Attention-Deficit/Hyperactivity Disorder (ADHD) frequently persists into adulthood and is associated with substantial functional impairment. Beyond classical neurotransmitter dysregulation, increasing evidence points to oxidative stress and impaired cellular defense mechanisms as key contributors to ADHD pathophysiology. However, data on upstream redox-regulatory pathways in adult ADHD remain limited. To evaluate serum tumor necrosis factor-alpha (TNF-α), heme oxygenase-1 (HO-1), nuclear factor…
