Cadmium (Cd) is a persistent toxic metal that bioaccumulates in human tissues and may disrupt redox and endocrine pathways, yet the metabolic mechanisms linking Cd exposure to both endothelial and prostate dysfunctions remain insufficiently defined. This study investigated whether chronic occupational Cd exposure alters methylated arginine metabolism and prostate-specific antigen (PSA) levels, indicating a shared toxicometabolic axis. A total of 150 male workers were enrolled, including 75 metallurgical employees with documented Cd exposure and 75 matched controls. All participants were non-smokers, eliminating confounding from tobacco-related oxidative or endocrine effects. Urinary Cd concentrations were quantified using Inductively Coupled Plasma–Mass Spectrometry (ICP–MS), and serum asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), L-arginine, citrulline, and PSA were measured by Liquid Chromatography Tandem Mass Spectrometry (LC-MS/MS) and electrochemiluminescence. The use of Inductively Coupled Plasma–Mass Spectrometry for arsenic quantification and LC-MS/MS for methylated arginine profiling provided high analytical specificity and sensitivity, strengthening the validity of biomarker measurements. Correlation and multivariable analyses adjusted for age and body mass index. Cd-exposed workers demonstrated significantly elevated urinary Cd, PSA, ADMA, and SDMA levels, alongside reduced arginine/ADMA ratios, consistent with impaired nitric oxide bioavailability. Urinary Cd strongly correlated with PSA and ADMA levels. These findings indicate that Cd may disrupt the nitric oxide pathway and elevates PSA, supporting a mechanistic link between vascular and prostate stress. Combined ADMA, SDMA, and PSA profiling may serve as an early biomarker panel for Cd-related metabolic injury in occupational settings.
Gözükara et al. (Thu,) studied this question.