TY - JOUR
T1 - Sulphydryl blocker induced gastric damage is ameliorated by scavenging of free radicals
AU - Karmeli, F.
AU - Okon, E.
AU - Rachmilewitz, D.
PY - 1996
Y1 - 1996
N2 - Background - Sulphydryl compounds and nitric oxide are essential in maintaining gastric mucosal integrity. Aims - To characterise the gastric damage induced by a sulphydryl blocker, to evaluate the role of nitric oxide in its pathogenesis, and to reveal its possible prevention by scavenging of free radicals. Methods - Gastritis was induced in rats by addition of iodoacetamide (0.1%) to the drinking water, with and without dally intragastric administration of TEMPOL. After death, the stomach was resected, washed, lesion area assessed, and mucosal inflammatory mediators, myeloperoxidase and nitric oxide synthase activities were determined. Results - Administration of iodoacetamide induced gastric mucosal erosions present for up to two weeks. Myeloperoxidase activity was increased for up to seven days and nitric oxide synthase activity was significantly decreased for up to 14 days. Treatment for seven days with the free radical scavenger, TEMPOL, decreased by 68% the damage induced by iodoacetamide. Conclusions - Gastric damage induced by iodoacetamide, a sulphydryl alkylator, accompanied by inhibition of nitric oxide synthase activity shows the important contribution of sulphydryl compounds and nitric oxide to the maintenance of gastric mucosal integrity. Nitric oxide donation and scavenging of free radicals may be a novel approach to prevent gastric damage.
AB - Background - Sulphydryl compounds and nitric oxide are essential in maintaining gastric mucosal integrity. Aims - To characterise the gastric damage induced by a sulphydryl blocker, to evaluate the role of nitric oxide in its pathogenesis, and to reveal its possible prevention by scavenging of free radicals. Methods - Gastritis was induced in rats by addition of iodoacetamide (0.1%) to the drinking water, with and without dally intragastric administration of TEMPOL. After death, the stomach was resected, washed, lesion area assessed, and mucosal inflammatory mediators, myeloperoxidase and nitric oxide synthase activities were determined. Results - Administration of iodoacetamide induced gastric mucosal erosions present for up to two weeks. Myeloperoxidase activity was increased for up to seven days and nitric oxide synthase activity was significantly decreased for up to 14 days. Treatment for seven days with the free radical scavenger, TEMPOL, decreased by 68% the damage induced by iodoacetamide. Conclusions - Gastric damage induced by iodoacetamide, a sulphydryl alkylator, accompanied by inhibition of nitric oxide synthase activity shows the important contribution of sulphydryl compounds and nitric oxide to the maintenance of gastric mucosal integrity. Nitric oxide donation and scavenging of free radicals may be a novel approach to prevent gastric damage.
KW - TEMPOL
KW - free radicals
KW - gastric damage
KW - iodoacetamide
KW - nitric oxide
UR - http://www.scopus.com/inward/record.url?scp=0030035210&partnerID=8YFLogxK
U2 - 10.1136/gut.38.6.826
DO - 10.1136/gut.38.6.826
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C2 - 8984018
AN - SCOPUS:0030035210
SN - 0017-5749
VL - 38
SP - 826
EP - 831
JO - Gut
JF - Gut
IS - 6
ER -