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PREVENTION BY ZINC OF CADMIUM‐INDUCED ALTERATIONS IN PANCREATIC AND HEPATIC FUNCTIONS
Author(s) -
MERALI Z.,
SINGHAL R.L.
Publication year - 1976
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1976.tb10387.x
Subject(s) - medicine , endocrinology , cadmium , glucagon , insulin , zinc , gluconeogenesis , chemistry , glycogen , glycogenolysis , cyclase , basal (medicine) , adenylate kinase , stimulation , homeostasis , glucose homeostasis , metabolism , enzyme , biology , biochemistry , insulin resistance , organic chemistry
1 Subacute cadmium treatment (CdCl 2 , 1 mg/kg twice daily for 7 days) in rats disturbs glucose homeostasis as shown by hyperglycemia and decreased glucose tolerance associated with suppression of insulin release, enhancement of hepatic gluconeogenic enzymes and decrease in hepatic glycogen content. 2 Exposure to cadmium increases hepatic cyclic adenosine 3′,5′‐monophosphate (cyclic AMP) and this is accompanied by stimulation of basal, adrenaline‐as well as glucagon‐stimulated form(s) of adenylate cyclase. 3 In contrast to cadmium, subacute administration of zinc (ZnCl 2 , 2 mg/kg twice daily for 7 days) fails to alter the activities of hepatic gluconeogenic enzymes, cyclic AMP synthesis, as well as glucose clearance and insulin release in response to a glucose load. 4 Zinc, when administered at the same time as cadmium, prevents the cadmium‐induced lesions in both hepatic and pancreatic functions. 5 The results are discussed in relation to the possible mechanisms of cadmium toxicity and to the role of sulphydryl groups in the protection exercised by zinc.