Acrolein induces a cellular stress response and triggers mitochondrial apoptosis in A549 cells

Roy, Julie; Pallepati, Pragathi; Bettaieb, Ahmed; Tanel, André; Averill‐Bates, Diana A.

doi:10.1016/j.cbi.2009.07.001

Cited by 65 publications

(37 citation statements)

References 64 publications

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“…It was reported that acrolein caused apoptosis in the colon cancer cells by production of a cellular stress response [23,24]. In this study, we demonstrated that acrolein can cause cardiac myocytes injury and cell death in concentrationdependent manner.…”

Section: Acrolein-induced Cardiomyocytes Apoptosissupporting

confidence: 50%

Acrolein, an Environmental Toxin, Induces Cardiomyocyte Apoptosis via Elevated Intracellular Calcium and Free Radicals

Wang

Sun

Asahi

et al. 2011

Cell Biochem Biophys

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Acrolein, an unsaturated aldehyde, is an environmental toxin known to inhibit mitochondrial electron transport chain in brain and induce lipid peroxidation and apoptosis. However, the nature of the effects of acrolein on cardiac function and myocardium is not known. The objective of this study is to examine whether acrolein induces apoptosis in cardiomyocytes and alters cytosolic calcium concentration and the intracellular oxygen free-radical levels. Adult mouse cardiomyocytes exposed to 1 μmol/l of acrolein showed a marked increase in the intracellular oxygen free-radicals and calcium concentration, by 12- and 2-fold, respectively, compared to the resting value. Moreover, the cardiomyocyte viability decreased significantly in a dose-dependent manner by treatment with 25, 50, and 100 μmol/l of acrolein compared to controls. Morphological changes and DNA laddering typical of apoptosis were found in acrolein-exposed cardiomyocytes. Our finding suggested that acrolein caused apoptotic death of adult mice cardiomyocytes by increasing intracellular oxygen free-radicals and calcium concentration.

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Section: Acrolein-induced Cardiomyocytes Apoptosissupporting

confidence: 50%

Acrolein, an Environmental Toxin, Induces Cardiomyocyte Apoptosis via Elevated Intracellular Calcium and Free Radicals

Wang

Sun

Asahi

et al. 2011

Cell Biochem Biophys

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“…Cigarette smoking intake reduces inner mitochondrial membrane fluidity, inhibits respiration, and reduces ATP production through a switch from mitochondrial state 3 to state 4 respiration (50,75). Recent data also demonstrate that acrolein, a reactive aldehyde in cigarette smoke, induces hyperpolarization of DJ m with a resultant increase in ROS production (135). In addition, lipid-soluble components of cigarette smoke induce excessive mitochondrial ROS production in lung epithelial cells, contributing to toxicity in that organ (159).…”

Section: Smoking and Mitochondrial Rosmentioning

confidence: 99%

Regulation of Endothelial Function by Mitochondrial Reactive Oxygen Species

Widlansky

Gutterman

2011

Antioxidants & Redox Signaling

169

152

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Mitochondria are well known for their central roles in ATP production, calcium homeostasis, and heme and steroid biosynthesis. However, mitochondrial reactive oxygen species (ROS), including superoxide and hydrogen peroxide, once thought to be toxic byproducts of mitochondrial physiologic activities, have recently been recognized as important cell-signaling molecules in the vascular endothelium, where their production, conversion, and destruction are highly regulated. Mitochondrial reactive oxygen species appear to regulate important vascular homeostatic functions under basal conditions in a variety of vascular beds, where, in particular, they contribute to endothelium-dependent vasodilation. On exposure to cardiovascular risk factors, endothelial mitochondria produce excessive ROS in concert with other cellular ROS sources. Mitochondrial ROS, in this setting, act as important signaling molecules activating prothrombotic and proinflammatory pathways in the vascular endothelium, a process that initially manifests itself as endothelial dysfunction and, if persistent, may lead to the development of atherosclerotic plaques. This review concentrates on emerging appreciation of the importance of mitochondrial ROS as cell-signaling molecules in the vascular endothelium under both physiologic and pathophysiologic conditions. Future potential avenues of research in this field also are discussed. Antioxid. Redox Signal. 15, 1517-1530.

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“…Whether apoptosis or necrosis ensues after acrolein exposure appears to be related to dose and cell type. In regards to activation of caspases as part of the mitochondrial death pathway it was shown that apoptosis could be both caspase-dependent: in human neuroblastoma cells (Dong et al, 2013) and in A549 lung cells (Roy et al, 2009), as well as caspase-independent: in CHO cells (Tanel and Averill-Bates, 2005). It was suggested that the activation of certain caspases may arise from a partial inhibition of their active site cysteine residue through direct alkylation by acrolein (Kern and Kehrer, 2002).…”

Section: Empirical Support For Linkagementioning

confidence: 99%

Adverse Outcome Pathway on Protein Alkylation Leading to Liver Fibrosis

Landesmann

2016

OECD Series on Adverse Outcome Pathways

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Acrolein induces a cellular stress response and triggers mitochondrial apoptosis in A549 cells

Cited by 65 publications

References 64 publications

Acrolein, an Environmental Toxin, Induces Cardiomyocyte Apoptosis via Elevated Intracellular Calcium and Free Radicals

Acrolein, an Environmental Toxin, Induces Cardiomyocyte Apoptosis via Elevated Intracellular Calcium and Free Radicals

Regulation of Endothelial Function by Mitochondrial Reactive Oxygen Species

Adverse Outcome Pathway on Protein Alkylation Leading to Liver Fibrosis

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