Efecto secuestrador del D-002 sobre radicales hidroxilo en mucosa gástrica

introduction: the etiology of the gastric ulceration is associated to the imbalance between aggressive and defensive factors acting upon the gastric mucosa. d-002, a mixture of 6 higher primary alcohols purified from the beeswax, cause some multiple mechanism-mediated gastroprotective effects and decrease of lipid peroxidation in the gastric mucosa. objective: to determine whether d-002 can scavenge the in vivo added or in vivo generated hydroxyl radical in rats with indometacin-induced gastric ulcer or not. methods: for the in vitro experiment, d-002 was added at concentrations 0.9 and 1 000 mg/ml for the in vivo experiment, the rats were randomized into 6 groups: one negative control, and five indometacin-treated groups as follows a positive excipient-treated control, three under d-002 treatment (5, 25 or 100 mg/kg, respectively, p.o.), and another group treated with omeprazole (20 mg/kg i.p.). these lines of treatment were given 1 hour (excipient and d-002) or 30 min (omeprazole) prior to inducing the ulcers. in both experiments, aliquots from the gastric mucosa were taken and the damage infringed to 2-deoxiribose by the hydroxyl radical was determined. results: oral administration of d-002, rather than in vitro addition, significantly protected 2-desoxiribose from the oxidative damage depending on the dosage as compared to the positive control. conclusions: these results indicate that the ability of the orally administered d-002 (25 and 100 mg/kg) to scavenge the hydroxyl radical endogenously generated on the gastric mucosa by indometacin could contribute to its antioxidant and gastroprotective effects against the damage that the non-steroidal anti-inflammatory drugs carry to the gastric mucosa.