title: Erythrocyte glucose-6-phosphate dehydrogenase activity in laboratory rats treated with amoxiclav, lidaprim and 1-chloro-2,4-dinitrobenzen.
abstract: The enzyme glucose-6-phosphate dehydrogenase (G6P-DH, EC.1.1.1.49) catalyzes the oxidation of glucose-6-phosphate in 6-phosphogluconat which is indispensable in the defence of erythrocytes from oxidative insult. The aim of this study was to examine the influence of commonly used drugs in our medical practice, amoxiclav (amoxicillin-clavulanate combination) and lidaprim (trimethoprim-sulfamethrole combination) respectively, upon the erythrocyte G6P-DH activity in experimental rats. In addition, the effect of the toxic drug 1-chloro-2,4-dinitrobenzen (CDNB) on the activity of G6P-DH was examined. The experiment was conducted in fresh blood haemolysates of white laboratory rats, Wistar type, of both genders (n=80). The enzyme activity was determined by "Boehringer-Mannheim" diagnostic assay kits (Kornberg et al., 1955). However, the measured enzyme activity in the control group of rats was found to be a statistically insignificant difference between the genders (140.2 +/- 21.2 mU/10(9)Er in male rats, 144.3 +/- 20.6 mU/10(9) in the female group). Hence, the established enzyme activity does not differ from the activity of the same enzyme in healthy human subjects. The administered dose of lidaprim did not affect the activity of G6P-DH in the treated group of rats, thus attaining levels similar to the control group. By contrast, amoxiclav administration provoked a significant reduction in enzyme activity of 13.6% in male and 19.5% in female rats (p < 0.001), while the treatment with CDNB significantly increased the activity of the latter to 49.7% in male and 30.1% in female rats (p < 0.001) in comparison with the control ones. Testing of haemolitical potential is strongly recommended prior to the use of new drugs, particularly in the Mediterranean region, were this enzymopathy is found to be frequent bearing in mind that there is an established list of drugs which affect the G6P-DH activity in the erythrocytes. The above-mentioned method may be used in experimental animal models allowing for administration of a wider selection of drugs in this type of research.
authors.affiliation: Pediatric Clinic, Clinical Centre, Skopje, R. Macedonia.
authors.forename: Violeta
authors.initials: V
authors.lastname: Anastasovska
authors.forename: Bozidarka
authors.initials: B
authors.lastname: Dosić-Markovska
authors.forename: Velimir
authors.initials: V
authors.lastname: Stojkovski
authors.forename: Jasmina
authors.initials: J
authors.lastname: Dimitrova-Sumkovska
mesh_terms: D019980:Amoxicillin-Potassium Clavulanate Combination / Q000494:pharmacology*; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D004137:Dinitrochlorobenzene / Q000633:toxicity*; D004338:Drug Combinations; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism*; D006801:Humans; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013424:Sulfanilamides / Q000494:pharmacology*; D014295:Trimethoprim / Q000494:pharmacology*
chemical_list: D000900:Anti-Bacterial Agents; D004137:Dinitrochlorobenzene; D004338:Drug Combinations; D004791:Enzyme Inhibitors; D013424:Sulfanilamides; C011900:lidaprim; D019980:Amoxicillin-Potassium Clavulanate Combination; D014295:Trimethoprim; D005954:Glucosephosphate Dehydrogenase