Cardiac Tissue Injury Resistance During Myocardial Infarction at Adulthood by Developmental Exposure to Cadmium

Zepeda, Ramiro; Castillo, Paula; Saez, Daniel Martinez; Llanos, Miguel; Ronco, Ana María

doi:10.1007/s12012-011-9139-6

Cited by 5 publications

(4 citation statements)

References 41 publications

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“…In particular, high susceptibility of the heart to cadmium was reported in a human 15 year follow-up study in line with the fact that the heart is a relatively sensitive organ due to its low anti-oxidant capacity [7]. Similarly, animal studies also shows cadmium cause some changes in cardiovascular functions [8][9][10]. Environmental exposure to cadmium has been found to be associated with an increased prevalence of heart failure, although the precise toxic effects of cadmium exposure on myocardial function remain unknown [11].…”

Section: Introductionmentioning

confidence: 69%

Effects of age, gender, BMI, settlement and smoking on lead and cadmium accumulation in heart tissue

Dip¹,

İritaş²,

Mergen³

et al. 2017

Med-Science

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Cadmium (Cd) and lead (Pb) are well-known risk factors for peripheral arterial and some other cardiovascular diseases. The aim of the study was to determine the level of both toxic metals, in the human heart tissue and compare the accumulation to their age, gender, body mass index, living environment and smoking habit. Heart tissues of the 112 autopsy cases, representing a sample set of population living in capital city of Turkey: Ankara Province (both in city center and suburban), were collected from Turkey Ministry of Justice, Council of Forensic Medicine in Ankara Branch. Lead and cadmium analysis was carried out by Graphite Furnace Atomic Spectrometry technique. Cd/Pb results and individuals' information were assessed by SPSS statistically. Average value of Pb was found as 1374.99±237.01ppb and Cd was found as 287.54±66.43ppb in all heart tissue samples. Consideration of metal levels in autopsy heart tissues by age, statistically significant positive correlation in Cd was observed (p<0.05). There was no correlation found between metal levels with gender and BMI values. Both Pb and Cd levels of the samples who lived in urban was significantly greater than in suburban areas (p<0.05). Significant increase Cd level were observed in smokers' heart tissues (p<0.05), however, contrary to expectations, Pb has no statistically significant result.

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Section: Introductionmentioning

confidence: 69%

Effects of age, gender, BMI, settlement and smoking on lead and cadmium accumulation in heart tissue

Dip¹,

İritaş²,

Mergen³

et al. 2017

Med-Science

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“…We and others have previously reported that cadmium (Cd), a ubiquitously distributed environmental toxicant and main component of tobacco smoke, accumulates in the placenta of pregnant rats inducing low birth weight in high correlation with placental levels of this heavy metal [7] , [11] , [12] . We have reported that Cd exposure during pregnancy increases levels of circulating corticosterone – the main active GC of rodents – in mothers and offspring, suggesting an involvement of the GC system in some toxic effects induced by Cd [10] , [13] . This steroidogenic hormone is regulated by the 11β-hydroxysteroid dehydrogenase enzymes (11β-HSD; isoforms 1 and 2) and mediated by intracellular glucocorticoid receptor (GR) [9] .…”

Section: Introductionmentioning

confidence: 99%

“…We have reported that Cd exposure during pregnancy increases levels of circulating corticosterone – the main active GC of rodents – in mothers and offspring, suggesting an involvement of the GC system in some toxic effects induced by Cd [10], [13]. This steroidogenic hormone is regulated by the 11β-hydroxysteroid dehydrogenase enzymes (11β-HSD; isoforms 1 and 2) and mediated by intracellular glucocorticoid receptor (GR) [9].…”

Section: Introductionmentioning

confidence: 99%

Impact of Cadmium Exposure during Pregnancy on Hepatic Glucocorticoid Receptor Methylation and Expression in Rat Fetus

et al. 2012

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Adverse fetal environment due to maternal undernutrition or exposure to environmental chemicals alters glucocorticoid (GC) metabolism increasing the risk of metabolic disorders in adulthood. In this study, we investigated the effects of maternal exposure to cadmium (Cd, 50 ppm) during pregnancy in the methylation of fetal hepatic glucocorticoid receptor promoter (GR) and the correlation with its expression and that of the DNA methyltransferases (DNMT1a and 3a). We also studied the expression of liver phosphoenolpyruvate carboxykinase (PEPCK) and acyl-CoA oxidase (AOX), two enzymes involved in the metabolism of carbohydrates and lipids respectively. The methylation of the rat GR gene exon 110 (GR110) in nucleotides -2536 to -2361 was analyzed by pyrosequencing. Quantitative real time PCR was used to assess hepatic GR, PEPCK and AOX mRNA, and their protein levels using Western blotting analysis. Differential methylation was noted across groups at all CpG sites in the GR exon 110 in a sex-dependent manner. In males, CpG were more methylated than the controls (185±21%, p<0.001) but only CpG sites 1,6,7 and 9 showed a significantly different extent of methylation. In addition, a lower expression of GR (mRNA and protein) was found. On the contrary, in females, CpG were less methylated than the controls (62±11%, p<0.05) and overexpressed, affecting PEPCK and AOX expression, which did not change in males. The GR methylation profile correlates with DNMT3a expression which may explain epigenetic sex-dependent changes on GR110 promoter induced by Cd treatment. In conclusion, Cd exposure during pregnancy affects fetal liver DNMT3a resulting in sex-dependent changes in methylation and expression of GR110. Although these effects do not seem to be directly involved in the low birth weight and height, they may have relevant implications for long-term health.

