Amoxillin- and pefloxacin-induced cholesterogenesis and phospholipidosis in rat tissues

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• 作者：Solomon O Rotimi (1)
  David A Ojo (2)
  Olusola A Talabi (3)
  Regina N Ugbaja (4)
  Elizabeth A Balogun (4) (5)
  Oladipo Ademuyiwa (4)
  
  1. Department of Biological Sciences ; Covenant University ; Ota ; Nigeria
  2. Department of Microbiology ; Federal University of Agriculture ; Abeokuta ; Nigeria
  3. Medical Centre ; Federal University of Agriculture ; Abeokuta ; Nigeria
  4. Department of Biochemistry ; Federal University of Agriculture ; Abeokuta ; Nigeria
  5. Department of Biochemistry ; University of Ilorin ; Ilorin ; Nigeria
  
• 关键词：Amoxillin ; Pefloxacin ; Dyslipidemia ; Cholesterogenesis ; Phospholipidosis
• 刊名：Lipids in Health and Disease
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：14
• 期：1
• 全文大小：975 KB
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• 刊物主题：Lipidology; Medical Biochemistry;
• 出版者：BioMed Central
• ISSN：1476-511X

文摘

Background To investigate whether amoxillin and pefloxacin perturb lipid metabolism. Methods Rats were treated with therapeutic doses of each antibiotic for 5 and 10 days respectively. Twenty four hours after the last antibiotic treatment and 5 days after antibiotic withdrawal, blood and other tissues (liver, kidney, brain, heart and spleen) were removed from the animals after an overnight fast and analysed for their lipid contents. Results Both antibiotics produced various degrees of compartment-specific dyslipidemia in the animals. While plasma and erythrocyte dyslipidemia was characterised by up-regulation of the concentrations of the major lipids (cholesterol, triglycerides, phospholipids and free fatty acids), hepatic and renal dyslipidemia was characterised by cholesterogenesis and phospholipidosis. Splenic dyslipidemia was characterised by cholesterogenesis and decreased phospholipid levels. Cardiac and brain cholesterol contents were not affected by the antibiotics. A transient phospholipidosis was observed in the brain whereas cardiac phospholipids decreased significantly. Lipoprotein abnormalities were reflected as down-regulation of HDL cholesterol. Furthermore, the two antibiotics increased the activity of hepatic HMG-CoA reductase. Although erythrocyte phospholipidosis was resolved 5 days after withdrawing the antibiotics, dyslipidemia observed in other compartments was still not reversible. Conclusion Our findings suggest that induction of cholesterogenesis and phospholipidosis might represent additional adverse effects of amoxillin and pefloxacin.