NDLI: Cardiac toxic effects of trans-2-hexenal are mediated by induction of cardiomyocyte apoptotic pathways

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Acknowledgements

Cardiovascular Toxicology : Volume 3, Issue 3, September 2003

Cardiovascular Toxicology : Volume 3, Issue 2, June 2003

Cardiovascular Toxicology : Volume 3, Issue 1, March 2003

Cardiovascular Toxicology : Volume 2

Cardiovascular Toxicology : Volume 1

Cardiac toxic effects of trans-2-hexenal are mediated by induction of cardiomyocyte apoptotic pathways

Content Provider	Springer Nature Link
Author	Ping, Peipei Baines, Christopher P. Gu, Yan Prabhu, Sumanth D. Zhang, Jun Tsai, Linda L. Cardwell, Ernest Zong, bel C. Vondriska, Thomas M. Korge, Paavo Bhatnagar, Aruni Wang, Guang Wu
Copyright Year	2003
Abstract	Aldehydes are ubiquitous pollutants with well-indicated but ill-defined cardiovascular toxicity. To investigate the direct toxic effects of environmental aldehyde exposure on the myocardium, 8-wk-old male ICR (Institute of Cancer Research) strain mice were gavage fed trans-2-hexenal (0.1, 1, 10, or 50 mg/kg/wk) or corn oil (vehicle) for 4 wk, during which cardiac function, myocardial morphology, cardiomyocyte apoptosis, and the cytochrome c-mediated caspase activation apoptotic pathway were determined. Quantification by enzyme-linke immunosorbent assay (ELISA) revealed that aldehyde-protein adducts increase in mouse hearts following hexenal treatment, whereas echocardiographic analysis displayed a significant impairment of basal left-ventricular contractile function. Both histological analysis and TUNEL (terminal deoxynucleotidyl transferase-mediated nick-end labeling) staining indicated condensed nuclei and a significant increase in cardiomyocyte apoptosis in these mice, but immunohistochemistry-based confocal microscope revealed no marked myofibril disarray. Release of cytochrome c from mitochondria into the cytosol, concomitant with activation of caspase-3 and-9, was also found in hexenal-treated groups. In addition, isolated cardiac mitochondria formed hexenal-protein adducts when treated with hexenal, providing indirect evidence that the cardiac mitochondrion is one of primary subcellular targets of aldehyde toxins. These findings suggest that trans-2-hexenal exposure results in direct cardiac toxicity through, at least in part, induction of mitochondrial cytochrome c release-mediated apoptosis in cardiomyocytes, indicating that the cardiac mitochondrion is one of principal subcellular targets of aldehyde toxins.
Starting Page	341
Ending Page	351
Page Count	11
File Format	PDF
ISSN	15307905
Journal	Cardiovascular Toxicology
Volume Number	3
Issue Number	4
e-ISSN	15590259
Language	English
Publisher	Humana Press
Publisher Date	2003-01-01
Publisher Place	Totowa
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Trans-2-hexenal aldehyde-protein adducts cytochrome c release caspase activation myocardial dysfunction Pharmacology/Toxicology Cardiology
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Toxicology Cardiology and Cardiovascular Medicine

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