1989•Journal of Clinical Biochemistry and NutritionOpen access

Effect of Ascorbic Acid on Antioxidant Defense Systems and Lipid Peroxidation in Guinea Pig

Ashwani Koul, Krishan Lal KHANDUJA, Indu Bala KOUL, Mahesh P. Gupta, Sabhiya Majid, Rati Ram SHARMA

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Abstract

In view of the antioxidant properties of ascorbic acid (AA), effects of inadequate and excessive doses of AA on hepatic and pulmonary antioxidant enzymes and NADPH-dependent lipid peroxidation were investigated in the present study. Male guinea pigs, dosed daily with 0.2mg AA/100g b wt (inadequate) or 50mg AA/100g b wt (excessive) for 8 weeks, demonstrated no difference in body growth, liver and lung weights, and post-10, 000×g supernatant protein contents as compared with the control group, which was daily fed with 2mg AA/ 100g b wt. Inadequacy of AA decreased the hepatic and pulmonary contents of catalase, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD), but it significantly increased glutathione reductase (GR) activity (p<0.005) in lung. However, levels of hepatic and pulmonary NADPH-dependent lipid peroxidation remained unaltered when the supply of AA was inadequate. Excessive doses of AA did not influence any pulmonary antioxidant enzyme, level of NADPH-dependent lipid peroxidation and content of reduced glutathione (GSH), but increased the hepatic GSH-Px and GR activities. Hepatic SOD activity showed a significant decrease (p<0.01), whereas NADPH-dependent lipid peroxidation and GSH contents remained unchanged. It appears that the changes in antioxidant enzymes may be a nonspecific response to AA or these changes may not be sufficient to bring about any shift in the levels of NADPH-dependent lipid peroxidation in the presence of unaltered GSH contents or other biomolecules which may act as antioxidants or free radical scavengers in the cell system.

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In view of the antioxidant properties of ascorbic acid (AA), effects of inadequate and excessive doses of AA on hepatic and pulmonary antioxidant enzymes and NADPH-dependent lipid peroxidation were investigated in the present study. Male guinea pigs, dosed daily with 0.2mg AA/100g b wt (inadequate) or 50mg AA/100g b wt (excessive) for 8 weeks, demonstrated no difference in body growth, liver and lung weights, and post-10, 000×g supernatant protein contents as compared with the control group, which was daily fed with 2mg AA/ 100g b wt. Inadequacy of AA decreased the hepatic and pulmonary contents of catalase, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD), but it significantly increased glutathione reductase (GR) activity (p<0.005) in lung. However, levels of hepatic and pulmonary NADPH-dependent lipid peroxidation remained unaltered when the supply of AA was inadequate. Excessive doses of AA did not influence any pulmonary antioxidant enzyme, level of NADPH-dependent lipid peroxidation and content of reduced glutathione (GSH), but increased the hepatic GSH-Px and GR activities. Hepatic SOD activity showed a significant decrease (p<0.01), whereas NADPH-dependent lipid peroxidation and GSH contents remained unchanged. It appears that the changes in antioxidant enzymes may be a nonspecific response to AA or these changes may not be sufficient to bring about any shift in the levels of NADPH-dependent lipid peroxidation in the presence of unaltered GSH contents or other biomolecules which may act as antioxidants or free radical scavengers in the cell system.

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Available abstract

In view of the antioxidant properties of ascorbic acid (AA), effects of inadequate and excessive doses of AA on hepatic and pulmonary antioxidant enzymes and NADPH-dependent lipid peroxidation were investigated in the present study. Male guinea pigs, dosed daily with 0.2mg AA/100g b wt (inadequate) or 50mg AA/100g b wt (excessive) for 8 weeks, demonstrated no difference in body growth, liver and lung weights, and post-10, 000×g supernatant protein contents as compared with the control group, which was daily fed with 2mg AA/ 100g b wt. Inadequacy of AA decreased the hepatic and pulmonary contents of catalase, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD), but it significantly increased glutathione reductase (GR) activity (p<0.005) in lung. However, levels of hepatic and pulmonary NADPH-dependent lipid peroxidation remained unaltered when the supply of AA was inadequate. Excessive doses of AA did not influence any pulmonary antioxidant enzyme, level of NADPH-dependent lipid peroxidation and content of reduced glutathione (GSH), but increased the hepatic GSH-Px and GR activities. Hepatic SOD activity showed a significant decrease (p<0.01), whereas NADPH-dependent lipid peroxidation and GSH contents remained unchanged. It appears that the changes in antioxidant enzymes may be a nonspecific response to AA or these changes may not be sufficient to bring about any shift in the levels of NADPH-dependent lipid peroxidation in the presence of unaltered GSH contents or other biomolecules which may act as antioxidants or free radical scavengers in the cell system.

Key concepts: Lipid peroxidation, Ascorbic acid, Antioxidant, Glutathione, Superoxide dismutase, Chemistry, Glutathione reductase, Catalase

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