Aluminum oxide nanoparticles (Al2O3 NPs) are widely utilized in vaccine manufacturing and other medical preparations. Melatonin has numerous effects as an antioxidant and anti-apoptotic. The purpose of this study was to examine the beneficial impact of melatonin on Al2O3 NPs toxicity in the spinal cord. Forty male rats were divided into four groups: Group I, the negative controls (received standard diet and distilled water); Group II, Al2O3 NPs (received 30 mg/kg bw Al2O3 NPs); Group III, melatonin and Al2O3 NPs (received 30 mg/kg bw Al2O3 NPs + 10 mg/kg bw melatonin); Group IV, melatonin (received 10 mg/kg bw melatonin). All treatments were administered daily for 28 days by gastric gavage. After that, all rats were sacrificed, then, the samples from different spinal cords were subjected to histopathological, biochemical, and immunohistochemical analyses. Al2O3 NPs markedly elevated malondialdehyde and 8-hydroxydeoxyguanosine while inhibiting superoxide dismutase and catalase. Al2O3 NPs also induced histological alterations in both gray and white matter manifested by neuronal degeneration, vacuolation, axonal degeneration, ballooning, and fusion of myelin sheaths. Furthermore, immunohistochemical results displayed a strong positive expression of caspase-3. Conversely, melatonin significantly mitigated the effects of Al2O3 NPs by increasing the activities of antioxidant enzymes and inhibiting malondialdehyde and 8-hydroxydeoxyguanosine. Moreover, melatonin alleviated most histological alterations induced by Al2O3 NPs and reduced caspase-3 immunoreactivity. Collectively, melatonin could protect the spinal cord and mitigate Al2O3 NPs-induced neurotoxicity.
Keywords: Aluminum oxide nanoparticles; apoptosis; histopathology; melatonin; spinal cord.
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