Sulfur dioxide induces apoptosis via reactive oxygen species generation in rat cardiomyocytes

Li, Shuyue; Xu, Zhifang; Xia, Jin; Qin, Guohua; Sang, Nan

doi:10.1007/s11356-019-04319-7

Cited by 12 publications

(3 citation statements)

References 38 publications

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“…In some studies, SO 2 promoted cardiomyocytic apoptosis in vitro and in vivo (Li et al, 2019). The data showed that the SO 2 increased the proportion of apoptotic cells, activated caspase-9 and caspase-3, destroyed the MMP, reduced bcl-2 expression and the ratio of bcl-2/bax, and upregulated the expression of bax and p53, which could be blocked by antioxidant N-acetylcysteine.…”

Section: Endogenous So 2 Regulates Cardiomyocyte Apoptosismentioning

confidence: 98%

Endogenous SO2 Controls Cell Apoptosis: The State-of-the-Art

Feng

et al. 2021

Front. Cell Dev. Biol.

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SO2, previously known as the product of industrial waste, has recently been proven to be a novel gasotransmitter in the cardiovascular system. It is endogenously produced from the metabolism pathway of sulfur-containing amino acids in mammalians. Endogenous SO2 acts as an important controller in the regulation of many biological processes including cardiovascular physiological and pathophysiological events. Recently, the studies on the regulatory effect of endogenous SO2 on cell apoptosis and its pathophysiological significance have attracted great attention. Endogenous SO2 can regulate the apoptosis of vascular smooth muscle cells, endothelial cells, cardiomyocytes, neuron, alveolar macrophages, polymorphonuclear neutrophils and retinal photoreceptor cells, which might be involved in the pathogenesis of hypertension, pulmonary hypertension, myocardial injury, brain injury, acute lung injury, and retinal disease. Therefore, in the present study, we described the current findings on how endogenous SO2 is generated and metabolized, and we summarized its regulatory effects on cell apoptosis, underlying mechanisms, and pathophysiological relevance.

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Section: Endogenous So 2 Regulates Cardiomyocyte Apoptosismentioning

confidence: 98%

Endogenous SO2 Controls Cell Apoptosis: The State-of-the-Art

Feng

et al. 2021

Front. Cell Dev. Biol.

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“…In this context, it has been reported that the improvements in the vascular remodeling in hypertension and pulmonary hypertension are achieved through increasing apoptosis of vascular smooth muscle cells (VSMCs) and prohibiting the apoptosis of vascular endothelial cells (ECs) [ 65 ]. Endogenous SO 2 also provides cardio-protection by suppressing the apoptosis of cardiomyocytes [ 66 ]. Whether or not such initially beneficial actions are—at closer inspection—really desirable and may even be used in the context of therapy is a major and so far not really answered question.…”

Section: Inorganic Vscsmentioning

confidence: 99%

A Whiff of Sulfur: One Wind a Day Keeps the Doctor Away

et al. 2022

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Reactive Sulfur Species (RSS), such as allicin from garlic or sulforaphane from broccoli, are fre-quently associated with biological activities and possible health benefits in animals and humans. Among these Organic Sulfur Compounds (OSCs) found in many plants and fungi, the Volatile Sulfur Compounds (VSCs) feature prominently, not only because of their often-pungent smell, but also because they are able to access places which solids and solutions cannot reach that easily. Indeed, inorganic RSS such as hydrogen sulfide (H2S) and sulfur dioxide (SO2) can be used to lit-erally fumigate entire rooms and areas. Similarly, metabolites of garlic, such as allyl methyl sulfide (AMS), are formed metabolically in humans in lower concentrations and reach the airways from inside the body as part of one’s breath. Curiously, H2S is also formed in the gastrointestinal tract by gut bacteria, and the question of if and for which purpose this gas then crosses the barriers and enters the body is indeed a delicate matter for equally delicate studies. In any case, nature is surprisingly rich in such VSCs, as fruits (for instance, the infamous durian) demonstrate, and therefore these VSCs represent a promising group of compounds for further studies.

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“…The systemic inflammatory response was excluded since no systemic acute phase or coagulant response was observed during exposure (159). Besides, several studies have suggested that SO 2 could cause mitochondrial dysfunction and induce ROS production (162,163), which provide possible underlying mechanisms for the significant association of SO 2 to ischemic heart diseases. Above two pathological pathways for promoting arrhythmias have been discussed in previous sections and are not discussed here.…”

Section: Potential Proarrhythmic Mechanismsmentioning

confidence: 99%

Air Pollution and Cardiac Arrhythmias: From Epidemiological and Clinical Evidences to Cellular Electrophysiological Mechanisms

Zhang

Lü

Wei

et al. 2021

Front. Cardiovasc. Med.

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Cardiovascular disease is the leading cause of death worldwide and kills over 17 million people per year. In the recent decade, growing epidemiological evidence links air pollution and cardiac arrhythmias, suggesting a detrimental influence of air pollution on cardiac electrophysiological functionality. However, the proarrhythmic mechanisms underlying the air pollution-induced cardiac arrhythmias are not fully understood. The purpose of this work is to provide recent advances in air pollution-induced arrhythmias with a comprehensive review of the literature on the common air pollutants and arrhythmias. Six common air pollutants of widespread concern are discussed, namely particulate matter, carbon monoxide, hydrogen sulfide, sulfur dioxide, nitrogen dioxide, and ozone. The epidemiological and clinical reports in recent years are reviewed by pollutant type, and the recently identified mechanisms including both the general pathways and the direct influences of air pollutants on the cellular electrophysiology are summarized. Particularly, this review focuses on the impaired ion channel functionality underlying the air pollution-induced arrhythmias. Alterations of ionic currents directly by the air pollutants, as well as the alterations mediated by intracellular signaling or other more general pathways are reviewed in this work. Finally, areas for future research are suggested to address several remaining scientific questions.

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Sulfur dioxide induces apoptosis via reactive oxygen species generation in rat cardiomyocytes

Cited by 12 publications

References 38 publications

Endogenous SO2 Controls Cell Apoptosis: The State-of-the-Art

Endogenous SO2 Controls Cell Apoptosis: The State-of-the-Art

A Whiff of Sulfur: One Wind a Day Keeps the Doctor Away

Air Pollution and Cardiac Arrhythmias: From Epidemiological and Clinical Evidences to Cellular Electrophysiological Mechanisms

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