Abstract
The pathophysiological events leading to anthracycline cardiomyopathy remain unclear in spite of intensive investigations. Major factors are thought to include stimulation of chemical processes giving rise to superoxide or hydroxyl radicals capable of causing oxidative damage to cellular membranes and thereby changes in subcellular organelles (1,2). It has also been suggested that anthracycline toxicity may arise from increased myocardial permeability resulting from induced deficiency of protective mechanisms. This could be reflected by an alterations in such enxymes as catalase, superoxide dismutase and glutathione peroxidase (3,4,5).
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© 1987 Martinus Nijhoff Publishing, Boston
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Tomlinson, C.W., McNeill, J.H., Godin, D.V. (1987). Pathophysiology of Anthracycline-Induced Cardiomyopathy. In: Dhalla, N.S., Singal, P.K., Beamish, R.E. (eds) Pathophysiology of Heart Disease. Developments in Cardiovascular Medicine, vol 65. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2051-7_21
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