Role of iron and lipid peroxidation in mediating peroxynitrite-induced toxicity to cultured gastric mucosal cells

Abstract

that endoscopically negative patients with GER-related symptoms may have enhanced protective mechanisms. Aims: 1. To assess bicarbonate, non-bicarbonate, protein, transforming growth factor ct (TGFtx) and prostaglandin E 2 (PGE2) in salivary secretion in patients with endoscopically negative [E(-)] GERD. 2. To compare the obtained results with corresponding values in asymptomatic controls (C) and patients with RE~ Subjects & Methods: The study was conducted in 30 patients with RE (12F & 18M, mean age of 49), in 39 asymptomatic volunteers (16F & 23M, mean age of 40), and in 10 patients with E(-) GERD (SF & 5M, mean age of 40). Salivary secretions were collected under basal conditions, daring mastication, and during intraesophageal mechanical and chemical stimulation, mimicking the GER scenario, using an esophageal perfusion catheter. Salivary bicarbonate and non-bicarbonate were measured using Titra-Lab (Radiometer America, IL). Salivary protein was quantitated using Lowry method, whereas TGFot, and PGE z by RIA (Amersham, IL and Biomed. Technol. Inc. MA). Statistical analysis was implemented by E-Stat (Jandel Sci. CA) software. Results: Salivary bicarbonate in patients with E(-) GERD was significantly higher than in C and in RE during intraesophageal chemical stimulation (P < 0.05). Salivary protein was significantly higher in GERD E(-) than in and RE during intraesophageai mechanical and chemical stimulation (P < 0.05). Salivary TGFot output in GERD E(-) was significantly higher than in RE (P < 0.05) but not controls during intraesophageal mechanical stimulation. Salivary PGE z output, on the other hand, in GERD E(-) was significantly higher than in C (P < 0.05) but not RE during intraesophageal chemical stimulation. Conclusion: . A strong salivary secretory response to intraesophageal mechanical and chemical stimuli in patients with GERD E(-) in terms of bicarbonate, protein, TGFa, and PGE z seem to mediate resistance to the development of endoscopic mucosal changes by GER. ° This could explain t he lack of endoscopic esophagitis in the majority of GERD patients and could be a therapeutic target in future treatment strategies.