[Changes in gastric mucosal glycosidases and thiobarbituric acid reactants induced by burn stress in obstructive jaundice rats].
To elucidate the pathogenesis of acute gastric mucosal lesion (AGML), burn stress was loaded in rats with and without obstructive jaundice. The activation of gastric mucosal glycosidases (beta-N-acetyl-D-glucosaminidase (NAG), beta-glucuronidase (BG)), which were released into the cytoplasm as a results of instability of the lysosomal membrane, was studied biochemically, enzymatically and histochemically after burn stress with and without obstructive jaundice. The latent enzyme activity calculated by NAG or BG, which represented the stability of lysosomal membrane, was lowest at 2-3 hour after burn stress in both groups. In other words, the degree of activation of the glycosidases was highest at 2-3 hour after burn stress. The latent enzyme activity calculated by NAG decreased significantly (p < 0.05) at 1 hour after burn stress in obstructive jaundice group compared with the non-obstructive jaundice group. The staining of NAG before burn stress was observed in mucus neck cell and surface epithelial cell in granular shape and it was observed diffusely after burn stress, especially in obstructive jaundice group. The changes in staining of BG was similar to NAG. Before activation of glycosidases, the thiobarbituric acid reactants, which are considered products of lipid peroxidation, increased promptly at 30 min after burn stress in both groups. Ulcer index increased gradually after burn stress and the significance was found between in the obstructive jaundice group and in non-obstructive jaundice group at 3 hour after burn stress. It's concluded that obstructive jaundice accelerated the fragility of lysosomal membrane after burn stress and these change were considered to be the reasons of frequent occurrence of AGML.
Kunisaki
C
C
Second Department of Surgery, Yokohama City University, School of Medicine.
D000118:Acetylglucosaminidase / Q000378:metabolism; D000818:Animals; D002056:Burns / Q000201:enzymology*; D002779:Cholestasis / Q000201:enzymology*; D005753:Gastric Mucosa / Q000201:enzymology* / Q000473:pathology; D006026:Glycoside Hydrolases / Q000378:metabolism*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000503:physiopathology; D013858:Thiobarbiturates / Q000494:pharmacology*
D013858:Thiobarbiturates; D006026:Glycoside Hydrolases; D000118:Acetylglucosaminidase; C029684:thiobarbituric acid