Abstract

Aim: Gatifloxacin (GTX) - an 8 - methoxy fluoroq uinolone antibacterial agent has been considered very effective in the treatment of respiratory and urinary tract infections. This study investigates the toxic potentials of GTX in Wistar rats. Methodology: Twenty male rats (180 - 220 g) were randomised int o four groups: I - Control, II - 4 mg/kg body weight (b.w.) GTX, III - 8 mg/kg b.w GTX, and IV - 16 mg/kg b.w GTX. Results: After seven days of GTX administration, the levels of plasma creatinine, urea and bilirubin were increased significantly ( P< 0.05 ) in GTX - tr eated rats compared to control. ALP, ALT, AST and GGT activities were also elevated significantly in the plasma of the treated animals relative to control. Similarly, hepatic malondialdehyde level increased significantly in the GTX treated groups relative to control. Hepatic levels of ascorbic acid, reduced glutathione as well as activities of hepatic GST, catalase, and SOD were reduced significantly in a dose dependent manner in the GTX - treated animals compared to control. Besides, histopathological studie s revealed very mild, moderate and severe hepatic portal congestion and cellular infiltration by mononuclear cells by the three doses of GTX. Conclusion: Overall, three different doses of Gatifloxacin (half - therapeutic, therapeutic and double - therapeutic) induced renal and hepatic damages, as well as oxidative stress in rats. Original Research Article

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.