ABSTRACT
Cardiovascular diseases (CVDs) are the major causes of arsenic-related morbidity and mortality. Hypertension is a major risk of CVDs. Atherosclerosis is the main biochemical event of all forms of CVDs including hypertension. Atherosclerosis is a complex biochemical process in which several molecules are involved. However, underlying mechanism of arsenic exposure-related atherosclerosis leading CVDs especially hypertension has not yet been clearly understood. In our research, we have focused on the pathophysiology of arsenic-induced atherosclerosis leading to CVDs recruiting human subjects from arsenic-endemic and non-endemic rural areas in Bangladesh. We found that arsenic exposure metrics were positively associated with the elevated levels of diastolic (DBP) and systolic blood pressure (SBP) of the study subjects. We have also analyzed several circulating molecules related to vascular endothelial dysfunction and atherosclerosis including vasoconstrictors, and inflammatory, oxidative and adhesion molecules. We have demonstrated the relationship of arsenic exposure with these molecules. Our results suggest that exposure to arsenic is associated endothelial dysfunction probably through its pro-oxidative and pro-inflammatory properties. Our results also suggest that chronic exposure to arsenic impairs the vascular homeostasis leading to the development of hypertension and other forms CVDs. Thus, endothelial dysfunction and related biochemical events are the hallmarks of arsenic-induced cardiovascular diseases.
