ABSTRACT
Experimental and clinical gastrointestinal data reported that nitrosative stress development involved in impaired barrier function, altered motility and a lowered threshold to noxious stimuli, but its pathogenetic role in diabetic esophagopathy remains unexplored. We tested the hypothesis that an imbalance in nonenzymatic glycation and glycooxidation, enhanced peroxynitrite formation, may play an important role in development esophageal mucosa (EM) lesions during streptozotocin-induced experimental hyperglycemia (EHG). To understand the biological significance of EM resistance in vivo used a glycomic approach to identification of lectin receptors glycosylation pattern. Were enrolled rat groups without/with EHG & modification of NO/NOS activity by L-arginine (L-arg) and indomethacin pre-treatment. Survival rate, destruction occurrence ratio, the size of EM lesions, and the number of EM lesions was investigated. To access the oligosaccharide residues the peroxidase conjugated lectin (HPA, SNA, WGA, PNA)-diaminobenzidine procedure was performed to EM sections. EHG was monitored daily by glucometer. Content of NO (NO(n)) was determinated by Griess reagent and reactive oxygen-scavenging systems (ROSS) activity - generally accepted biochemical methods. In EHG and L-arg pretreatment group reduced NO(n) and EM injury with markedly rise ROSS activity significantly vs to control; in the group with indomethacin pretreatment existed different ROSS activity. Presence of heterogeneous glycosylation pattern in different layers of EM was shown. In EHG staining with PNA and SNA were strongly positive. NS and ROSS play a critical role in esophagoprotection induced by EHG, because both involved increases in iNOS expression. These results indicate the usefulness of glycomic approach as multifunctional substrate of early evaluation of NS in esophageal physiopathy.