Ammonium Acetate

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Jianwei Mao - One of the best experts on this subject based on the ideXlab platform.

Yanli Cui - One of the best experts on this subject based on the ideXlab platform.

Periyasamy Giridharan - One of the best experts on this subject based on the ideXlab platform.

Cheng Zhaodong - One of the best experts on this subject based on the ideXlab platform.

Perumal Subramanian - One of the best experts on this subject based on the ideXlab platform.

  • Effects of melatonin on the levels of antioxidants and lipid peroxidation products in rats treated with Ammonium Acetate.
    Die Pharmazie, 2004
    Co-Authors: Peter J. Lena, Perumal Subramanian
    Abstract:

    The antioxidant potential of melatonin (MLT) on hyperammonemia (induced by Ammonium Acetate treatment) were studied in rats. The levels of circulatory ammonia, urea and non-protein nitrogen increased significantly in Ammonium Acetate treated rats and decreased significantly in rats treated with melatonin and Ammonium Acetate. In brain tissues, the same pattern of alterations across groups was observed in the levels of thiobarbituric acid reactive substances and lipid profile variables (free fatty acids, triglycerides, phospholipids, and cholesterol). Further, enzymatic (superoxide dismutase, catalase and glutathione peroxidase) and non-enzymatic (reduced glutathione) antioxidants in brain tissues decreased significantly in Ammonium Acetate treated rats and increased significantly in rats treated with melatonin and Ammonium Acetate. These biochemical alterations could be due to the ability of melatonin to (i) scavenge a variety of radicals and reactive oxygen species (ii) induce antioxidative enzymes which reduce steady state levels of reactive oxygen species and (iii) stabilize cell membranes which assist them in reducing oxidative damage and thus could prevent oxidative stress in rats.

  • Evaluation of the antiperoxidative effects of melatonin in Ammonium Acetate-treated Wistar rats.
    Polish journal of pharmacology, 2003
    Co-Authors: Peter J. Lena, Perumal Subramanian
    Abstract:

    The efficacy of melatonin (MLT) against Ammonium Acetate-induced neurotoxicity was biochemically studied in the experimental rats. The activities of serum transaminases and the levels of thiobarbituric acid reactive substances were significantly increased in Ammonium Acetate-treated rats. These levels were significantly decreased in MLT and Ammonium Acetate-treated rats. Further, non-enzymatic (vitamin C and E) and enzymatic (super-oxide dismutase and catalase) antioxidants were significantly decreased in Ammonium Acetate-treated rats and were increased in MLT and Ammonium Acetate-treated rats. These biochemical alterations during MLT treatment could be due to its ability to: (i) scavenge a variety of radicals and reactive species, (ii) induce antioxidative enzymes which reduce steady state levels of reactive species, (iii) inhibit nitric oxide synthase which generates nitric oxide and (iv) stabilize cell membranes which assists them in reducing oxidative damage and, thus, prevents the oxidative stress in rats.

  • Effects of Ornithine α-Ketoglutarate on Circulatory Antioxidants and Lipid Peroxidation Products in Ammonium Acetate Treated Rats
    Annals of nutrition & metabolism, 2002
    Co-Authors: K.b. Dakshayani, Velvizhi S, Perumal Subramanian
    Abstract:

    The effects of ornithine α-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.

  • Ornithine α-ketoglutarate modulates the levels of antioxidants and lipid peroxidation products in Ammonium Acetate treated rats
    Indian journal of biochemistry & biophysics, 2002
    Co-Authors: K.b. Dakshayani, Velvizhi S, Perumal Subramanian
    Abstract:

    The effects of ornithine alpha-ketoglutarate (OKG) on Ammonium Acetate induced hepatotoxicity were studied in experimental rats. The levels of urea, non-protein nitrogen and thiobarbituric acid reactive substances were significantly increased in Ammonium Acetate treated rats; but these levels were significantly decreased in Ammonium Acetate-OKG treated rats. Similar patterns were observed in the levels of free fatty acids, triglycerides and phospholipids. Furthermore, non-enzymatic (reduced glutathione) and enzymatic (glutathione peroxidase, superoxide dismutase and catalase) antioxidants were significantly decreased in Ammonium Acetate treated rats, when compared with control and were significantly increased in Ammonium Acetate-OKG treated rats compared to Ammonium Acetate treatment alone.

  • Protective influences of α-ketoglutarate on lipid peroxidation and antioxidant status in Ammonium Acetate treated rats
    Indian journal of experimental biology, 2002
    Co-Authors: Velvizhi S, K.b. Dakshayani, Perumal Subramanian
    Abstract:

    The effects of alpha-ketoglutarate on Ammonium Acetate induced hyperammonemia were studied biochemically in experimental rats. The levels of circulatory, non-protein nitrogen, serum transaminases and thiobarbituric acid reactive substances were significantly increased in Ammonium Acetate treated rats. These levels were significantly decreased in alpha-ketoglutarate and Ammonium Acetate treated rats. Similar patterns of alterations were observed in the levels of free fatty acids, triglycerides, phopholipids and cholesterol inbetween various groups. Further non-enzymatic (vitamins C and E) and enzymatic (superoxide dismutase and catalase) antioxidants were significantly decreased in Ammonium Acetate treated rats; and were significantly increased in alpha-ketoglutarate and Ammonium Acetate treated rats. The biochemical alterations during alpha-ketoglutarate treatment could be due to (i) the detoxification of excess ammonia, (ii) by participating in the non-enzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process and (iii) by enhancing the proper metabolism of fats which could suppress oxygen radicals generation and thus prevent the lipid peroxidative damages in rats.