EFFECTS OF L-ASCORBIC ACID AND ALPHA-TOCOPHEROL ON BIOCHEMICAL PARAMETERS OF SWIMMING-INDUCED OXIDATIVE STRESS IN SERUM OF GUINEA PIGS

There is ample evidence implicating reactive oxygen species in a number of human degenerative diseases such as atherosclerosis and haemochromatosis. Although lipid peroxidation underlies many of the toxic effects of oxidative stress, there is a lack of a sensitive and reliable method for its assessment in vivo. To understand the implications of oxidative stress in vivo, we have used dietary iron overload (IO) in the rat. Oxidant status in these animals was determined by assessing depletion of endogenous antioxidants and formation of various lipid peroxidation products, including acylated F2-isoprostanes, a novel class of free-radical-derived prostaglandin-F2-like compounds. IO led to a significant decrease in the concentration of the antioxidants alpha-tocopherol and ascorbic acid in plasma, and alpha-tocopherol, beta-carotene and ubiquinol-10 in liver. Whereas there was no significant lipid peroxidation in plasma, hepatic F2-isoprostane levels were moderately but significantly increased in IO. In addition, IO caused a significant increase in plasma total and high-density lipoprotein cholesterol levels, an effect that was correlated with depletion of plasma ascorbic acid but not alpha-tocopherol. The data demonstrate that IO causes lipid metabolism disturbances and oxidative stress which is associated with substantial depletion of endogenous antioxidants and moderate lipid peroxidative damage.

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Chlorpyrifos-induced oxidative stress and histological changes in retinas and kidney in rats: Protective role of ascorbic acid and alpha tocopherol

Pesticide Biochemistry and Physiology ◽

10.1016/j.pestbp.2010.04.006 ◽

2010 ◽

Vol 98 (1) ◽

pp. 33-38 ◽

Cited By ~ 20

Author(s):

Nadia S. Ahmed ◽

Aneesa S. Mohamed ◽

Mosaad A. Abdel-Wahhab

Keyword(s):

Oxidative Stress ◽

Ascorbic Acid ◽

Protective Role ◽

Alpha Tocopherol ◽

Histological Changes

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Prolonged Marginal Ascorbic Acid Deficiency Induces Oxidative Stress in Retina of Guinea Pigs

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831.72.2.63 ◽

2002 ◽

Vol 72 (2) ◽

pp. 63-70 ◽

Cited By ~ 2

Author(s):

Yoshiji Ohta ◽

Taku Okubo ◽

Takafumi Niwa ◽

Takashi Yamasaki ◽

Masayuki Horiguchi

Keyword(s):

Oxidative Stress ◽

Ascorbic Acid ◽

Vitamin E ◽

Guinea Pigs ◽

Serum Vitamin ◽

Thiobarbituric Acid ◽

Reduced Form ◽

Ascorbic Acid Deficiency ◽

Acid Deficiency ◽

Deficient Group

We examined whether prolonged marginal ascorbic acid deficiency induces oxidative stress in the retina of guinea pigs. Male guinea pigs aged four weeks were given a scorbutic diet (20 g/animal per day) with either marginally deficient ascorbic acid (0.5 mg/animal per day) or adequate ascorbic acid (1 g/animal per day) in drinking water for three and six months. The retinal contents of the reduced form of ascorbic acid in the deficient group at three and six months were 68.1 and 43.5%, respectively, of that in the corresponding adequate group. The retinal contents of the oxidized form of ascorbic acid in the deficient group at three and six months were 1.9- and 2.7-fold, respectively, higher than that in the corresponding adequate group. The content of retinal thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, in the deficient group was 2.5-fold higher than that in the adequate group at six months. The retinal contents of reduced glutathione (GSH) in the deficient group at three and six months were 84.8 and 66.7%, respectively, of that in the corresponding adequate group. The deficient group had 37.5% of retinal vitamin E content of the adequate group at six months. The deficient group had higher serum vitamin E concentration than the adequate group in both experimental periods. There were no differences in serum TBARS and GSH concentrations between the groups at both periods. These results indicate that prolonged marginal ascorbic acid deficiency induces oxidative stress in the retina of guinea pigs without systemic oxidative stress.

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