Effect of Enrofloxacin on the Joint Fluid/Blood Oxidative Status and Organ Damage Markers
Devran Coskun, Kurtulus Parlak, Burak Dik, Hatice Eser Faki, Emre Bahcivan, Enver Yazar, Ayse Er
Annual Research & Review in Biology · pp. 1–7 · Published 27 Mar 2018
10.9734/ARRB/2018/40537Abstract
Aim: It has been hypothesized that chondrotoxicity, the main side effect of enrofloxacin use, may be derived from oxidative stress, and this side effect can be confirmed by measuring malondialdehyde and endogen antioxidants following drug application. The primary aim of this research is to determine the effect of enrofloxacin on the joint fluid and blood oxidative status parameters, and it is also to determine the effect on the organ damage parameters. Materials and Methods: In the study, 10 rams received enrofloxacin (10 mg/kg/day, SC) for 14 days. Blood and joint fluids were taken on day 0 (Control) before drug application and 1.5 hours after the last drug application. Plasma and joint fluid malondialdehyde, total antioxidant status, superoxide dismutase, glutathione peroxidase and catalase levels were determined by an ELISA reader. Cardiac (CK-MB mass, troponin I), liver (AST, ALT, ALP, GGT, total protein, albumin) and kidney (Creatinine, BUN) damage markers and hemogram (WBC, RBC, platelet, hematocrit, haemoglobin) values were measured. Results: Enrofloxacin decreased the joint fluid catalase level (P<0.05), while there was no effect observed in the other oxidative status parameters of joint fluid or blood samples. Statistically significant changes (P<0.05) were found in some hemogram and biochemical parameters within the reference range. However, enrofloxacin increased (P<0.05) the levels of cardiac damage markers (CK-MB mass, troponin I). Conclusion: It may be stated that enrofloxacin does not cause oxidative stress in the joint fluid and blood in rams, and it is generally accepted to be safe when the effect on the organ/system is considered, but the long-term use and high doses require caution in terms of possible heart related damage.
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