Research Article Influence of Moxifloxacin on Hepatic Redox Status and Plasma Biomarkers of Hepatotoxicity and Nephrotoxicity in Rat Ayokanmi Ore and Ebenezer Tunde Olayinka Biochemistry Unit, Department of Chemical Sciences, Ajayi Crowther University, PMB 1066, Oyo 211213, Oyo State, Nigeria Correspondence should be addressed to Ayokanmi Ore; oreayokanmi@gmail.com Received 31 July 2015; Accepted 20 September 2015 Academic Editor: Andrei Surguchov Copyright © 2015 A. Ore and E. T. Olayinka. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Moxifoxacin is a broad spectrum fuoroquinolone antibacterial agent. We examined the hepatic redox status and plasma biomarkers of nephrotoxicity and hepatotoxicity in rat following administration of moxifoxacin (MXF). Twenty-four Wistar rats, 180–200 g, were randomized into four groups (I–IV). Animals in group I (control) received 1mL of distilled water, while animals in groups II, III, and IV received 1 mL each of MXF equivalent to 4 mg/kg b.w., 8 mg/kg b.w., and 16 mg/kg b.w., respectively. Afer seven days, plasma urea, bilirubin, and creatinine were signifcantly ( < 0.05) elevated in the MXF-treated animals. Activities of alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase were signifcantly increased in the plasma of MXF- treated animals compared to control. Also plasma total cholesterol, HDL-cholesterol, LDL-cholesterol, and triglycerides increased signifcantly in the MXF-treated groups relative to control. Moreover, MXF triggered a signifcant decrease in hepatic catalase, superoxide dismutase, and glutathione- transferase activities. Likewise, MXF caused a decrease in the hepatic levels of glutathione and vitamin C. A signifcant increase in hepatic MDA content was also observed in the MXF-treated animals relative to control. Overall, our data suggest that the half-therapeutic, therapeutic, and twice the therapeutic dose of MXF induced nephrotoxicity, hepatotoxicity, and altered hepatic redox balance in rats. 1. Introduction Moxifoxacin (MFX) is a fourth-generation synthetic fuo- roquinolone antibacterial agent with a broad spectrum of bactericidal action. MXF possess enhanced activity against Gram-positive bacteria, most notably against penicillin- susceptible and penicillin-resistant strains of S. pneumoniae. It is available for oral and intravenous administration, respec- tively, as a once-daily 400 mg antibiotic for the treatment of respiratory tract infections, chronic bronchitis, and acute bacterial sinusitis and in some cases pelvic infammatory dis- ease, complicated and uncomplicated skin and skin structure infections, complicated intra-abdominal infections, ocular bacterial keratitis, and community acquired pneumonia [1– 3]. MXF like other quinolones have a bicyclic aromatic core with a carbon at position 8 and demonstrate an N-1 cyclo- propyl moiety (Figure 1). Following oral administration, MXF is well absorbed from the gastrointestinal tract with approximately 50% bound to serum proteins [4]. It binds weakly to plasma proteins and penetrates well into most tissue and fuid compartments. MXF is metabolized to an N- sulfate conjugate and an acyl glucuronide in humans [5]. Like other fuoroquinolones, MXF exhibit bactericidal activity by binding to bacterial topoisomerases II (DNA gyrase) and topoisomerase IV [6]. By binding to these enzymes, the fuoroquinolones interfere with DNA replication, repair, and transcription, resulting in bacterial death. Te ability to target both enzymes has been promoted as a major advantage of the fuoroquinolones in preventing or delaying the emergence of resistance [7]. Most fuoroquinolones are known to be associated with some adverse efects on vital organs [8]. Previous reports suggest that free radical formation might play a role in the mechanism of some of these adverse efects [9]. Moreover, certain members of the fuoroquinolones are known to Hindawi Publishing Corporation Biochemistry Research International Volume 2015, Article ID 192724, 8 pages http://dx.doi.org/10.1155/2015/192724