The Effect of Chronic Cadmium Toxicity on Blood Pressure and Plasma Viscosity

Koçak, Mukadder; Yazıhan, Nuray; Akçıl, Ethem; Bay, Meltem; Aslan, Önder

doi:10.1159/000323702

Cited by 11 publications

(7 citation statements)

References 74 publications

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“…The present study did not include the role of chronic cadmium exposure on the kidneys and its relation to the described cardiac dysfunction has not been examined. On the other hand, several prior studies have reported that cadmium at the same dose has resulted in renal and cardiac injuries ( Kacar Kocak et al, 2009 ; Yazihan et al, 2011b ; Erdem et al, 2016 ). The authors reported hypertension associated with renal injury which may be mediated by oxidative stress, deteriorating bioelements like zinc, inducing apoptosis and inflammation.…”

Section: Discussionmentioning

confidence: 98%

Chronic Cadmium Exposure Alters Cardiac Matrix Metalloproteinases in the Heart of Sprague-Dawley Rat

et al. 2021

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The aim of this study was to evaluate the role of chronic cadmium exposure in modulating cardiac matrix metalloproteinases (MMPs) in the heart of rats. Adult male Sprague-Dawley rats were exposed to 15 ppm CdCl2 in drinking water for 10 weeks followed by withdrawal of cadmium treatment for 4 weeks. Following the completion of the treatment, gene expression of inflammatory mediators (IL-1β, IL-6, IL-10, TNF-α and NF-κB), protein expression of MMP-2, MMP-9 and their respective inhibitors- TIMP-1 and TIMP-2, and gelatinolytic activity of MMP-2 and MMP-9 were determined. At the protein level, cadmium incites a differential effect on the expression and activity of gelatinases and their endogenous inhibitors in an exposure-dependent manner. Results also show that the administered cadmium dose elicits an inflammatory response until week 10 that slightly diminishes after 4 weeks. This study provides evidence of cadmium-induced imbalance in the MMP-TIMP system in the cardiac tissue. This imbalance may be mediated by cadmium-induced inflammation that could contribute to various cardiovascular pathologies.

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Section: Discussionmentioning

confidence: 98%

Chronic Cadmium Exposure Alters Cardiac Matrix Metalloproteinases in the Heart of Sprague-Dawley Rat

et al. 2021

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“…According to Lee et al (2011), BCd may be related to an increased risk for hypertension among men in a general Korean adult population. In a study by Kacar Kocak et al (2011), a rat experiment suggested that Cd exposure affected blood pressure by increasing plasma viscosity. In the present study, we excluded participants with hypertension to reduce potential confounding effects of high blood pressure, which is a risk factor for renal dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Renal Function after Reduction in Cadmium Exposure: An 8-Year Follow-up of Residents in Cadmium-Polluted Areas

Liang

Nilsson

et al. 2012

Environ Health Perspect

104

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Background and objective: Long-term exposure to cadmium (Cd) causes renal dysfunction, but the change in renal function with exposure is unknown. We assessed the evolution of Cd-induced renal effects after a reduction in dietary exposure to Cd in rice.Methods: Four hundred twelve residents in previously Cd-polluted and nonpolluted areas were examined twice, in 1998 and in 2006. Changes in blood Cd, urinary Cd, and kidney function [N-acetyl-β-d-glucosaminidase (NAG), β2-microglobulin, and albumin in urine] were measured.Results: In the most polluted area, mean blood Cd was 8.9 μg/L and 3.3 μg/L in 1998 and in 2006, respectively, and urinary Cd was 11.6 and 9.0 μg/g creatinine. Urinary albumin in 1998 increased with urinary Cd, but no such exposure–response relation appeared for 2006 albumin versus urinary Cd 1998, indicating recovery. Other biomarkers of kidney function were also elevated in 1998. Partial recovery was observed for NAG among women and was suggested for β2-microglobulin among young individuals. The probability of having β2-microglobulin levels above the 95th percentile in 2006 was high in those with elevated β2-microglobulin in 1998 [odds ratio (OR) = 24.8; 95% confidence interval (CI): 11.2, 55.3] compared with albumin (OR = 3.0; 95% CI: 1.2, 7.5) and NAG (OR = 2.6; 95% CI: 1.6, 4.4).Conclusions: Results suggest that a Cd-mediated increase in urinary albumin excretion is reversible upon substantial reduction of exposure. For markers of tubular effects, we observed a tendency toward improvement but not complete recovery. Data from repeated observations suggest that β2-microglobulin may be more informative than NAG as an indicator for an individual’s future tubular function.

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“…These outcomes are contrary to those reported to show a negative correlation between Cd exposure and elevated blood pressure (Staessen et al 1984(Staessen et al , 1991(Staessen et al , 2000Nawrot et al 2008;Garner and Levallois 2017). Animal studies have shown the effect of Cd exposure to elevation of blood pressure, particularly systolic pressure (Kacar Kocak et al 2009). However, hypertension is associated with alteration in vascular structure and function.…”

Section: Discussionmentioning

confidence: 79%

Cadmium-induced endothelial dysfunction mediated by asymmetric dimethylarginine

Al‐Naemi

Das

2020

Environ Sci Pollut Res

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Cadmium (Cd) is a naturally occurring toxic heavy metal with no known essential biological functions. Exposure to Cd increases the risk of cardiovascular disease by disrupting vascular homeostasis at the endothelium. The aim of the study was to evaluate the effect of chronic low-dose Cd on vascular structure and function. Fifty adult male Sprague Dawley rats were grouped and assigned to one of two treatments for 14 weeks. The control group received normal water for 14 weeks while the Cd-treated group received 15 mg Cd/kg B.W. as CdCl 2 in water for 10 weeks. A subset of the Cd-treated group received 15 mg Cd/kg B.W. as CdCl 2 in water for 10 weeks followed by 4 weeks of normal water. Results show an overall decline in vascular function and structure. Withdrawal of Cd treatment showed a considerable restoration of vascular structure and vasorelaxation function. Additionally, asymmetric dimethylarginine (ADMA) bioavailability was found to be lowered over time. Interestingly, the expression of eNOS in the Cd-treated group was found to be significantly elevated during the exposure by more than 3-fold in comparison with that in the control group. This protein expression was similar to the control group after the withdrawal of Cd treatment. Taken together, the results suggest that ADMA, an eNOS inhibitor, may play a role in altering endothelial function in the presence of cadmium. In conclusion, the findings indicate that even at low doses, Cd leads to endothelial dysfunction mediated by ADMA.

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The Effect of Chronic Cadmium Toxicity on Blood Pressure and Plasma Viscosity

Cited by 11 publications

References 74 publications

Chronic Cadmium Exposure Alters Cardiac Matrix Metalloproteinases in the Heart of Sprague-Dawley Rat

Chronic Cadmium Exposure Alters Cardiac Matrix Metalloproteinases in the Heart of Sprague-Dawley Rat

Renal Function after Reduction in Cadmium Exposure: An 8-Year Follow-up of Residents in Cadmium-Polluted Areas

Cadmium-induced endothelial dysfunction mediated by asymmetric dimethylarginine

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