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Cardiac membrane vitamin E and malondialdehyde levels in heart muscle of normotensive and spontaneously‐hypertensive rats
Author(s) -
Janero David R.,
Burghardt Barbara
Publication year - 1989
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02535261
Subject(s) - malondialdehyde , vitamin e , thiobarbituric acid , medicine , endocrinology , cardiac muscle , clinical chemistry , lipidology , chemistry , vitamin , oxidative stress , biochemistry , antioxidant , lipid peroxidation
The vitamin E (α‐tocopherol) and free and bound malondialdehyde (MDA) in ventricular heart muscle and myocardial membrane from Wistar‐Kyoto (W/K) normotensive and spontaneously hypertensive (SH) rats have been measured directly by high performance liquid chromatography (HPLC). Thiobarbituric acid‐reactive substance (TBA‐RS) in the myocardium and heart‐muscle membrane of the two strains was also quantified by a colorimetric TBA test. It was found that SH‐rat myocardium and myocardial membrane contained more than 3‐fold less α‐tocopherol than did heart muscle and cardiac membrane of the normotensive rat. Coincident with this relative vitamin E deficiency were several‐fold greater amounts of MDA and TBA‐RS in SH‐rat myocardium and myocardial membrane. Most (87%) of the MDA in SH‐rat heart muscle, but only 40% in W/K‐rat heart muscle, was free (i.e., unbound). These results offer direct evidence that SH‐rat myocardium is vitamin E‐deficient and highly peroxidative, relative to cardiac muscle of the normotensive W/K parent strain. The lower vitamin E content of SH‐rat myocardium is particularly striking, because SH‐rat myocardial membrane was found to contain ∼35% more phospholipid than myocardial membrane in the W/K rat. Although the amounts of myocardial TBA‐RS are greater in the SH strain, they do not reflect the actual MDA profiles of the heart muscles or the heart membranes and cannot be used as a quantitative index of cardiac oxidative‐injury status due to non‐MDA TBA‐RS in both strains.