Hamza AVCI, Kenan YILDIZHAN
Kastamonu Medical Journal - 2026;6(2):169-175
Aims: Neurotoxicity is characterized by structural and functional neuronal disorders resulting from exposure to toxic substances in the central and peripheral nervous systems. Cadmium (Cd), a toxic heavy metal with widespread industrial uses, is known to have significant neurotoxic effects on the nervous system. This study investigated the protective effect of selenium (Se) against CdCl?-induced neurotoxicity in rat brain tissue and evaluated the possible involvement of the Transient Receptor Potential Melastatin-2 (TRPM2) channel in this process. Methods: In the study, 40 male Wistar Albino rats were randomly divided into five groups (n=8): Control, CdCl?, CdCl?+Se, CdCl?+2-APB, and CdCl?+Se+2-APB. For five days, CdCl? (25 mg/kg) was administered intragastrically, and Se (0.5 mg/kg) and the TRPM2 inhibitor 2-Aminoethoxydiphenyl Borate (2-APB; 3 mg/kg) were administered intraperitoneally. Results: Total antioxidant levels (TAS), total oxidant levels (TOS), reactive oxygen species (ROS), poly (ADP-ribose) polymerase-1 (PARP-1), and TRPM2 levels in brain tissues were analyzed using "ELISA kits". In the CdCl? group, TOS, ROS, PARP-1, and TRPM2 levels were significantly increased compared to the control group, while TAS levels were significantly decreased (p<0.05). Se and 2-APB administrations significantly reversed these changes; the most significant improvement was observed in the CdCl?+Se+2-APB group (p<0.05). Conclusion: The present findings suggest that CdCl? exposure is associated with increased oxidative stress-related markers and TRPM2 levels in rat brain tissue, whereas Se and 2-APB treatment partially attenuate these alterations.
