Assessment of oxidative stress and lipid peroxidation in cats infected with toxoplasma

Document Type : Original Articles

Authors

1 Department of Veterinary, Ka.C., Islamic Azad University, Karaj,Iran

2 Department of veterinary clinical sciences, Karaj branch, Islamic Azad University, Karaj, Iran

10.22092/ari.2025.368791.3566

Abstract

Toxoplasmosis, caused by the intracellular protozoan Toxoplasma gondii, is a widespread zoonotic infection that frequently remains asymptomatic in humans and animals. During parasitic infections, oxidative stress can increase due to excessive free radical production, potentially contributing to disease pathogenesis. The present study investigates oxidative stress biomarkers in cats, the definitive hosts of Toxoplasma gondii. Blood samples were collected from 55 cats. Among them, 10 infected and 10 uninfected cats were selected based on serological screening using the Modified Agglutination Test (MAT). Serum levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and total antioxidant capacity (TAC) were analyzed. Data were evaluated using independent t-tests, with statistical significance set at P ≤ 0.05. Although serum MDA concentrations were elevated in infected cats (10.68 ± 1.07 µM) compared to controls (9.12 ± 0.56 µM), the difference was not statistically significant. Enzyme activities of SOD showed no significant difference. Infected cats had lower GPx (128.66 ± 35.62 U/mL vs. 235.66 ± 74.13 U/mL), CAT (12.19 ± 1.03 U/mL vs. 13.12 ± 2.60 U/mL), and TAC (0.118 ± 0.004 mM vs. 0.126 ± 0.005 mM), but these reductions were not statistically significant (p > 0.05).
This study evaluated serum oxidative markers and lipid peroxidation in cats naturally infected with Toxoplasma gondii. The lack of significant differences suggests that oxidative stress and lipid peroxidation induced by the infection may be localized within cells, consistent with the intracellular nature of Toxoplasma gondii, an obligate intracellular protozoan. Moreover, the absence of overt clinical signs in infected cats might account for the minimal changes in systemic antioxidant parameters. Further research incorporating tissue-specific analyses and experimental infection models is necessary to more accurately elucidate the oxidative stress mechanisms associated with Toxoplasma gondii infection.

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