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Balasubramaniyan V, Nalini N
Correspondence: Dr. Namasivayam Nalini, firstname.lastname@example.org
Introduction This study aimed to assess the leptin dependent changes on adenosine triphosphatase (ATPase) activities of the central nervous system during chronic ethanol supplementation.
Methods The mice were divided into four groups. Group 1 consisted of control animals that received isocaloric glucose, Group 2 animals received isocaloric glucose plus exogenous mouse recombinant leptin (230 microgrammes/kilogramme body weight intraperitoneally) every alternate day, Group 3 were alcohol-fed mice (6.32 grammes/kilogramme body weight orally), and Group 4 were alcohol-fed mice that received leptin (230 microgrammes/kilogramme body weight intraperitoneally) every alternate day. The experiment was terminated after giving the mice leptin injections for 15 days.
Results Ethanol feeding for a total period of 45 days (p-value is less than 0.05) significantly elevated the brain lipid hydroperoxide levels and total ATPases, sodium, potassium-ATPase and magnesium-ATPase activities but significantly decreased the calcium-ATPase activity. Leptin injections to ethanol-fed animals further elevated the levels of lipid hydroperoxides, total ATPases, sodium, potassium-ATPase and magnesium-ATPase, while calcium-ATPase activity was reduced significantly.
Conclusion Leptin plays an important role in the pathogenesis of ethanol-induced neurotoxicity by enhancing brain lipid peroxidation and regulating brain ATPase activities in mice. Thus, hyperleptinaemia-induced oxidative stress and enhanced ATPase activities may be important pathogenic factors in brain toxicity.
Keywords: adenosine triphosphatase, brain, ethanol, leptin, lipid peroxidation, mice, neurotoxicity
Singapore Med J 2006; 47(10): 864-868