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“…9, 10 Prenatal exposure to cadmium is known to lead to change of cardiovascular function during adulthood. 1, 11, 12 Environmental exposure to cadmium has been found to be associated with an increased prevalence of heart failure 1 although the precise toxic response of cadmium exposure on myocardial function remains elusive. More recent data from the National Health and Nutrition Examination Survey have strongly suggested that cadmium, at substantially low levels of exposure, remains a rather important determinant of all-cause cardiovascular mortality in certain populations of U.S. adults.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of DNA methylation attenuates low‐dose cadmium‐induced cardiac contractile and intracellular Ca²⁺ anomalies

Turdi

Sun

Tan

et al. 2013

Clin Exp Pharma Physio

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Cadmium is a human carcinogen with unfavorable health impact probably associated with its DNA methylation property. Recent data suggest that environmental cadmium exposure is associated with incidence of myocardial infarction and peripheral arterial disease. Nonetheless, the effect of chronic cadmium exposure on cardiac contractile function remains elusive. This study was designed to examine the impact of low-dose cadmium exposure on cardiac contractile function and intracellular Ca2+ homeostasis. Adult male mice were exposed to cadmium for 4 weeks with or without the DNA methylation inhibitor (5-aza-2’-deoxyctidene, 5-AZA). Cardiac contractile and intracellular Ca2+ properties were analyzed including echocardiographic left ventricular parameters, fractional shortening (FS), peak shortening amplitude (PS), maximal velocity of shortening/relengthening (± dL/dt), time-to-PS (TPS), time-to-90% relengthening (TR90), electrically-stimulated increase of intracellular Ca2+ and intracellular Ca2+ decay. Our results revealed that cadmium exposure depressed FS, PS, ± dL/dt and electrically-stimulated rise in intracellular Ca2+ without affecting TPS, TR90, intracellular Ca2+ level and decay rate, the effects of which were significantly attenuated or nullified by 5-AZA. Cadmium exposure led to overt interstitial fibrosis (collagen deposition), the effect of which was mitigated by 5-AZA. Western blot analysis showed unchanged expression of ICAM-1, TNF-α and Cleaved caspase-3 in response to cadmium exposure and/or 5-AZA treatment, suggesting a relatively minor role of pro-inflammatory cytokines and apoptosis in cadmium- and 5-AZA-induced cardiac responses. Taken together, our data demonstrated for the first time direct cardiac depressant effect following cadmium exposure, which may be rescued by DNA methylation inhibition.

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Cardiac Tissue Injury Resistance During Myocardial Infarction at Adulthood by Developmental Exposure to Cadmium

Cited by 5 publications

References 41 publications

Effects of age, gender, BMI, settlement and smoking on lead and cadmium accumulation in heart tissue

Effects of age, gender, BMI, settlement and smoking on lead and cadmium accumulation in heart tissue

Impact of Cadmium Exposure during Pregnancy on Hepatic Glucocorticoid Receptor Methylation and Expression in Rat Fetus

Inhibition of DNA methylation attenuates low‐dose cadmium‐induced cardiac contractile and intracellular Ca²⁺ anomalies

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Cardiac Tissue Injury Resistance During Myocardial Infarction at Adulthood by Developmental Exposure to Cadmium

Cited by 5 publications

References 41 publications

Effects of age, gender, BMI, settlement and smoking on lead and cadmium accumulation in heart tissue

Effects of age, gender, BMI, settlement and smoking on lead and cadmium accumulation in heart tissue

Impact of Cadmium Exposure during Pregnancy on Hepatic Glucocorticoid Receptor Methylation and Expression in Rat Fetus

Inhibition of DNA methylation attenuates low‐dose cadmium‐induced cardiac contractile and intracellular Ca2+ anomalies

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Inhibition of DNA methylation attenuates low‐dose cadmium‐induced cardiac contractile and intracellular Ca²⁺ anomalies