RESUMO
Experimental studies performed on 227 rats showed that Zn-aspartate and Zn-glycinate administered ip lowered the incidence, number, and severity of the reserpine-induced gastric lesions ensuring significant protection indices. Histochemical methods revealed increased amount of mucosal glycoproteins. The activity of dehydrogenases involved in energy metabolism that modulates acid secretion in the parietal cells was depressed. RNA content in the chief cells, as premises of pepsinogen synthesis, was decreased. ATPase reaction in the periglandular capillaries was uniform and stronger, showing an improvement of gastric mucosal microcirculation. Since these histochemical changes were also noted in healthy rats receiving Zn salts, it might be suggested that they are not the mere expression of an anti-ulcer protective effect of zinc, but rather reflect its mechanism of action, relating to the complex metabolic events induced by the trace element. Our results are in agreement with those previously reported concerning the noxious influence of Zn depletion, the accelerated healing of peptic ulcer patients after Zn treatment, and the protective effect of Zn against ulcerogenesis in several experimental models involving different pathomechanisms.
