E. O ALOAMAKA

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNpc), leading to severe motor and cognitive impairments. Its complex pathophysiology involves oxidative stress, mitochondrial dysfunction, and glutamatergic excitotoxicity. Hyperthermia, or high body temperature, is also known to cause cellular damage by impairing mitochondrial function and increasing oxidative stress. This study aimed to investigate physiological alterations associated with hyperthermia in MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) induced Neurotoxicity using the MPTP rat model. Adult Wistar rats were divided into Control, Heat only, and MPTP + heat groups, receiving intranasal administration of MPTP (0.1ml/nostril)daily for 2 days. Heat exposure was carried out with heat bulbs for 6hours/day for one week at a temperature range of 28°c - 43°c. The study assessed key biochemical parameters, including oxidative stress markers (Superoxide Dismutase (SOD), Catalase (CAT), Glutathione Peroxidase (GPx), and Malondialdehyde (MDA)), and Total Protein levels. Biochemical analysis confirmed that MPTPt + HEAT treatments induced a severe state of oxidative stress. This was evidenced by a significant increase in the activities of antioxidant enzymes (SOD, CAT, GPx) alongside a decrease in the lipid peroxidation marker MDA. This pattern indicates that the cellular antioxidant defenses were overwhelmed by the toxin and heat.. Furthermore, there was a statistically significant decrease in total protein levels across the Heat only and MPTP+ heat groups, suggesting widespread cellular injury and apoptotic death consistent with severe heat exposure and MPTP neurotoxicity. This study confirms the physiological alterations caused by heat, demonstrating that MPTP administration and heat exposure promote molecular damage, oxidative stress, and widespread protein loss.