OXYGEN-METABOLISM IN BLOOD OF PATIENTS WITH GASTRIC AND DUODENAL-ULCER DISEASE

Citation
K. Kedziorakomatowska et al., OXYGEN-METABOLISM IN BLOOD OF PATIENTS WITH GASTRIC AND DUODENAL-ULCER DISEASE, Hepato-gastroenterology, 42(3), 1995, pp. 246-249
Citations number
27
Categorie Soggetti
Surgery,"Gastroenterology & Hepatology
Journal title
ISSN journal
01726390
Volume
42
Issue
3
Year of publication
1995
Pages
246 - 249
Database
ISI
SICI code
0172-6390(1995)42:3<246:OIBOPW>2.0.ZU;2-0
Abstract
Among multiagent mechanisms causing peptic ulcer disease, oxygen free radicals hypothesis is reasonable. Our investigation concerned the det ermination of oxygen free radicals generation lipid peroxidation and e nzymatic antioxidative defense in blood of patients with peptic ulcer disease. The examinations were performed in 79 males, non- smokers, ag ed 20-51 with peptic ulcer disease, clinically diagnosed as gastric or duodenal ulcer. Biochemical investigations were carried out on blood platelets obtained from venous blood according to the centrifugation f ractionation technique. Superoxide dismutase (CuZn-SOD) (EC 1. 15. 1. 1.) activity and malonyl dialdehyde (MDA) concentration were determine d according to Misra and Fridovich (1972) and Placer et al (1966) meth ods, respectively. Oxygen free radicals as the superoxide anion O-2(-) generation in blood according to Bellavite et al, (1983) method was d etermined. The results indicate that patients with peptic ulcer diseas e have a higher level of malonyl dialdehyde in blood platelets, wherea s the superoxide dismutase activity is significantly decreased in comp arison with the control group. Oxygen free radicals generation both in patients with peptic ulcer disease as in healthy men is maintained at normal level. Our data suggest that in spite of similar range of oxyg en free radicals generation both in patients with peptic ulcer disease and healthy men, the injury to patients by superoxide anion is more d estructive and harmful to cells, because the enzymatic antioxidative d efense is decreased. The increase of lipid peroxidation in patients wi th peptic ulcer disease also supports this conclusion.