Kedziora-Kornatowska K, Tkaczewski W, Blaszczyk J, Buczyn'ski A, Chojnacki J, Kedziora J
Department of Gastroenterology, Military Medical University, Kódz, Poland.
Hepatogastroenterology. 1995 Jul;42(3):246-9.
Among multiagent mechanisms causing peptic ulcer disease, oxygen free radicals hypothesis is reasonable. Our investigation concerned the determination of oxygen free radicals generation lipid peroxidation and enzymatic antioxidative defense in blood of patients with peptic ulcer disease. The examinations were performed in 79 males, non-smokers, aged 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 fractionation technique. Superoxide dismutase (CuZn-SOD) (EC 1.15.1.1.) activity and malonyl dialdehyde (MDA) concentration were determined according to Misra and Fridovich (1972) and Placer et al (1966) methods, respectively. Oxygen free radicals as the superoxide anion O2- generation in blood according to Bellavite et al. (1983) method was determined. The results indicate that patients with peptic ulcer disease have a higher level of malonyl dialdehyde in blood platelets, whereas the superoxide dismutase activity is significantly decreased in comparison 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 oxygen free radicals generation both in patients with peptic ulcer disease and healthy men, the injury to patients by superoxide anion is more destructive and harmful to cells, because the enzymatic antioxidative defense is decreased. The increase of lipid peroxidation in patients with peptic ulcer disease also supports this conclusion.
在导致消化性溃疡疾病的多种因素中，氧自由基假说是合理的。我们的研究涉及对消化性溃疡疾病患者血液中氧自由基生成、脂质过氧化和酶促抗氧化防御的测定。对79名年龄在20 - 51岁、临床诊断为胃溃疡或十二指肠溃疡的男性非吸烟者进行了检查。根据离心分级技术，对从静脉血中获取的血小板进行生化研究。分别根据米斯拉和弗里多维奇（1972年）以及普拉塞等人（1966年）的方法测定超氧化物歧化酶（铜锌超氧化物歧化酶）（EC 1.15.1.1.）活性和丙二醛（MDA）浓度。根据贝拉维特等人（1983年）的方法测定血液中作为超氧阴离子O2-生成的氧自由基。结果表明，消化性溃疡疾病患者血小板中的丙二醛水平较高，而与对照组相比，超氧化物歧化酶活性显著降低。消化性溃疡疾病患者和健康男性的氧自由基生成均维持在正常水平。我们的数据表明，尽管消化性溃疡疾病患者和健康男性的氧自由基生成范围相似，但超氧阴离子对患者细胞的损伤更具破坏性和危害性，因为酶促抗氧化防御能力下降。消化性溃疡疾病患者脂质过氧化的增加也支持这一结论。
