Gentamicin potentiate tigecycline induced cardiotoxicity in rats: the cardiac susceptibility to oxidative stress

Abstract

Tigecycline (TIG) toxicity is a threat to health because of the mortality risk attributed to its overdose. Large doses result in fatal cardiomyopathy and acute cardiotoxicity. Gentamicin (GEN) is an aminoglycoside antibacterial agent that affects kidney function, causing nephrotoxicity. Six groups of rats (n=5) were used. Control (DW), TIG 7 (TIG 7 mg/kg IP), TIG14 (TIG 14 mg/kg IP), gentamicin (GEN), TIG 7+ GEN, and TIG 14+ GEN groups. Cardiac catalase (CAT) activity, glutathione (GSH), and malondialdehyde (MDA) levels in the heart, as well as histopathological changes were recorded. Myocardium from TIG 14+ GEN group exhibited typical changes for myocardial apoptosis and degeneration, as well as an increase in interleukin-6 (IL-6) and annexin-V levels, were recorded specially in the TIG 14+ GEN group. GEN, in addition to its nephrotoxicity, increases TIG-induced cardiotoxicity. GEN may increase the cardiotoxicity of high dose TIG. Particularly large doses of GEN have a negative impact on the cardiac oxidative stress caused by TIG.