With 12 different isozymes, Carbonic anhydrase plays a key role in acid-base balance, CO 2 and ion transport…etc. Any change in the enzymatic activity may cause disturbances in these processes leading to different disorders. The study focuses on the association of electromorphs of Carbonic anhydrase-II (CAII) with peptic ulcers and ulcerated cancers, which result due to an imbalance between the aggressive and defensive factors necessary for maintaining the pH of the gastric lumen. Endoscopically confirmed 210 duodenal ulcer, 50 gastric ulcer and 50 gastric cancer cases were considered along with 110 healthy individuals for comparative study. Since H.pylori infection is considered as primary risk factor, Rapid Urease Test (RUT) was performed to identify the infection status in both disease and control groups. Phenotyping of CA II was carried out in both control and disease by subjecting the haemolysate to PAGE and detecting the bands based on esterase activity of CA II using α or β-napthol acetate. Frequency distribution of different phenotypes with respect to various factors was compiled and relative risk estimates were obtained using Woolf's δ-method.The allelic frequencies of CA II calculated, were tested for Hardy-Weinberg equilibrium. Frequency distribution of CA II phenotypes showed increased number of heterozygotes (2-1) in controls, against higher number of homozygotes (2-2) in diseased group. Similarly, blood group O was predominant in disease group as against group B in controls. Most of the controls were negative for H.pylori infection and almost 100% individuals in disease group were positive. In conclusion, the allele CA II 2 was found to be associated with peptic ulcers and ulcerated cancers along with blood group O and positive H.pylori infectivity status, predisposing an individual to the disease condition.
Background: Duodenal ulcers are mucosal erosions that penetrate into the muscularis propria of the duodenum. They are a result of an imbalance between aggressive and defensive factors. Various environmental factors like Helicobacter pylori infection, addictions to smoking and alcohol etc. and genetic factors have been reported to be associated with duodenal ulceration. Alpha-1-antitrypsin was studied for its role as a genetic marker and specific allelic association to protein functioning and alteration. Serum samples from 185 normal subjects and 210 duodenal ulcer cases were typed for the phenotypes following PAGE (polyacrylamide gel electrophoresis) and immunofixation using specific commercial antisera with appropriate staining protocols. In general, 'M' allele of alpha-1-antitrypsin was found to be predominant in healthy normal subjects, with the gene frequencies being 0.679 (M), 0.299 (Z) and 0.0214 (S). Whereas in duodenal ulcer cases, Z and S alleles were found to be predominant with a significant association of MS, ZZ and MZ phenotypes (χ 2: 49.98) and the gene frequencies being 0. 113 (M), 0. 347 (Z) and 0.506 (S). Predominance of Z and S alleles indicates that these alleles may encode for reduced synthesis of alpha-1-antitrypsin, hence decreased neutralization of proteases like trypsin and chymotrypsin inhibited by alpha-1-antitrypsin, thereby resulting in ulcers. The study highlights the association of Z and S alleles of the potent protease inhibitor alpha-1-antitrypsin and also suggests its role as a genetic marker in ulcerogenesis.
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