[Changes in the activities of lysosomal enzyme (glycosidase) in experimental acute gastric mucosal lesion].
In order to study the pathogenesis of stress-induced ulcer, we induced experimental acute gastric mucosal lesion (AGML) by loading the rats with heat-burn stress, and we monitored the activities of four glycosidases having mucolytic action. The activity of beta-N-Acetyl-D-glucosaminidase was 59.50 +/- 3.27 micrograms 4 MU/h/mg protein before stress, increasing significantly one to three hours after burn, and that of beta-N-Acetyl-D-galactosaminidase was 17.50 +/- 1.60 micrograms 4 MU/h/mg protein before stress, increasing significantly two hours after burn. The activities of two uronic acid exoglycosidases, alpha-L-Iduronidase and beta-D-Glucuronidase were 4.52 +/- 0.37 and 8.68 +/- 0.89 micrograms phenol/h/mg protein before stress; both increased significantly one to three hours after burn. Burn stress caused microcirculatory disturbance in the gastric mucosa, release of histamine and other vasoactive substances, and accelerated release of lysosomal enzymes. Triggered by these reaction, glycosidases were released to cause the degradation of glycoprotein in the tissue and resulted in the breakdown of the defense mechanisms.
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Watanabe
D000208:Acute Disease; D000818:Animals; D005753:Gastric Mucosa / Q000201:enzymology*; D006026:Glycoside Hydrolases / Q000378:metabolism*; D008247:Lysosomes / Q000201:enzymology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013276:Stomach Ulcer / Q000201:enzymology* / Q000473:pathology
D006026:Glycoside Hydrolases