Prevention by zinc of cadmium-induced alterations in pancreatic and hepatic functions.

Document Type

Article

Department

Brain and Mind Institute

Abstract

1.Subacute cadmium treatment (CdCl2, 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 (ZnCl2, 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.

Comments

This work was published before the author joined Aga Khan University.

Publication (Name of Journal)

British Journal of Pharmacology

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