Volume 89, Issue 6, June (2003), pp. 777-786 © The Author 2003
doi:10.1079/BJN2003845

Medline/PubMed Citation | Related Articles in PubMed | Download to Citation Matcher  

Protective effect of dietary nitrate on experimental gastritis in rats

Muriel Larauche¹, Pauline M. Anton¹, Rafaël Garcia-Villar¹, Vassilia Theodorou², Jacques Frexinos³, Lionel Buéno¹ and Jean Fioramonti^1
1Neuro-Gastroenterology and Nutrition Unit, Institut National de la Recherche Agronomique, 180 chemin de Tournefeuille, BP3, 31931 Toulouse cedex 9, France
²Department of Physiology, Ecole Supérieure d'Agriculture de Purpan, Toulouse, France
³Department of Gastroenterology, Rangueil Hospital, Toulouse, France

 (Received 6 June 2002–Revised 10 December 2002–Accepted 19 January 2003)

Nitrates have long been considered as harmful dietary components and judged responsible for deleterious effects on human health, leading to stringent regulations concerning their levels in food and water. However, recent studies demonstrate that dietary nitrate may have a major role in human health as a non-immune mechanism for host defence, through its metabolism to NO in the stomach. NO is a versatile molecule and although evidence exists showing that administration of low doses of exogenous NO protects against gastrointestinal inflammation, higher NO doses have been shown to exacerbate injury. So, the effect of an ingestion of nitrates in doses corresponding to a normal diet in human consumers on an experimental gastritis induced by iodoacetamide in rats was investigated. During gastritis one of the following compounds was given orally: water; KNO₃; the NO donor sodium nitroprusside; the NO scavenger haemoglobin given with either water or KNO₃. N(G)-nitro-L-arginine methyl ester (L-NAME), a non-specific NO synthase inhibitor, was administered with either water, iodoacetamide alone, or combined with KNO₃. After killing, the stomach was resected and microscopic damage scores, myeloperoxidase and NO synthase activities were determined. Iodoacetamide-induced gastritis was significantly reduced by KNO₃ administration, an effect which was reproduced by sodium nitroprusside and reversed by haemoglobin. L-NAME induced gastric mucosal damage in itself, and KNO₃ did not prevent the gastritis induced by iodoacetamide associated with L-NAME. In conclusion, dietary nitrate exerts a protective effect against an experimental gastritis in rats by releasing NO in the stomach but such an effect requires the production of endogenous NO.

Abbreviations: cNOS; constitutive NO synthase; EGTA; ethylene-glycol-bis(a-aminoethyl)-N,N,N¢,N¢-tetra-acetic acid; HEPES; 4-(2-hydroxy- ethyl)piperazine-1-ethanesulfonic acid; iNOS; inducible NO synthase; L-NAME; N(G)-nitro-L-arginine methyl ester; MPO; myeloperoxidase; NOS; nitric oxide synthase; SNP; sodium nitroprusside

Keywords:
Nitric oxide, Inflammation, Dietary nitrate, Stomach