Restorative effects of zinc and selenium on nitrergic relaxations impaired by cadmium in the mouse corpus cavernosum

Göçmen, Cemil; Kumcu, Eda Karabal; Secilmis, Ata; Uçar, Peyman; Dikmen, Atilla; Baysal, Firuz

doi:10.1016/s0378-4274(99)00182-4

Cited by 13 publications

(6 citation statements)

References 21 publications

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“…Finally, both zinc and selenium restore anti‐nitrergic effects of Cd in mice (Göçmen et al. ). Thus, Cd, iron, zinc, and selenium may coordinately regulate the potential contribution of Cd to AHR by direct interaction (Cd–selenium), competition for transporters (Cd–iron), or regulation of protective factors (Cd–zinc).…”

Section: Discussionmentioning

confidence: 99%

Low-dose oral cadmium increases airway reactivity and lung neuronal gene expression in mice

et al. 2016

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Inhalation of cadmium (Cd) is associated with lung diseases, but less is known concerning pulmonary effects of Cd found in the diet. Cd has a decades‐long half‐life in humans and significant bioaccumulation occurs with chronic dietary intake. We exposed mice to low‐dose CdCl2 (10 mg/L in drinking water) for 20 weeks, which increased lung Cd to a level similar to that of nonoccupationally exposed adult humans. Cd‐treated mice had increased airway hyperresponsiveness to methacholine challenge, and gene expression array showed that Cd altered the abundance of 443 mRNA transcripts in mouse lung. In contrast to higher doses, low‐dose Cd did not elicit increased metallothionein transcripts in lung. To identify pathways most affected by Cd, gene set enrichment of transcripts was analyzed. Results showed that major inducible targets of low‐dose Cd were neuronal receptors represented by enriched olfactory, glutamatergic, cholinergic, and serotonergic gene sets. Olfactory receptors regulate chemosensory function and airway hypersensitivity, and these gene sets were the most enriched. Targeted metabolomics analysis showed that Cd treatment also increased metabolites in pathways of glutamatergic (glutamate), serotonergic (tryptophan), cholinergic (choline), and catecholaminergic (tyrosine) receptors in the lung tissue. Protein abundance measurements showed that the glutamate receptor GRIN2A was increased in mouse lung tissue. Together, these results show that in mice, oral low‐dose Cd increased lung Cd to levels comparable to humans, increased airway hyperresponsiveness and disrupted neuronal pathways regulating bronchial tone. Therefore, dietary Cd may promote or worsen airway hyperresponsiveness in multiple lung diseases including asthma.

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Section: Discussionmentioning

confidence: 99%

Low-dose oral cadmium increases airway reactivity and lung neuronal gene expression in mice

et al. 2016

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“…The studies on aorta reported that cadmium-accumulation in aortas increased vasocontractility (Sakurada and Wakabayashi 1999), but the studies on myocardium reported that Cd +2 decreased the contractions (Asqrimsson et al 1995). It was determined that the contractions in the mouse corpus cavernosum decreased by the neurogenic effect of Cd +2 (Göçmen et al 2000). Also, in another study, it was reported that the contractions in the rat detrusor muscle decreased by the myogenic effect of Cd +2 (Bayazit et al 2002).…”

Section: Discussionmentioning

confidence: 99%

Determination of acute and chronic effects of cadmium on the cardiovascular system of rats

Ozturk

Büyükakıllı

Ballı

et al. 2009

Toxicology Mechanisms and Methods

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In this study, the systemic hemodynamics induced by acute and chronic cadmium (Cd+2) intoxication in the cardiovascular system of rats using thoracic electrical bioimpedance were examined and the acute and chronic effects of Cd+2 intoxication on the activities of antioxidant enzymes and malondialdehyde (MDA) were compared. Also, in this study, ultrastructural changes in the heart and aorta of rats were evaluated. Thirty-eight male Wistar albino rats were randomly divided into control, acute, and chronic groups. Chronic group was administered by oral gavage an aqueous solution of CdCl2 for 60 days, at dose of 15 mg Cd+2/kg/day. Acute group was administered by oral gavage an aqueous solution of CdCl2 with a single dose of 15 mg Cd+2/kg. Cadmium increased the stroke volume and cardiac output of rats in the chronic group, but did not change the heart rate significantly. Antioxidant enzymes activities and MDA level significantly increased in the chronic group. In ultrastructural examination, there were widespread degenerative changes in heart muscle cells of the chronic group but endothelial cells and smooth muscle cells in the aorta tissue samples had normal morphological features in all groups. All of the findings indicate that Cd+2 toxication can cause deformation in heart muscle cells due to an increase in free radicals and lipid peroxidation. Also, this study has confirmed that a long-term-Cd+2 exposure increased stroke volume (SV) and cardiac output (CO), but did not change the heart rate (HR).

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“…However, this restoration of vasorelaxation response was not statistically significant. Earlier studies reported a decrease in the Ach-induced vasorelaxation (Göçmen et al 2000;Gökalp et al 2009). Yoopan et al (2008) predicted that Cd may interact with the thiol groups of muscarinic receptors altering the ligand binding site consequently decreasing the muscarinic receptor responses to Ach.…”

Section: Discussionmentioning

confidence: 99%

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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Restorative effects of zinc and selenium on nitrergic relaxations impaired by cadmium in the mouse corpus cavernosum

Cited by 13 publications

References 21 publications

Low-dose oral cadmium increases airway reactivity and lung neuronal gene expression in mice

Low-dose oral cadmium increases airway reactivity and lung neuronal gene expression in mice

Determination of acute and chronic effects of cadmium on the cardiovascular system of rats

Cadmium-induced endothelial dysfunction mediated by asymmetric dimethylarginine

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