Inhibition of rat heart mitochondrial respiration by cadmium chloride

Kisling, Gregory M.; Kopp, Stephen J.; Paulson, Dennis J.; Hawley, Philip L.; Tow, June P.

doi:10.1016/0041-008x(87)90149-9

Cited by 21 publications

(6 citation statements)

References 20 publications

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“…Cadmium toxicity has been showed to impair energy productions in cardiomyocytes, as well as glucose oxidations. It has been reported that cadmium acted solely as an inhibitor of rat heart pyruvate–malate-supported mitochondrial respiration [ 17 ]. Considering that glucose oxidation primarily occurs in mitochondria, we would like to confirm whether mitochondria respiratory gene expression is altered by cadmium toxicity in cardiomyocytes.…”

Section: Resultsmentioning

confidence: 99%

“…For example, cadmium perfusion significantly decreased contractile tension, rate of tension development, heart rate, coronary flow rate and atrioventricular node conductivity [ 16 ]. Moreover, cadmium acted solely as an inhibitor of rat heart pyruvate-malate supported mitochondrial respiration [ 17 ]. And cadmium treatment of rats decreased activities of the selenoenzyme, glutathione peroxidase and copper-containing enzyme superoxide dismutase, together with a rise in thiobarbiturate-reactive substances in the heart [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

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Cadmium toxicity induces ER stress and apoptosis via impairing energy homoeostasis in cardiomyocytes

et al. 2015

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cadmium toxicity induces ER stress and apoptosis via impairing energy homoeostasis in cardiomyocytes

et al. 2015

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“…24,25 It is reported that atractyloside poisoning causes fatal renal and hepatic necrosis in humans and experimental animals; 1,12,15,17 it also has cardiotoxic effects. 15,26,27 Sharply demarcated and severe centrilobular hepatocellular necrosis associated with haemorrhage and congestion 9,12,24,[28][29][30] were demonstrated in the liver. However, the toxic damage in the kidney was confined to the proximal tubular cells and the thick ascending loop of Henle while the glomeruli appeared unaffected.…”

Section: Discussionmentioning

confidence: 99%

Carboxyatractyloside poisoning in humans

Turğut

Alhan

Gürgöze

et al. 2005

Annals of Tropical Paediatrics

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“…In rats, the heart muscle cells could be deformed by cadmium poisoning because of the increment of free radicals and lipid peroxidation, based on ultrastructural examination 22. Another rat study indicated that cadmium acted solely as an inhibitor of heart pyruvate-malate-supported mitochondrial respiration, suggesting that disturbances in myocardial metabolism and function may occur following cadmium exposure 23. Furthermore, an epidemiologic study of 12,049 US participants demonstrated that urinary cadmium levels were significantly correlated with self-reported prevalence of heart failure 24.…”

Section: Discussionmentioning

confidence: 99%

“…Then, the absorbed cadmium accumulates in the kidneys for a long time with a low rate of urinary excretion 6. Although cadmium exposure is a risk factor of cardiovascular diseases in humans,25,26 and may disturb myocardial metabolism (suggested by animal studies),22,23 it is uncertain whether the basic metabolism of cadmium would be changed in patients with cardiac diseases, including heart failure. Hence, further studies are needed to elucidate its specific role in AHF patients.…”

Section: Discussionmentioning

confidence: 99%

Urinary cadmium levels predict mortality of patients with acute heart failure

Hsu

Weng

Lee

et al. 2017

TCRM

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BackgroundAcute heart failure (AHF) is a serious condition that is associated with increased mortality in critically ill patients. Previous studies indicated that environmental exposure to cadmium increases mortality of general populations. However, the relationship of cadmium exposure and mortality is unclear for AHF patients.Materials and methodsA total of 153 patients with AHF in intensive care units (ICUs) met the inclusion criteria and were followed up for 6 months. Demographic data, AHF etiology, hematological and biochemical data, and hospital mortality were recorded. The scores of two predictive systems (Sequential Organ Failure Assessment [SOFA], Acute Physiology and Chronic Health Evaluation II [APACHE II]) for mortality in critically ill patients were calculated, and urinary cadmium levels were recorded.ResultsAt the end of the follow-up period, the mortality rate was 24.8%. The survivors (n=115) had higher urinary cadmium levels on day 1 (D1UCd) of ICU admission than non-survivors (n=38). A multiple linear regression analysis revealed a positive correlation between D1UCd and acute kidney injury, but a negative correlation between D1UCd and the level of serum albumin. A multivariate Cox analysis indicated that D1UCd was an independent predictor of mortality in AHF patients. For each increment of 1 μg of D1UCd, the hazard ratio for ICU mortality was 1.20 (95% confidence interval [CI]: 1.09–1.32, P<0.001). The area under the receiver operating characteristic curve for D1UCd was 0.84 (95% CI: 0.78–0.91), better than the values for the SOFA and APACHE II systems.ConclusionThe D1UCd may serve as a single predictor of hospital mortality for AHF patients in the ICU. Because of the high mortality and smaller sample size, more investigations are required to confirm these observations and elucidate the underlying mechanisms.

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Inhibition of rat heart mitochondrial respiration by cadmium chloride

Cited by 21 publications

References 20 publications

Cadmium toxicity induces ER stress and apoptosis via impairing energy homoeostasis in cardiomyocytes

Cadmium toxicity induces ER stress and apoptosis via impairing energy homoeostasis in cardiomyocytes

Carboxyatractyloside poisoning in humans

Urinary cadmium levels predict mortality of patients with acute heart failure

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