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ORAL PRESENTATION / TAM METİN SÖZLÜ SUNUM

The Effect of Infliximab on Oxidative Stress Markers in the Temporal Cortex
in a Propionic Acid-Induced Experimental Autism Model

Ahmet ATEŞŞAHİN 1 Nur AKMAN
2,*

1 Fırat University, Faculty of Veterinary Medicine, Department of Pharmacology and
Toxicology, Elazığ, TÜRKİYE

2 Van Yüzüncü Yıl University, Faculty of Health Sciences, Department of Midwifery, Van,
TÜRKİYE

*Correspond Author: nurakman@yyu.edu.tr

Abstract
In this study, the effects of infliximab administration on oxidative stress parameters

in the temporal cortex of rats were investigated using an experimental autism model
induced by propionic acid (PPA). A total of 32 Wistar albino rats aged 3–5 weeks were

randomly divided into four groups: control, PPA (autism), PPA + infliximab, and infliximab.
The autism model was established by oral administration of PPA at a dose of 250 mg/kg

for three consecutive days. Infliximab was administered intraperitoneally at a dose of 5
mg/kg for five weeks. At the end of the experiment, temporal cortex tissues were

dissected and analyzed for malondialdehyde (MDA), glutathione (GSH), catalase (CAT),
glutathione peroxidase (GPx), and advanced oxidation protein products (AOPP) levels

using the ELISA method. The results showed a significant increase in MDA and AOPP

levels in the PPA group compared to the control group (P<0.05), while GSH, GPx1, and
CAT levels were significantly decreased (P<0.05). In the PPA + infliximab group, oxidative

stress was further elevated, and in the infliximab-only group, MDA and AOPP levels were
highest, whereas antioxidant parameters were lowest (P<0.05). These findings indicate

that a marked oxidative stress develops in the PPA-induced autism model and that
infliximab treatment exerts adverse effects on certain antioxidant parameters in the

temporal cortex. Based on these results, it is suggested that TNF-α inhibitors may disrupt
oxidative balance in neurodevelopmental disorders by contributing to mitochondrial

dysfunction through Tumor Necrosis Factor Receptor 2 (TNFR2) signaling.
Keywords: Antioxidant Enzymes, Experimental Autism Model, Infliximab, Oxidative Stress,

Temporal Cortex.

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