TY - JOUR
T1 - Mechanism of Diethyldithiocarbamate‐Induced Gastric Ulcer Formation in the Rat
AU - Ogino, Keiki
AU - Hobara, Tatsuya
AU - Kawamoto, Toshihiro
AU - Kobayashi, Haruo
AU - Iwamoto, Susumu
AU - Oka, Shinji
AU - Okazaki, Yukinori
PY - 1990/2
Y1 - 1990/2
N2 - 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. 1990 Nordic Pharmacological Society
AB - 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. 1990 Nordic Pharmacological Society
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U2 - 10.1111/j.1600-0773.1990.tb00719.x
DO - 10.1111/j.1600-0773.1990.tb00719.x
M3 - Article
C2 - 2156249
AN - SCOPUS:0025233601
SN - 1742-7835
VL - 66
SP - 133
EP - 137
JO - Basic and Clinical Pharmacology and Toxicology
JF - Basic and Clinical Pharmacology and Toxicology
IS - 2
ER -