Modulatory Role of Vitamin E on Oxidative Stress, Inflammation, and Autophagy in Oxytetracycline Induced Renal Toxicity

Abstract

The present study aimed to investigate the nephrotoxic effects of oxytetracycline (OTC) and to evaluate the protective role of vitamin E (Evit) through oxidative stress, inflammation, and autophagy pathways. A total of 28 rats were randomly assigned to four experimental groups: control, Evit, OTC, and OTC + Evit and treated for seven consecutive days. At the end of the experimental period, kidney tissues were collected for biochemical and molecular analyses. Oxidative stress parameters, including malondialdehyde (MDA), reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT), were determined using spectrophotometric methods. In addition, the gene expression levels of nuclear factor kappa B (NF-κB), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF α), and the autophagy-related marker Beclin-1 were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). OTC administration significantly increased MDA levels while decreasing GSH content and the activities of antioxidant enzymes, indicating enhanced oxidative stress. Furthermore, the expression levels of NF-κB, IL-1β, TNF-α, and Beclin-1 were markedly elevated, suggesting activation of inflammatory and autophagic pathways. Evit co administration significantly reduced MDA levels, restored antioxidant enzyme activities, and suppressed the expression of inflammatory and autophagy-related markers compared with the OTC group, although these parameters did not fully return to control levels. In conclusion, Evit exerts a protective effect against OTC-induced renal injury by attenuating oxidative stress and modulating inflammation and autophagy pathways, highlighting its potential as a supportive therapeutic strategy against antibiotic-induced nephrotoxicity.