TREATMENT OF RATS WITH DEXAMETHASONE OR THYROXINE REVERSES ZINC DEFICIENCY-INDUCED INTESTINAL DAMAGE

Structural and functional damage to the intestine and the potential be neficial effects of dexamethasone (Dex) and thyroxine (T4) were examin ed in zinc-deficient rats. Rats were assigned to zinc deficient (ZD), control (C) or pair-fed (PF) groups and fed for 40 d a zinc deficient (1 mg/kg) diet (ZD rats) or a similar diet supplemented with 50 mg Zn/ kg (C and PF rats). Some rats of the ZD group were treated for the las t 10 d with low (250 mg/kg) or high (5 mg/kg) doses of Dex or with T4 (100 mg/kg). Serum corticosterone of T4-treated ZD rats did not differ from untreated ZD rats. Serum T4 of T4-treated ZD rats did not differ from C rats. ZD rats developed ulcerations, inflammation and edema in the small intestine, particularly in the jejunum. PF rats did not sho w mucosal changes relative to C rats. ZD rats showed significantly low er crypt cell production rate (CCPR) and labeling index (LI) in the th ree intestinal regions, and lower cell migration rate and higher turno ver time in the duodenum relative to C rats. Sucrase and maltase activ ities of ZD rats were significantly lower than C rats in the three muc osal regions. Treatment with the tow dose of Dex resulted in fewer ulc erations compared with ZD rats. In rats administered the high dose of Dex or T4, all morphological alterations disappeared; the CCPR, tl, ce ll migration rate, cell turnover time and disaccharidase activities di d not differ from C rats. In conclusion, Dex and T4 exert beneficial e ffects on zinc deficiency-induced intestinal alterations in rats.