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ORAL PRESENTATION / TAM METİN SÖZLÜ SUNUM

electron donor. In individuals with ASD, CAT levels have been reported to be decreased in
erythrocytes, unchanged in plasma, and increased in serum (Altun et al., 2018).

Significant decreases in CAT levels have been found in the brain tissue (Bhat et al., 2023)
and serum (El-Ansary et al., 2017) of children with ASD. Al-Amin et al. (2015) reported

decreased CAT levels in the brain tissue of rat models of ASD, while Ornoy et al. (2019)

found increased CAT levels in the prefrontal cortex of such rat models (Ornoy et al., 2019).
In the present study, decreased CAT levels were detected in the autism group compared

to controls.
Advanced oxidation protein products (AOPP), formed during oxidative stress via

myeloperoxidase activation, are considered markers of oxidative protein damage
(Campara et al., 2025). Yenkoyan et al. (2018) found no changes in serum AOPP levels

in children with ASD, whereas Jasenovec et al. (2023) reported increased AOPP levels in

the serum of ASD individuals. Similarly, Al-Amin et al. (2015) observed significant
increases in AOPP levels in the brain tissue of rat ASD models. AOPP may contribute to

ASD pathogenesis by increasing pro-inflammatory cytokine production through monocyte
activation (Nasrallah and Alzeer, 2022). Ahmad et al. (2013) reported significantly higher

AOPP levels in severely autistic individuals compared to those with mild to moderate ASD
and healthy controls. Nasrallah and Alzeer (2022) also found a positive correlation

between AOPP levels and ASD severity. These findings suggest that AOPP may not only
be a marker of oxidative stress but also a potential biomarker reflecting ASD severity. In

the present study, AOPP levels were significantly elevated in the autism group compared
to controls, supporting increased oxidative stress in autism.

Mitochondria are both the primary source of ROS production and responsible for

their neutralization. Mitochondrial dysfunction observed in ASD leads to excessive ROS
production, resulting in oxidative stress (Wen et al., 2021). Studies have shown increased

mitochondrial activity in autistic children, making them more susceptible to oxidative
stress (Khaliulin et al., 2025). Mitochondrial dysfunction in ASD may lead to oxidative

stress and cellular damage. As mitochondria play a crucial role in cellular repair,
mitochondrial impairment may increase brain cells’ susceptibility to oxidative damage,

potentially affecting ASD development and severity (Długosz et al., 2025).
In the present study, an experimental autism model induced by propionic acid (PPA)

demonstrated significantly increased oxidative stress in the temporal cortex of the autism
group, characterized by decreased GSH, GPX1, and CAT levels alongside elevated MDA

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