Intestinal damage induced by zinc deficiency is associated with enhanced CuZn superoxide dismutase activity in rats effect of dexamethasone or thyroxine treatment

Zinc has a wide spectrum of biological activities and its deficiency has be en related to various tissue dysfunctions and alterations of normal cell me tabolism Zinc also plays an important role in the antioxidant cellular defe nses being a structural element of the non-mitochondrial form of the enzyme superoxide dismutase (CuZnSOD). We have already reported that Zn deficienc y induces severe alterations in the rat intestine, that are reverted by tre atment with dexamethasone (Dex) or thyroxine (T4). Here we report a paradox ical increase of CuZnSOD activity in rat intestine after 20 and 40 days of zinc deficiency. The increase of CuZnSOD activity is not due to an upregula tion of gene expression because both Northern and Western blot analysis ind icate that CuZnSOD mRNA and protein levels are not affected by zinc deficie ncy. A significant increase of lipid peroxidation was also observed in duod enum and jejunum associated with zinc deficiency. Treatment with either Dex or T4 to zinc-deficient rats protects against intestinal oxidative damage and results in SOD activity similar to control rats. Because glutathione pe roxidase and catalase activities decreased in zinc deficiency, we speculate that the increase in SOD activity may be associated with an accumulation o f hydrogen peroxide that may activate inflammatory molecules, further worse ning tissue damage. (C) 1999 Elsevier Science Inc.Zinc has a wide spectrum of biological activities and its deficiency has been related to various tis sue dysfunctions and alterations of normal cell metabolism Zinc also plays an important role in the antioxidant cellular defenses being a structural e lement of the non-mitochondrial form of the enzyme superoxide dismutase (Cu ZnSOD). We have already reported that Zn deficiency induces severe alterati ons in the rat intestine, that are reverted by treatment with dexamethasone (Dex) or thyroxine (T4). Here we report a paradoxical increase of CuZnSOD activity in rat intestine after 20 and 40 days of zinc deficiency. The incr ease of CuZnSOD activity is not due to an upregulation of gene expression b ecause both Northern and Western blot analysis indicate that CuZnSOD mRNA a nd protein levels are not affected by zinc deficiency. A significant increa se of lipid peroxidation was also observed in duodenum and jejunum associat ed with zinc deficiency. Treatment with either Dex or T4 to zinc-deficient rats protects against intestinal oxidative damage and results in SOD activi ty similar to control rats. Because glutathione peroxidase and catalase act ivities decreased in zinc deficiency, we speculate that the increase in SOD activity may be associated with an accumulation of hydrogen peroxide that may activate inflammatory molecules, further worsening tissue damage. (C) 1 999 Elsevier Science Inc.