51.   There was no significant difference in the concentration of -tocopherol in the gastric mucosa among the normal, the control, and the SOD plus catalase groups.

52.   Even when SOD was administered, its activity in the gastric mucosa did not increase.

53.   These findings suggest that in the gastric mucosa free radicals or lipid peroxides are injurious offensive factors and GSH is a protecting defensive factor.

54.   The decrease in GSH in our study was accompanied by an increase in lipid peroxides measured as a TBA-reactive substances in the gastric mucosa.

55.   These findings suggest that indomethacin itself, or depletion of prostaglandins, inhibits GSH peroxidase activity of the gastric mucosa.

56.   Our findings are in line with those of Banergee, who recently showed the inhibition of peroxidase activity in the mitochondrial fraction of rat gastric mucosa by indomethacin.

57.   Twenty patients taking NSAIDs had a histologically normal antral gastric mucosa.

58.   Perhaps the most striking finding in the present study was the histological analysis of the gastric mucosa surrounding the tumour.

59.   An effort to correlate mucosal pepsinogen accumulation with total peptic activity and peptic cell mass shows good correlation between these parameters in normal and inflamed gastric mucosa.

60.   The fact that H pylori infected gastric mucosa has normal pepsinogen activity indicates adequate zymogen production and storage.