Mechanism of Diethyldithiocarbamate‐Induced Gastric Ulcer Formation in the Rat

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Abstract
Diethyldithiocarbamate (DDC) was injected subcutaneously in the rat and the mechanism of gastric ulcer formation was investigated. DDC induced gastric ulcers in a dose‐dependent manner. DDC significantly suppressed gastric mucosal copper‐zinc superoxide dismutase (Cu, Zn‐SOD) activity at 2 hr. However, manganese‐superoxide dismutase (Mn‐SOD) activity was not changed. Gastric mucosal blood flow (GMBF) decreased to 52% of the control level at 2 hr after administration of DDC and gradually increased to reach the control level by 7 hr. A Shay rat preparation (4 hr) was used to study gastric secretion. DDC (200, 400 and 800 mg/kg) inhibited acid secretion to about 80% of the control level. Histopathological examination of the gastric mucosa after administration of DDC revealed mucosal congestive findings from 1 hr to 3 hr. These data suggested that the mechanism of DDC‐induced gastric ulcer formation may be attributable to a decreased level of GMBF and O2‐ production owing to decreased SOD activity.