Abstract
The role that copper (Cu) plays in encouraging lipid peroxidation reveals the aggressive aspect of copper overload in both human and animal bodies. This process disrupts membrane integrity by generating hydroxyl radicals, leading to increased membrane permeability and uncontrolled leakage of cellular contents, which ultimately contributes to neuronal injury. D-penicillamine, a chelating agent, was used here in our study as its known mechanism is to bind free copper ions and facilitate their urinary excretion. Our point of view is to determine the protective role of D-penicillamine in diminishing the challenges that occurred from over-exposure to copper sulfate (CuSO₄) material on brain tissue, especially at the caudate nucleus (the center of movement and learning in the brain). Thirty adult male albino rats were divided into three groups (10 rats each): control, CuSO₄ (0.2 mg/kg bw), and CuSO₄ (0.2 mg/kg bw) + D-penicillamine (100 mg/kg bw) concurrently once daily for 30 days. We found that CuSO₄ exposure led to oxidative stress, as evidenced by a significant elevation of Malondialdehyde (MDA) and reduction of total antioxidant capacity (TAC), increased levels of interleukin-6 (IL-6) and tissue necrosis factor-α (TNF-α), and raised the Bax/Bcl-2 ratio for provoking apoptosis in brain tissue, which was supported by histopathological examination as marked degenerative changes in the neurons of the caudate nucleus. Apoptotic genes and histopathological images showed a more pragmatic beneficial effect of D-penicillamine on neurons of the caudate nucleus compared to the CuSO₄-treated group. The study highlights the potential role of D-penicillamine as a therapeutic option to counteract CuSO₄-induced toxicity, especially in ecologically affected areas where both humans and animals may be exposed to elevated copper levels.