Effects of ornithine (alpha)-ketoglutarate on circulatory antioxidants and lipid peroxidation products in ammonium acetate treated rats
The effects of ornithine alpha-ketoglutarate (OKG) on ammonium acetate induced hepatotoxicity were studied biochemically in rats. The levels of urea, nonprotein nitrogen, and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; these levels were sign...
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Veröffentlicht in: | Annals of nutrition and metabolism 2002-05, Vol.46 (3/4), p.93 |
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description | The effects of ornithine alpha-ketoglutarate (OKG) on ammonium acetate induced hepatotoxicity were studied biochemically in rats. The levels of urea, nonprotein nitrogen, and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; these levels were significantly decreased in rats treated with ammonium acetate and OKG. Similar patterns of alterations were observed in the levels of free fatty acids, triglycerides, and phospholipids. Furthermore, nonenzymatic antioxidants (vitamins C and E) were significantly decreased in ammonium acetate treated rats, when compared with control rats, and increased in OKG and ammonium acetate treated rats. The biochemical alterations during OKG treatment could be (1) by detoxifying excess ammonia; (2) by participating in nonenzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process, and (3) by enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus prevent the lipid peroxidative damages in rats. |
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The levels of urea, nonprotein nitrogen, and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; these levels were significantly decreased in rats treated with ammonium acetate and OKG. Similar patterns of alterations were observed in the levels of free fatty acids, triglycerides, and phospholipids. Furthermore, nonenzymatic antioxidants (vitamins C and E) were significantly decreased in ammonium acetate treated rats, when compared with control rats, and increased in OKG and ammonium acetate treated rats. The biochemical alterations during OKG treatment could be (1) by detoxifying excess ammonia; (2) by participating in nonenzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process, and (3) by enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus prevent the lipid peroxidative damages in rats.</description><identifier>ISSN: 0250-6807</identifier><identifier>EISSN: 1421-9697</identifier><language>eng</language><publisher>Basel: S. Karger AG</publisher><subject>Ammonia ; Ammonium ; Antioxidants ; Fatty acids ; Hepatotoxicity ; Hydrogen peroxide ; Lipid peroxidation ; Lipids ; Nitrogen ; Peroxidation ; Plasma ; Proteins ; Triglycerides ; Urea ; Vitamin C ; Vitamin E ; Vitamins</subject><ispartof>Annals of nutrition and metabolism, 2002-05, Vol.46 (3/4), p.93</ispartof><rights>Copyright S. 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The levels of urea, nonprotein nitrogen, and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; these levels were significantly decreased in rats treated with ammonium acetate and OKG. Similar patterns of alterations were observed in the levels of free fatty acids, triglycerides, and phospholipids. Furthermore, nonenzymatic antioxidants (vitamins C and E) were significantly decreased in ammonium acetate treated rats, when compared with control rats, and increased in OKG and ammonium acetate treated rats. The biochemical alterations during OKG treatment could be (1) by detoxifying excess ammonia; (2) by participating in nonenzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process, and (3) by enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus prevent the lipid peroxidative damages in rats.</description><subject>Ammonia</subject><subject>Ammonium</subject><subject>Antioxidants</subject><subject>Fatty acids</subject><subject>Hepatotoxicity</subject><subject>Hydrogen peroxide</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Nitrogen</subject><subject>Peroxidation</subject><subject>Plasma</subject><subject>Proteins</subject><subject>Triglycerides</subject><subject>Urea</subject><subject>Vitamin C</subject><subject>Vitamin E</subject><subject>Vitamins</subject><issn>0250-6807</issn><issn>1421-9697</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNjEtOwzAQhi1EJULhDiNWsIhku69kjYo4APtqFE_otI4d7LEEJ-DauIgDsPr0P_RdqcasrWn7bb-7Vo22G91uO727Ubc5n7Q2tltvGvW9H0caJEMcIabAcuRA8Ih-PuJTeyaJ774IJhSCGGDgNBSPEtMXYBCOn-wqcw0OPM_sYKb029YxwJyiKxc9B8BpioHLBDiQXHySqMJBlec7tRjRZ7r_41I9vOzfnl_bavgolOVwiiWFOh3syurOGNOv_nX6AQjVVZM</recordid><startdate>20020501</startdate><enddate>20020501</enddate><creator>Dakshayani, K B</creator><creator>Velvizhi, S</creator><creator>Subramanian, P</creator><general>S. 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The levels of urea, nonprotein nitrogen, and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; these levels were significantly decreased in rats treated with ammonium acetate and OKG. Similar patterns of alterations were observed in the levels of free fatty acids, triglycerides, and phospholipids. Furthermore, nonenzymatic antioxidants (vitamins C and E) were significantly decreased in ammonium acetate treated rats, when compared with control rats, and increased in OKG and ammonium acetate treated rats. The biochemical alterations during OKG treatment could be (1) by detoxifying excess ammonia; (2) by participating in nonenzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process, and (3) by enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus prevent the lipid peroxidative damages in rats.</abstract><cop>Basel</cop><pub>S. Karger AG</pub></addata></record> |
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source | Jstor Complete Legacy; Karger Journals; Alma/SFX Local Collection |
subjects | Ammonia Ammonium Antioxidants Fatty acids Hepatotoxicity Hydrogen peroxide Lipid peroxidation Lipids Nitrogen Peroxidation Plasma Proteins Triglycerides Urea Vitamin C Vitamin E Vitamins |
title | Effects of ornithine (alpha)-ketoglutarate on circulatory antioxidants and lipid peroxidation products in ammonium acetate treated rats |
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