Arsenic induces cardiac rhythm dysfunction and acylcarnitines metabolism perturbation in rats

Phan, Nam Nhut; Li, Kuan-Lun; Lin, Yansong

doi:10.1080/15376516.2018.1440679

Cited by 6 publications

(3 citation statements)

References 39 publications

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“…Arsenic exposure is known to induce the hyper phosphorylation of protein tau [27], and increase the production of amyloid-β [28], both of which are involved in the formation of neurofibrillary tangles and brain amyloid plaques [29]. Arsenic is a well-known cardiovascular toxicant that causes cardiovascular diseases [30,31], which is in agreement with the vascular hypothesis of AD. The current vascular hypothesis of AD proposes that the AD is the result of vascular damages which reduces the cerebral blood perfusion rate and therefore indirectly impairs neuron [32,33].…”

Section: Discussionmentioning

confidence: 66%

Positive association between soil arsenic concentration and mortality from alzheimer’s disease in mainland China

Zhan

Zheng

et al. 2020

Journal of Trace Elements in Medicine and Biology

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Objectives: The current study was designed to investigate the relationship between the soil arsenic (As) concentration and the mortality from Alzheimer's disease (AD) in mainland China. Study design: Ecological study. Methods: Twenty-two provinces and 3 municipal districts in mainland China were included in this study. The As concentrations in soil in 1990 was obtained from the China State Environmental Protection Bureau; the data on annual mortality of AD from 1991 to 2000 were obtained from the National Death Cause Surveillance Database of China. Using these data, we calculated the spearman correlation coefficient between soil As concentration and AD mortality, and the relative risk (RR) between soil As levels and AD mortality by quartile-dividing study groups. Results: The spearman correlation coefficient between As concentration and AD mortality was 0.552 (p = 0.004), 0.616 (p = 0.001) and 0.622 (p = 0.001) in the A soil As (eluvial horizon), the C soil As (parent material horizon), and the Total soil As (A soil As + C soil As), respectively. When the A soil As concentration was over 9.05 mg/kg, 10.40 mg/kg and 13.10 mg/kg, the relative risk was 0.835 (95 % CI: 0.832, 0.838), 1.969 (95 %CI: 1.955, 1.982), and 2.939 (95 % CI: 2.920, 2.958), respectively; when the C soil As reached 9.45 mg/kg, 11.10 mg/kg and 13.55 mg/kg, the relative risk was 4.349 (95 % CI: 4.303, 4.396), 6.108 (95 % CI: 6.044, 6.172), and 9.125 (95 %CI: 9.033, 9.219), respectively. No correlation was found between lead, cadmium, and mercury concentration in the soil and AD mortality. Conclusion: There was an apparent soil As concentration dependent increase in AD mortality. Results of this study may provide evidence for a possible causal linkage between arsenic exposure and the death risk from AD.

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Section: Discussionmentioning

confidence: 66%

Positive association between soil arsenic concentration and mortality from alzheimer’s disease in mainland China

Zhan

Zheng

et al. 2020

Journal of Trace Elements in Medicine and Biology

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“…Our study has confirmed the prolongation of QT interval as a major complication of As exposure. [40][41][42] Blocking potassium channels by As increases the risk of excessive repolarization delay in phase 3 of the cardiac action potential, causing changes in ventricular action potential duration (APD). 43 Increased APD is reflected by prolongation of the QT interval, displaying ventricular depolarization and repolarization.…”

