Abstract of research

BIOCHEMICAL EFFECT OF HYPERZINCEMIA ON EXPERIMENTALLY INDUCED HYPOMAGNESAEMIA IN RATS

Yakout A.Y. El-Senosi, Afaf D. Abdel-Mageid, Mohammed A. Hussein

Abstract

The clinical and experimental studies have demonstrated that the excessive bioavailability of Zn in diet causes magnesium (Mg) deficiency hyperglycemia and hyperinsulinemia/insulin resistance through activation of adrenal cortex for the synthesis and release of cortisol. These defects may be ameliorated if the ionic imbalance has been corrected. This study was carried out on male rats (n=80) divided into three groups: Group I (Control, n=20) received 20 mg Zn/kg diet orally daily for 8 weeks. Group II (Zn-induced-hypomagnesaemia, n=30) received daily oral dose of 80 mg ZnSO4.7H2O per kg diet for 8 weeks. Group III (Zn-induced-hypomagnesaemia, n=30) administered a daily oral dose of 160 mg ZnSO4.7H2O /kg diet for 8 weeks. Blood samples and tissue specimens (stomach) were collected from all groups at 2, 4, 6 and 8 week after treatment. All sera were processed for determination of Mg, acetylcholine esterase (AChE), creatine phosphokinase (CPK), lactate dehydrogenase (LDH), malondialdehyde (MDA), insulin, glucose, cortisone, glutathione peroxidase activity, reduced glutathione (GSH) concentration and nitric oxide (NO) were determined in stomach tissues in addition to plasma catalase activity. The obtained results revealed that hyperzincemia in male rats significantly increased the levels of serum glucose , serum cortisone, serum lactate dehydrogenase, serum creatine phosphokinase, serum malondialdehyde, erythrocytes catalase and significantly decreased the levels of serum magnesium, insulin, acetylcholine esterase, erythrocytes GSH-Px, erythrocytes reduced GSH and nitric oxide in stomach tissue compared to the control rats.