The clinical and experimental studies have demonstrated that the excessive bioavailability of Zn indiet causes magnesium (Mg) deficiency hyperglycemia and hyperinsulinemia/insulin resistancethrough activation of adrenal cortex for the synthesis and release of cortisol. These defects may beameliorated 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 perkg diet for 8 weeks. Group III (Zn-induced-hypomagnesaemia, n=30) administered a daily oral doseof 160 mg ZnSO4.7H2O /kg diet for 8 weeks. Blood samples and tissue specimens (stomach) werecollected from all groups at 2, 4, 6 and 8 week after treatment. All sera were processed fordetermination of Mg, acetylcholine esterase (AChE), creatine phosphokinase (CPK), lactatedehydrogenase (LDH), malondialdehyde (MDA), insulin, glucose, cortisone, glutathione peroxidaseactivity, reduced glutathione (GSH) concentration and nitric oxide (NO) were determined in stomachtissues in addition to plasma catalase activity. The obtained results revealed that hyperzincemia inmale rats significantly increased the levels of serum glucose , serum cortisone, serum lactatedehydrogenase, serum creatine phosphokinase, serum malondialdehyde, erythrocytes catalase andsignificantly decreased the levels of serum magnesium, insulin, acetylcholine esterase, erythrocytesGSH-Px, erythrocytes reduced GSH and nitric oxide in stomach tissue compared to the control rats. |
