Shinji Oka

Human serum immuno-reactive copper, zinc-superoxide dismutase assayed with an enzyme monoclonal immunosorbent in patients with digestive cancer.

Two types of monoclonal antibodies, N4 and N6, were raised against human copper, zinc-superoxide dismutase (Cu,Zn-SOD). An enzyme-linked immunosorbent assay for Cu,Zn-SOD was developed in sandwich method using these monoclonal antibodies. The measurable assay range was 1.0-100 micrograms/l and the coefficient of variation within and between series were 7.5% and 8.1%. Sera of 154 healthy control subjects displayed a low level (14 micrograms/l) of immunoreactive Cu,Zn-SOD with a logarithmic normal distribution. On the other hand, serum Cu,Zn-SOD levels were significantly elevated in patients with various digestive cancers.

Gastric mucosal protection and superoxide dismutase.

Diethyldithiocarbamate (DDC), an inhibitor of Cu,Zn-su-peroxide dismutase (SOD), at a dose of 500 mg/kg or aminotriazole (AT), an inhibitor of catalase, at a dose of 2,000 mg/kg reduced slightly gastric mucosal SOD activity, did not change gastric mucosal blood flow (GMBF), and did not cause gastric ulcers. However, when both DDC and AT were administered together, gastric mucosal SOD activity and GMBF remarkably decreased, and gastric ulcers appeared. Moreover, the administration of SOD attenuated gastric ulcer induced by DDC plus AT. These results suggested that SOD may play an important role in the gastric mucosal defense mechanisms against active oxygen species.

Role of active oxygen species in diethyldithiocarbamate-induced gastric ulcer in the rat.

Diethyldithiocarbamate, an inhibitor of Cu,Zn-superoxide dismutase, was recently found to be ulcerogenic in the rat stomach, and active oxygen species were found to be responsible for its ulcerogenicity. To clarify which active oxygen species play a role in ulcerogenesis, the effects of various scavengers and iron-chelators were studied. As superoxide dismutase and catalase reduced the ulcerogenesis induced by diethyldithiocarbamate, the superoxide radical and hydrogen peroxide were considered to play a pathogenic role in this ulcer model.