Lead is an environmental toxicant that can induce oxidative stress (OS) via reactive oxygen species (ROS) generation, which has been reported as an important mechanism underlying lead toxicity (Gurer and Ercal 2000; Pande and Flora 2002; Kasperczyk et al. 2004a; Farmand et al. 2005; Verstraeten et al. 2008; Wang et al. 2009; Martinez-Haro et al. 2011). OS occurs when the generation of ROS exceeds the antioxidant system's ability to defend cells against oxidized molecules. ROS is a term generally used to refer to free radicals derived from O2 (e.g., superoxide anions [O2-] and hydroxyl radicals [OH-]) or to non-radical species (e.g. hydrogen peroxide [H2O2]) (Halliwell and Cross 1994).
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Hypertension is an important public health concern that affects millions globally, leading to a large number of
morbidities and fatalities. The etiology of hypertension is complex and multifactorial, and it involves environmental
factors including heavy metals. Indeed, cadmium and mercury are toxic elements commonly distributed in the
environment which contribute to hypertension. We aimed to assess the role of cadmium and mercury-induced endothelial
dysfunction in the development of hypertension. A narrative review was carried out through database searches. In this
review, we discussed the critical roles of cadmium and mercury in the etiology of hypertension and provide new insights
into potential mechanisms of their effect, focusing primarily on endothelial dysfunction. Although, the mechanisms by
which cadmium and mercury induce hypertension have yet to be completely elucidated, evidence for both implicates
impaired nitric oxide signaling in their hypertensive etiology.
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