Section: Discussionmentioning

confidence: 99%

Melatonin ameliorates arsenic‐induced cardiotoxicity through the regulation of the Sirt1/Nrf2 pathway in rats

et al. 2023

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Chronic arsenic (As) exposure, mainly as a result of drinking contaminated water, is associated with cardiovascular diseases. Mitochondrial dysfunction, oxidative stress, inflammation, apoptosis, and autophagy have been suggested as the molecular etiology of As cardiotoxicity. Melatonin (Mel) is a powerful antioxidant. Mel improves diabetic cardiomyopathy, cardiac remodeling, and heart failure. Following pre-treatment with Mel (10, 20, or 30 mg/kg/day i.p.), rats were orally gavaged with As (15 mg/kg/day) for 28 days. Electrocardiographic findings showed that Mel decreased the As-mediated QT interval prolongation. The effects of As on cardiac levels of glutathione (GSH) and malondialdehyde (MDA) were reversed by Mel pretreatment. Mel also modulated the Sirt1 and Nrf2 expressions promoted by As. Mel down-regulated autophagy markers such as Beclin-1 expression and the LC3-II/I ratio. Moreover, the cardiac expression of cleaved-caspase-3 and Bax/Bcl-2 ratio was decreased by Mel pretreatment. Reduced expression of miR-34a and miR-144 by As were reversed by Mel. The histopathological changes of cardiac injury

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“…Arsenic is an ancient toxic metal that is commonly found in the environment. NaAsO2 is the most toxic, affecting people in many countries around the world, including China.Arsenic has been shown to cause many cardiovascular diseases and to cause cardiomyocyte damage and cardiomyocyte apoptosis 5,6) .Sodium tanshinone IIA sulfonate (STS) has been approved by China Food and Drug Administration (CFDA) for the treatment of cardiovascular disease. 7,8) However, the combination of NaAsO2 poisoning and STS has not been reported.…”

Section: Discussionmentioning

confidence: 99%

Effects of Sodium tanshinone IIA sulfonate on H9C2 cardiomyocyte injury induced by sodium arsenite

Zhang¹,

Li²,

Sheng³

et al. 2020

Preprint

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Arsenic is a grade I human carcinogen that can cause kinds of damage to the body.The heart is one of the main target organs of arsenic damage,but the preventive and curative measures underlying arsenic poisoning are not clear. To investigate the effect of tanshinone IIA sulfonate (STS) on the injury of H9C2 cardiomyocytes induced by NaAsO2,H9C2 cardiomyocyteswere divided into four groups where control group with general medium,arsenic (As) group received sodium arsenite (NaAsO2)-containing general medium,STS pretreatment+As group and finally the STS alone group . Compared with the control group, different concentrations of STS had no significant effect on the cell viability (n = 6, P > 0.05); Compared with the control group, there was no significant change in the viability of cells treated with arsenic for 12 h after STS pretreatment for 6 h (n = 6, P > 0.05),the viability of cells treated with NaAsO2 alone was decreased(n = 6, P < 0.05);Compared with the control group, the cell viability was decreased after STS pretreatment for 12h and arsenic for 24h,the cell viability of NaAsO2 group was also decreased,the viability of NaAsO2 cells was lower than that of STS pretreated for 12h with NaAsO2 for 24h(n=6,p<0.05).The content of Caspase 3/7 in the NaAsO2 group was higher than that in the STS and NaAsO2 group and the Control group and STS group after 12h,the differences were statistically significant(n=6,p<0.05).After STS pretreatment for 12h and NaAsO2 for 24 h, there was no significant difference in Caspase 8 content between NaAsO2 group and other groups (n=6,P>0.05) As a result,Sodium tanshinone IIA sulfonate can attenuate the injury of H9C2 cardiomyocytes induced by sodium arsenite.

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Arsenic induces cardiac rhythm dysfunction and acylcarnitines metabolism perturbation in rats

Cited by 6 publications

References 39 publications

Positive association between soil arsenic concentration and mortality from alzheimer’s disease in mainland China

Positive association between soil arsenic concentration and mortality from alzheimer’s disease in mainland China

Melatonin ameliorates arsenic‐induced cardiotoxicity through the regulation of the Sirt1/Nrf2 pathway in rats

Effects of Sodium tanshinone IIA sulfonate on H9C2 cardiomyocyte injury induced by sodium arsenite

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