Acute Cadmium Exposure Reduces the Local Angiotensin I Converting Enzyme Activity and Increases the Tissue Metal Content

Abstract

Cadmium exposure causes health problems that may result from increased oxidative stress and from changes in enzyme metalloproteases activities as angiotensin-converting enzyme (ACE). In fact, cadmium produces inhibition of serum ACE but is not known how cadmium acts on tissue ACE activity and whether following acute exposure tissue cadmium content is increased. In order to elucidate these issues, a cadmium bolus was injected intravenously in Wistar rats, and the cadmium content and the ACE activity were measured in the serum, lungs, aorta and kidneys. Moreover, in order to clarify if the cadmium affects directly tissue ACE activity, acute metal exposure in vitro was performed. Our results demonstrated that 120 min following cadmium administration, blood and organ cadmium content were both increased. Serum and lung ACE activity were reduced following acute cadmium exposure, but aortic and kidney ACE activities were not affected. The inhibitory effects induced by cadmium on ACE activity were also observed in the serum, as well as the lungs and the aorta, but not in the kidneys following in vitro exposure. Moreover, the inhibitory effects induced by cadmium on ACE activity were partially restored in vitro by zinc supplementation, suggesting a possible interaction or competition between cadmium and zinc by at the active site of ACE. Summarising, our results suggest that acute cadmium exposure promotes an increase in the tissue metal content that was accompanied by direct inhibition of serum, aorta and lung ACE activity, an effect that is cadmium concentration-dependent and is partially reversed by zinc.

Effects of omega-3 on androgenic activity in cadmium-induced hypertensive rats

“…Studies showed that one of the possible mechanism associated with hypertension development is disruption of the renin-angiotensin system which plays a major role in blood pressure regulation. 24 The result of cadmium-induced hypertension is in agreement with a study done by Angeli et al (2013) which demonstrated that acute exposure to Cd undoubtedly caused endothelial dysfunction by a mechanism relating to increased local release of angiotensin II, increased activity of COX-2, and NADPH oxidase. These mechanisms could contribute to the development of hypertension and atherosclerosis.…”

Single and Combined Aluminium and Cadmium Exposure during Pregnancy Mediate Changes in Cardio Metabolic Indices in Mice

“…Aluminium and other metals such as silica, barium, cobalt and gold have earlier been implicated in the development of granulomatous lung disease that mimics sarcoidosis (Newman, 1998;Fireman et al 2016;Bajer et al 2020;Judson 2020). Though the Cd group had a non-significantly elevated ACE activity, the findings in this study are in contrast to that reported by Broseghini-Filho et al, (2015) which noted a reduction in the serum concentration of ACE after acute cadmium exposure but agrees with Júnior et al, (2020) that reported a similar result stating an increase in serum ACE levels in mice exposed to Cd only. The increases signifies that the renin-angiotensin system plays an important role in the toxicity of the cardiovascular system and therefore may also promote the progression of hypertension.…”

In silico toxicogenomic data-mining to unraveling the influence of lead and cadmium co-exposure on molecular mechanisms involved in the development and progression of Hypertension

“…The inhibition was proposed to be via competitive replacement of zinc at the active site of ACE [24]. Furthermore, Carmignani et al [25] reported an increase in the activity of ACE following acute lead exposure, a result which is also consistent with the ndings of Shari et al [26].…”