelial cells and macrophages. Kim YJ, Chung HY. J Med Food. 2007 Jun;10(2):225-31. PMID: 17651056 doi:10.1089/jmf.2006.092.

Oral administration of both tetrahydrobiopterin and L-arginine prevents endothelial dysfunction in rats with chronic renal failure. Yamamizu K, Shinozaki K, Ayajiki K, Gemba M, Okamura T. J Cardiovasc Pharmacol. 2007 Mar;49(3):131-9. PMID: 17414224 doi: 10.1097/FJC.0b013e31802f9923

Artemisinin (pronounced /ɑːtə'misinən/) is a drug used to treat multi-drug resistant strains of falciparum malaria. The compound (a sesquiterpene lactone) is isolated from the plant Artemisia annua. Not all plants of this species contain artemisinin. Apparently it is only produced when the plant is subjected to certain conditions, most likely biotic or abiotic stress. It can be synthesized from artemisinic acid.[1] The drug is derived from a herb used in Chinese traditional medicine, though it is usually chemically modified and combined with other medications. Artemisinin is under early research and testing for treatment of cancer, primarily by researchers at the University of Washington.[7][8] Artemisinin has a peroxide lactone group in its structure. It is thought that when the peroxide comes into contact with high iron concentrations (common in cancerous cells), the molecule becomes unstable and releases reactive oxygen species. It has been shown to reduce angiogenesis and the expression of vascular endothelial growth factor in some tissue cultures.