Lysosomal acid hydrolase alterations in gastric mucosa from an experimental peptic ulcer model.
Ligation of the common bile duct in pigs causes esophagogastric ulceration in 100 per cent of instances within seven days postoperatively. The results of previous studies have suggested a peptic cause for these ulcers. The possible role of lysosomal acid hydrolases in the primary pathogenesis was investigated herein. The total activities of two lysosomal acid hydrolases in mucosal specimens taken at biopsy from ulcerated pars esophagea and one in ulcerated gastric cardia were significantly lower in pigs undergoing ligation of the bile duct postoperatively, than in comparable pigs undergoing sham operations while there was evidence of increased extracellular activity. Mucosal deoxythymidine kinase activity was increased in gastric cardia suggesting attempted repair. Pigs with parakeratosis of the pars esophagea and edema of the gastric cardia, consistent with the preulcerative state also showed lowered enzyme activity. These results in intact pigs suggest that release of lysosomal acid hydrolases occurs with and may precede peptic ulceration.
D000118:Acetylglucosaminidase / Q000378:metabolism; D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D002402:Cathepsin D / Q000378:metabolism; D004195:Disease Models, Animal; D005753:Gastric Mucosa / Q000201:enzymology* / Q000473:pathology; D006867:Hydrolases / Q000378:metabolism*; D008247:Lysosomes / Q000201:enzymology*; D010437:Peptic Ulcer / Q000201:enzymology* / Q000473:pathology; D013552:Swine; D013937:Thymidine Kinase / Q000378:metabolism; D013997:Time Factors; D001616:beta-Galactosidase / Q000378:metabolism
D013937:Thymidine Kinase; D006867:Hydrolases; D000135:Acid Phosphatase; D001616:beta-Galactosidase; D000118:Acetylglucosaminidase; D002402:Cathepsin D