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Title: [Nickel chloride and alloxan. I. Determination of glucose, insulin and superoxide dismutase in blood and pancreas of rats]. Author: Novelli EL, Rodrigues NL, Ribas Ozonas B. Journal: Acta Physiol Pharmacol Latinoam; 1987; 37(3):377-93. PubMed ID: 3332532. Abstract: Copper-zinc superoxide-dismutase (SOD-E.C. 1.15.1.1.) is present in high concentration in the beta-cells of pancreatic islets, and its specific activity correlates with maintenance of beta-cell function. In this paper the authors studied the effect of nickel chloride (s.c.) on alloxan toxicity. It was found that alloxan (100 mg x kg-1) inhibited insulin release of rats islets and thus, induced hyperglycemic response. The activity of erythrocytes and pancreatic SOD enzymes was partially inhibited upon alloxan treatment. It was found that nickel chloride (s.c. 10 mg x kg-1) produced stimulation of insulin release in rats treated by subcutaneous (s.c.) alloxan injection. The potential of NiCl2 to prevent alloxan induced diabetes was shown by the observed SOD specific activity increase in rats. In conclusion, our experiments show that nickel chloride prevented alloxan induced toxicity in rats.[Abstract] [Full Text] [Related] [New Search]