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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #76052
Title: INHIBITION OF HYPOXIA-REOXYGENATION INJURY IN THE HEART OF CATALASE OVEREXPRESSING TRANSGENIC MICE

Author
item CHEN, Y - U LOUISVILLE
item Saari, Jack
item KANG, Y - U LOUISVILLE

Submitted to: Toxicologist
Publication Type: Abstract Only
Publication Acceptance Date: 3/15/1997
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Oxygen-derived free radicals play important roles in hypoxia-reoxygenation or ischemia-reperfusion injury in the heart. Recent studies of isolated heart muscle and whole heart have strongly suggested that H2O2 is the primary free radical species responsible for postischemic myocardial damage. However, contradictory reports have been published on the possible effect of catalase on cardiac hypoxia-reoxygenation lesions although catalase is a major enzyme involved in detoxification of H2O2. The present study was undertaken to determine whether catalase overexpression in the heart of transgenic mice can provide protection against hypoxia-reoxygenation injury. Transgenic mice with elevated cardiac catalase (60-fold higher than normal) were selected to study the effects of catalase elevation on H2O2 and hypoxia-reoxygenation induced cardiotoxicity as determined by measuring functional and morphological changes in isolated atria. Catalase overexpression inhibited the reduction in contractile force and contraction rate caused by H2O2 and hypoxia-reoxygenation and eliminated reoxygentaiton-induced arrhythmia. The atria that overexpressed catalase were also highly resistant to hypoxia-reoxygenation-induced morphological alterations as examined by electron microscopy. The results demonstrate that catalase inhibits hypoxia-reoxygenation injury, most likely by its function in detoxifying H2O2.