Friday, 3 January 2014

Ameliorative Effect Of Epigallocatechin Gallate On Sodium Fluoride Induced Oxidative Stress Mediated Metabolism In Rat by S. Thangapandiyan , S. Miltonprabu

Fluorosis is the phenomenon caused by excessive ingestion of fluoride for a prolonged period of time. Intrinsic geological re-sources and more recently the arrival of increased industrialization and attendant ecological contaminated waste have contributed seriously to the increasing incidence of fluoride-related human health problem. High stratum of fluoride in drinking water has become a future health hazard all over the world, approximately with 66.62 million victims in India alone. Fluoride enters the hu-man and animal body through drinking water and to a slight extent through food (Susheela 2007). High quantity of fluoride ingestion causes metabolic anarchism, by interacting with a variety of cellu-lar processes such as gene expression, cell cycle, proliferation and migration, respiration, metabolism, ion transport, secretion, endo-cytosis, apoptosis, necrosis and oxidative stress, and disrupts the antioxidant security system in the body (Strunecka et al. 2007; Barbier et al. 2010). Numerous studies have shown that fluorosis may induce nucleotide damage, inhibition of protein synthesis and alters mitochondrial functions resulting in the energy deficient state of the cell (Jeng et al. 1998). Fluoride has already been re-ported to be hyperglycemic, hyperlipidemics, in fasting blood glucose levels in laboratory animals, which was attributed to lower Insulin levels (Rupal et al. 2010; Gracia-Montalvo et al. 2009). Philips and Hart (1935) first demonstrated that lipid metabolism was altered by toxic levels of fluoride given to rats. Fluoride expo-sure is resulting in generation of superoxide anion (O2-), and its downstream consequences such as hydrogen peroxide, peroxynitrite and hydroxyl radicals, which are important in medi-ating the toxic effects of fluoride (Barbier et al. 2010). Oxidative stress mediated free radical generation is known to be one of the most important mechanisms of fluoride toxicity (Nabavi et al. 2012). Fluoride has the ability to initiate respiratory burst and stimulate the generation of free radicals, which change the struc-ture and permeability of cell membranes and impair the cell func-tion (Chlubek 2003). Numerous studies have indicated an in-creased oxidative stress in the serum, liver and brain of animals exposed to fluoride (Grucka-Mamczar et al. 2009). Moreover, fluoride affects the activity of enzymes constituting the cell anti-oxidant system whose role is to protect against free radicals (Chinnoy 2003).

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