Calcium-dependent effects of cadmium on energy metabolism and function of perfused rat heart

Prentice, Robert C.; Hawley, Philip L.; Glonek, Thomas; Kopp, Stephen J.

doi:10.1016/0041-008x(84)90202-3

Cited by 29 publications

(8 citation statements)

References 23 publications

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“… 20 21 Cadmium also affects the cardiac conduction system by interfering with calcium-mediated physiological and biochemical processes. 22 Blockade of L-type calcium channels and altered outward potassium current in ventricular myocytes were also observed in vivo. 23 36 …”

Section: Discussionmentioning

confidence: 95%

Cadmium exposure and incidence of heart failure and atrial fibrillation: a population-based prospective cohort study

et al. 2015

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ObjectivesCadmium is a non-essential toxic metal with multiple adverse health effects. Cadmium has been shown to be associated with cardiovascular diseases, but few studies have investigated heart failure (HF) and none of them reported atrial fibrillation (AF). We examined whether cadmium exposure is associated with incidence of HF or AF.DesignA prospective, observational cohort study with a 17-year follow-up.SettingThe city of Malmö, Sweden.ParticipantsBlood cadmium levels were measured in 4378 participants without a history of HF or AF (aged 46–67 years, 60% women), who participated in the Malmö Diet and Cancer (MDC) study during 1992–1994.Primary and secondary outcome measuresIncidence of HF and AF were identified from the Swedish hospital discharge register.Results143 participants (53% men) were diagnosed with new-onset HF and 385 individuals (52% men) were diagnosed with new-onset AF during follow-up for 17 years. Blood cadmium in the sex-specific 4th quartile of the distribution was significantly associated with incidence of HF. The (HR, 4th vs 1st quartile) was 2.64 (95% CI 1.60 to 4.36), adjusted for age, and 1.95 (1.02 to 3.71) after adjustment also for conventional risk factors and biomarkers. The blood cadmium level was not significantly associated with risk of incident AF.ConclusionsBlood cadmium levels in the 4th quartile were associated with increased incidence of HF in this cohort with comparatively low exposure to cadmium. Incidence of AF was not associated with cadmium.

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Section: Discussionmentioning

confidence: 95%

Cadmium exposure and incidence of heart failure and atrial fibrillation: a population-based prospective cohort study

et al. 2015

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“…Effects on the cardiac conduction system are based on interactions of Cd with contraction and pacing systems. Observed phenomena include, among others, a blockade of L-type calcium channel (Shen et al 2000), and an alteration of outward potassium current (Follmer et al 1992), both in ventricular myocytes; an interaction with calcium-activated and calcium-mediated processes in the heart (Prentice et al 1984), and a blockade of fast Na channels of Purkinje fibres (DiFrancesco et al 1985). In several of the above studies Cd effects on cardiac performance were described.…”

Section: Cadmium and The Heartmentioning

confidence: 98%

Cadmium and cardiovascular diseases: cell biology, pathophysiology, and epidemiological relevance

2010

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Today cardiovascular diseases (CVDs) are the killer number one world wide. In 2004 an estimated 17.1 million people died due to CVDs and this number will further increase to an estimated 23.6 million by 2030. Importantly, currently known risk factors, like hypertension, and hypercholesterolemia, can only be made responsible for about 50-75% of all CVDs, highlighting the urgent need to search for and define new CVD risk factors. Cadmium (Cd) was shown to have the potential to serve as one such novel risk factor, as it was demonstrated-in vitro, in animal studies, and in human studies-that Cd causes atherosclerosis (the basis of most CVDs). Herein, we discuss the molecular and cellular biological effects of Cd in the cardiovascular system; we present concepts on the pathophysiology of Cd-caused atherosclerosis, and provide data that indicate an epidemiological relevance of Cd as a risk factor for CVDs.

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“…A possible mechanism to account for these findings is that Cd2+ might displace Ca2+ from binding sites on the E-cadherin molecule and thereby alter its adhesive properties. Although additional studies are needed to determine whether or not Cd 2+ does, in fact, bind directly to E-cadherin, it is well established that Cd 2 § can interact with many other types of Ca2+-binding sites (Chat et al 1984;Mazzei et al 1984;Prentice et al 1984;Akerman et al 1985). Furthermore, the removal of Ca 2 § from E-cadherin has been shown to profoundly disrupt the adhesive properties of the molecule (Gumbiner and Simons 1986;Ringwald et al 1987;Ozawa et al 1990).…”

Section: Discussionmentioning

confidence: 97%

Surface binding and uptake of cadmium (Cd2+) by LLC-PK1 cells on permeable membrane supports

Prozialeck¹,

Lamar²

1993

Arch Toxicol

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Recent studies have shown that Cd2+ has relatively specific damaging effects on cell-cell junctions in the renal epithelial cell line, LLC-PK1. The objective of the present studies was to examine the surface binding and uptake of Cd2+ by LLC-PK1 cells in relation to the disruption of cell-cell junctions. LLC-PK1 cells on Falcon Cell Culture Inserts were exposed to CdCl2 containing trace amounts of 109Cd2+ from either the apical or the basolateral compartments, and the accumulation of 109Cd2+ was monitored for up to 8 h. The integrity of cell-cell junctions was assessed by monitoring the transepithelial electrical resistance. The results showed that the cells accumulated 3-4 times more Cd2+ from the basolateral compartment than from the apical compartment. The accumulation of Cd2+ from the basolateral compartment occurred in two phases: a rapid, exponential phase that occurred in 1-2 h and coincided with a decrease in transepithelial resistance, and a slower, linear phase that continued for 6-8 h. The Cd2+ that accumulated during the rapid phase was easily removed by washing the cells in EGTA, indicating that most of it was bound to sites on the cell surface. By contrast, most of the Cd2+ that accumulated during the slower phase could not be removed by EGTA, indicating that it had been taken up by the cells. Additional studies showed that the rapid phase of Cd2+ accumulation was enhanced when Ca2+ was present at low concentrations (0.1 mM), and was greatly reduced when Ca2+ was present at high concentrations (10 mM).(ABSTRACT TRUNCATED AT 250 WORDS)

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Calcium-dependent effects of cadmium on energy metabolism and function of perfused rat heart

Cited by 29 publications

References 23 publications

Cadmium exposure and incidence of heart failure and atrial fibrillation: a population-based prospective cohort study

Cadmium exposure and incidence of heart failure and atrial fibrillation: a population-based prospective cohort study

Cadmium and cardiovascular diseases: cell biology, pathophysiology, and epidemiological relevance

Surface binding and uptake of cadmium (Cd2+) by LLC-PK1 cells on permeable membrane supports

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