Research Articles

2018  |  Vol: 4(5)  |  Issue: 5 (September- October)  |
Levofloxacin induced dyslipidemia in male albino rats

Abiodun Olusoji Owoade1, Augustine Ikhueoya Airaodion2, Adewale Adetutu1, Oluwatoyin Diana Akinyomi1

1Department of Biochemistry, Faculty of Basic Medical Science, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria

2Department of Biochemistry, Faculty of Biological Science, Federal University of Technology, Owerri, Imo State, Nigeria

*Address for Corresponding Author

Dr. Abiodun Olusoji Owoade

Department of Biochemistry,

Faculty of Basic Medical Sciences, Ladoke Akintola University of Technology,

Ogbomoso. Nigeria


Objective: This study was aimed to investigate whether levofloxacin perturb lipid metabolism. Materials and methods: Therapeutic dose (7.14 mg/kg body weight) of levofloxacin was administered intraperitoneally 12 hourly to rats for 5 and 10 days. Twenty-four hours after the last levofloxacin treatment and 7 days after levofloxacin withdrawal (for a group of rats), blood and other tissues (liver, kidney, brain, heart, lung and spleen) were removed from the animals after an overnight fast and analysed for their lipid contents. Results: Levofloxacin administration resulted in dyslipidemia in different compartments investigated. Plasma and erythrocyte dyslipidemia were characterised by increased concentrations of phospholipid, free fatty acids (FFA) and depletion of cholesterol. It also resulted in kidney and heart cholesterogenesis, while spleen and lung cholesterol were reduced. Liver cholesterol was unaffected. Administration of the drug equally produced phospholipidosis in the kidney, lung and liver while brain and heart phospholipids decreased. Lipoprotein abnormalities were reflected as up-regulation of HDL triglyceride and phospholipid as well as down-regulation of VLDL-LDL cholesterol and phospholipid. Hypertriglyceremia was the hallmark of dyslipidemia in the plasma, kidney, lung and brain while in the heart and erythrocyte triglyceride level was decreased. Conclusion: The distortion observed in the lipid profile in most of the compartments of the animals studied, suggest that induction of dyslipidemia might represent additional adverse effects of levofloxacin.

Keywords: Levofloxacin, lipid metabolism, cholesterogenesis, phospholipidosis, dyslipidemia

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