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標題: Effects of chloroacetaldehyde in 2-chloroethanol-induced cardiotoxicity
作者: Chen, Y.T.
Hsu, C.I.
Hung, D.Z.
Matsuura, I.
Liao, J.W.
Project: Food and Chemical Toxicology
期刊/報告no:: Food and Chemical Toxicology, Volume 49, Issue 5, Page(s) 1063-1067.
Cardiovascular effects have often been found in 2-chloroethanol (2-CE) intoxicated patients, but the 2-CE elicits cardiovascular toxicity mechanism is not clear. Recently, we have found that chloroacetaldehyde (CAA) accumulation in 2-CE-intoxicated rat's blood and play an important role in 2-CE intoxication. In this study, we used an isolated rat atrium model to examine the cardiotoxicity of 2-CE and CAA. Results indicated that 2-CE did not cause tension arrest in isolated rat right atria, but CAA did. 2-CE caused tension inhibition in the isolated rat left atria. In addition, CAA caused significant tension inhibition and contracture in the isolated rat left atria. Nifedipine, an L-type calcium channel blocker, decreased CAA-induced tension inhibition and contracture. Meanwhile, atrial nNOS and calmodulin (CaM) had significantly greater expression in the 2-CE group and the CM group than control group. Nifedipine could decrease CAA-induced nNOS and CaM expression. 2-CE-induced cardiovascular toxicity might be due to its metabolite CM. CAA-induced cardiovascular toxicity might be mediated by calcium channel and nifedipine protected against nNOS-triggered cardiovascular effects. (C) 2011 Elsevier Ltd. All rights reserved.
ISSN: 0278-6915
DOI: 10.1016/j.fct.2011.01.013
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