Methamphetamine-Induced Oxidative Stress and Inflammatory Markers as Indicators of Blood-Brain Barrier Disruption

Background: Methamphetamine (METH) abuse has been linked to neurotoxicity, oxidative stress, and dysfunction of the blood-brain barrier (BBB), potentially leading to cognitive impairments. This study aimed to evaluate the association between METH use, oxidative stress biomarkers, inflammation (NF-κB), endothelial permeability (MLCK), and memory impairment. Methods: A total of 150 male participants, aged 18–50 years, were recruited, including 75 METH users and 75 age-matched healthy controls. Serum levels of myosin light chain kinase (MLCK, NCBI Gene ID: 4638), nuclear factor kappa B (NF-κB, NCBI Gene ID: 4790), total oxidant status (TOS), total antioxidant capacity (TAC), catalase activity (CAT), and oxidative stress index (OSI) were measured. Receiver operating characteristic (ROC) curves and logistic regression were used to analyze biomarker sensitivity and risk association. Results: MLCK and NF-κB were significantly elevated in METH users compared to controls (p< 0.001*). TOS and OSI were higher, while TAC and CAT were lower in METH users (p< 0.001*). ROC analysis revealed MLCK (AUC = 0.978) and NF-κB (AUC = 0.959) as sensitive biomarkers for BBB dysfunction. Logistic regression indicated increased odds of memory impairment with elevated MLCK (OR = 1.246) and NF-κB (OR = 1.452), though these associations were not statistically significant (p > 0.05). Conclusion: Chronic METH use is associated with oxidative stress, inflammation, and increased BBB permeability, implicating MLCK and NF-κB as potential biomarkers for neurovascular damage and cognitive decline. Larger studies are warranted to confirm these associations.