Unraveling the enigma of cardiac damage caused by lead: Understanding the intricate relationship between oxidative stress and other multifactorial mechanisms.

Abstract

Lead (Pb) exposure remains a pressing concern in the realm of public health, with a mounting body of evidence underscoring its adverse impact on cardiovascular well-being. The exposure to Lead instigates the production of reactive oxygen species (ROS), leading to consequential cellular and physiological damage and a perturbation in redox equilibrium. The resultant oxidative stress, induced by ROS, disrupts endothelial functionality, propagates inflammatory processes, and initiates vascular remodeling, collectively contributing to the advancement of cardiovascular diseases (CVDs). The objective of this current review is to comprehensively expound upon the intricate mechanisms through which Lead induced toxicity affects cardiac cells. Additionally, it briefly addresses the ramifications of Lead exposure on the development of three interconnected cardiovascular conditions: atherosclerosis, hypertension, and myocardial infarction. Furthermore, the discourse delves into the specific repercussions of Lead exposure on lipid metabolism, blood pressure regulation, and cardiac performance, culminating in the initiation and progression of atherosclerotic plaque formation, elevated blood pressure, and an augmented risk of myocardial infarction. By understanding these intricate mechanisms, targeted interventions may be devised to counteract the deleterious effects of Lead on cardiovascular health. Thus, this review offers novel avenues for preventive and therapeutic strategies, ultimately serving to alleviate the burden of cardiovascular diseases associated with Lead toxicity.