This study evaluates the effects of elemental mercury on inflammation, oxidative stress, and myocardial injury in B6 mice, with a focus on neutrophil degranulation and TNF-alpha inflammatory pathways. Using controlled exposures, the research assesses changes in reactive oxygen species (ROS), neutrophil elastase (NE), and TNF-alpha levels, correlating these biomarkers with histological evidence of myocardial injury. Findings indicate that mercury exposure induces dose-dependent increases in inflammatory and oxidative markers, similar to other heavy metals like lead, potentially exacerbating myocardial damage. However, variations in response suggest adaptive physiological thresholds. The results emphasize the need for precise exposure assessments and interventions to mitigate mercury’s cardiovascular and systemic effects, highlighting implications for public health and safety standards.
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