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    Histopathological assessment of coenzyme Q10 mediated neuroprotection in the mouse cortex exposed to a glyphosate based herbicide
    (Fırat Üniversitesi Sağlık Bilimleri Enstitüsü, 2026) Saygı, Halil İbrahim; Ayla, Şule; Mutluay, Duygu; Dursun, İlknur
    Glyphosate-based herbicides (GBHs) are widely used globally, and their potential neurotoxicity is of increasing concern to researchers and the public. Mitochondrial-targeted antioxidants such as Coenzyme Q10 (CoQ10) have established neuroprotective effects yet approaches to neuroprotection against GBHs are still being developed. This study evaluates the potential of CoQ10 to reverse cortical damage caused by GBH exposure in mice. Fifty adult male ICR mice were assigned to five groups: control, sham, CoQ10 (200 mg/kg/day), GBH (Roundup, 500 mg/kg/day), and GBH+CoQ10. After 49 days of oral treatment, mice were euthanized and brains collected for histological examination using Hematoxylin and Eosin (H&E) and cresyl violet (Nissl) staining. Cortical histopathology was analyzed with QuPath software. Histological examination revealed that all normal cortical structures were found in the control, sham, and CoQ10 groups. Exposure to GBH produced shrunken, hyperchromatic, and pyknotic neurons with degenerative changes, as well as granulovacuolar degeneration and neuropil vacuolation. In the GBH+CoQ10 group, the cortical organization and neuronal morphology were well-preserved, with only mild focal vacuolation present. Cresyl violet staining revealed severe neuronal loss, Nissl substance depletion, and cytoplasmic pallor in GBH-treated mice, whereas GBH+CoQ10 sections showed higher neuronal density and clear Nissl granules. Quantitatively, GBH significantly reduced cortical neuron number compared with other treatment groups. However, GBH co-treatment with CoQ10 reversed this decline. GBH exposure induces neuronal degeneration in the mouse cerebral cortex, while CoQ10 supplementation preserves cortical cytoarchitecture and neuronal density, supporting its potential as a neuroprotective adjunct against GBH-induced brain toxicity.