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ORAL PRESENTATION / TAM METİN SÖZLÜ SUNUM

cerebral ischemia and epileptiform seizures, suggesting protective roles of TNF receptors
against neuronal damage.

Infliximab has been reported to exhibit antioxidant effects by reducing increased
oxidative stress in various tissues (Ozer et al., 2017; Dirik et al., 2021; Habib et al., 2019).

Habib et al. (2019) showed that infliximab decreased elevated MDA levels and increased

CAT and GSH levels, demonstrating antioxidant properties in testicular tissue exposed to
toxicity. Dirik et al. (2021) reported that infliximab reduced MDA and AOPP levels while

increasing CAT levels in rats with ovarian torsion. Infliximab prevented increases in MDA
levels in septic liver, lung, spleen, and kidney tissues and also prevented decreases in

GSH levels in septic liver, spleen, and kidney tissues (Ozer et al., 2017). In stressed rats,
infliximab attenuated decreases in GSH and superoxide dismutase (SOD) levels in the vas

deferens and inhibited increases in malondialdehyde (MDA) levels (Şahin et al., 2020).

No literature was found regarding the effects of infliximab in ASD. In the present
study, infliximab treatment further increased oxidative stress and disrupted antioxidant

balance in the temporal cortex of ASD. TNF-α has been reported to exert a protective
effect on the CNS, with its presence necessary for remyelination via TNFR2 activation

(Tristano et al., 2010). TNF-α signaling through TNFR2 enhances the expression of
enzymes detoxifying ROS, thereby contributing to intracellular oxidative balance

maintenance. This mechanism is supported by in vitro studies on oligodendrocyte
progenitor cells (Candel et al., 2014). According to Al-Azab et al. (2020), the TL1A/TNFR2

axis causes mitochondrial dysfunction and increases ROS production.
While TNF-α inhibitors like infliximab suppress inflammation by blocking TNF-α’s

biological effects, they may also induce mitochondrial dysfunction via TNFR2, increasing

ROS production and disrupting antioxidant balance. This can elevate the risk of cellular
damage in tissues where TNF-α plays a critical role in oxidative stress management, such

as the CNS, intestinal mucosa, and skin. The disruption of oxidative balance by infliximab
in ASD observed in this study may be due to increased TNFR2-mediated signaling linked

to mitochondrial dysfunction in ASD, leading to elevated ROS production via TNFR2
activation and increased cellular oxidative stress.

In this study, significant changes in oxidative stress markers were observed in the
temporal cortex of an experimental autism model induced by propionic acid. Levels of

MDA and AOPP, indicators of lipid peroxidation and protein oxidation respectively, were
increased in the autism group, while there was a marked decrease in key antioxidant

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