Doxycycline: An Antibiotic Attenuates Oxidant Stress, Perturbation of Lipid Metabolites, and Antioxidants against Vanadium Toxicity in Rat Hepatocytes

Background The liver is target following exposure to pentavalent vanadium (V5+). Doxycycline an antioxidant that prevents the progression of disease through inhibition lipid peroxidation. Aim present study was designed evaluate protective effects doxycycline against vanadium-induced hepatoxicity. Methods Sixty two male Sprague-Dawley rats (250–300 g) were equally divided into four groups: control group (received 0.2 mL physiological saline), 4 mg/kg body weight on day 1 and 2 daily thereafter), elemental 1.5 mg/kg-body in distilled water), concomitantly treated (doxycycline + vanadium) received thereafter weight), all given orally for 10 consecutive days. sacrificed by decapitation 24 hours after last dose. removed rapidly processed evaluation metabolic variables: phospholipids, cholesterol, cerebrosides, gangliosides, reduced glutathione (GSH), vitamin C, calcium, acetylcholinesterase enzyme, Results Vanadium administration significantly (−60 increased (+28%) relative compared with controls. exhibited neurological function deficits. decreased concentrations variables controls, cerebrosides (−50%), cholesterol (−39%), phospholipids (−18%), GSH (−45%), inhibited enzyme (–48%). Gangliosides (+ 38%), C 20%), calcium 80%) together enhancement (+64%) combined treatment (vanadium doxycycline) (+25 rat (+5%) administered group. levels reversed this order: (+17%), (+7%), (−14%), activity (−27%) (−16%) All (p < 0.05). presented no effect GSH, gangliosides. Conclusion suggested oxidation lipids sphingolipids hepatocytes much consumed high production reactive oxygen species. protected oxidative damage could be attributed its free radical scavenging membrane-bound enzyme.