Summary
Compelling evidence has been accumulated which indicates that myocardial tissue damage occurring during reperfusion after an ischaemic period may partly be due to the formation of oxygen free radicals and subsequent peroxidative processes. It has been well established that the actual toxicity of free radicals is dependent on the presence of free iron in the heart tissue. Based upon the hypothesis of McCord et al., proposing xanthine oxidase mediated formation of superoxide (O2-.) during the conversion of ATP-breakdown product(s) (hypo)xanthine to urate, we studied whether xanthine oxidase was able to mobilize free iron from the intra-and extracellular iron-binding proteins, ferritin and transferrin. It appeared that there was an O2-.-dependent and O2 -.-independent mechanism by which xanthine oxidase could mobilize iron from ferritin while no iron mobilization from transferrin was detectable. The capacity of xanthine oxidase to mobilize iron from ferritin by an O2-.-independent mechanism implies that already during the anoxic/ischaemic period, iron may become available in the tissue which, upon the re-entrance of O2, catalyzes the formation of the very reactive OH• radicals. The interaction between endothelial cells and cardiocytes in free radical homeostasis is discussed with the emphasis on the tissue localization of xanthine oxidase. The latter is located in endothelial cells implying an interaction between xanthine oxidase-induced endothelial cells initiated lipid peroxidation and the actual overall myocardial tissue damage.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Biemond P, Swaak AJG, Beinsdorff CM, Koster JF (1986) Superoxide-dependent and -independent mechanism of iron mobilization from ferritin by xanthine oxidase. Biochem J 239: 169–173
Biemond P, Van Eijk HG, Swaak MG, Koster JF (1984) Iron mobilization from ferritin by superoxide derived from stimulated polymorphonuclear leukocytes. Possible mechanism in inflammation diseases. J Clin Invest 73: 1576–1579
Del Maestro RF, Thans HH, Björk J, Planter M, Arfors K-E (1980) Free radicals as mediators of tissue injury. Acta Physiol Scand Suppl 492: 43–57
Esterbauer H, Cheeseman KH, Diazini MU, Slater TF (1982) Separation and characterization of the aldehydic products of lipid peroxidation stimulated by ADF-Fe2+ in rat liver microsomes. Biochem J 208: 129–140
Evenson SA, Galdal KS, Nilson E (1983) LDL-induced cytotoxicity and its inhibition by anti-oxidant treatment in human endothelial cells and fibroblasts. Atherosclerosis 49: 23–29
Fielding JF (1981) The endothelium, triglyceride-rich lipoproteins and atherosclerosis. Diabetes 30, suppl 2: 19–23
Gerlach E, Nees S, Becker BF (1985) The vascular endothelium: a survey of some newly evoking biochemical and physiological features. Basic Res Cardiol 80: 459–474
Hall ET (1977) The oxygen effect. Harper and Row, New York, p 48
Hessler JR, Moret DW, Levis LI, Chisolm GM (1983) Lipoprotein oxidation and lipoprotein-induced cytotoxicity. Arteriosclerosis 3: 215–222
Jolly R, Kane WJ, Bailie MB, Anrans GD, Luchesi BR (1984) Canine myocardial reperfusion injury: Its reduction by the combined administration of superoxide dismutase and catalase. Circ Res 54: 277–285
Kaminsk ZW, Jezewska MM (1982) Involvement of a single thiol group in the conversion of the NAD+-dependent activity of rat liver xanthine oxidoreductase to the O2 --dependent activity. Biochem J 207: 341–346
Koster JF, Biemond P, Montfoort A and Stam H (1986) Involvement of free radicals in pathological conditions. Life Chemistry Reports 3: 323–351
KosterJF, Slee RG (1986) Ferritin, a physiological iron donor for microsomal lipid peroxidation. FEBS Lett 199: 85–88
Koster JF, Slee RG, Stam H (1985) Studies on cumene hydroperoxideinduced lipid peroxidation in the isolated rat heart. J Mol Cell Cardiol 17: 701–708
Martinez-Sales V, Fornas E, Comanas A (1983) Prostacyclin production and lipid peroxidation in aorta of rats fed with cholesterol autooxidation products. Artery 12: 213–219
McCord JM, Roy RS (1983) The pathophysiology of superoxide: Roles in inflammation and ischemia. Can J Physiol 60: 1346–1352
Shingu M, Yoshioka M, Nobunaga M, Yoshida K (1985) Human vascular smooth muscle cell and endothelial cells lack catalase activity and are susceptible to hydrogen peroxide. Inflammation 9: 309–320
Stam H, Koster JF (1985) Fatty acid peroxidation in ischemia. In: Schrör K (ed) Regional ischemia and arcuculatory shock. Prostaglandins and other eicosanoids in the cardiovascular system. Karger, Basel, pp 131–148
Steinberger UP, Parthasarathy S, Xenke DS, Witztum JL, Steinberg D (1984) Modification of low-density lipoprotein by endothelial cells involves lipid peroxidation and degradation of low-density lipoprotein phospholipids. Proc Natl Acad Sci USA 81: 3883–3887
Turrens JF, Boveris A (1980) Generation of superoxide anion by the NADH dehydrogenase of bovin heart mitochondria. Biochem J 191: 421–427
Yaki K (1985) Increased serum lipid peroxides initiate atherosclerosis. Bio Essays 1: 58–60
Yaki K, Ohkawa H, Ohishi N, Yamashita M, Nakashima T (1981) Lesion of aortic intima caused by intravenous administration of linoleic acid hydroperoxide. J Appl Biochem 3: 58–61
Author information
Authors and Affiliations
Editor information
Rights and permissions
Copyright information
© 1987 Springer-Verlag Berlin Heidelberg
About this paper
Cite this paper
Koster, J.F., Biemond, P., Stam, H. (1987). Lipid peroxidation and myocardial ischaemic damage: cause or consequence?. In: Stam, H., van der Vusse, G.J. (eds) Lipid metabolism in the normoxic and ischaemic heart. Steinkopff, Heidelberg. https://doi.org/10.1007/978-3-662-08390-1_29
Download citation
DOI: https://doi.org/10.1007/978-3-662-08390-1_29
Publisher Name: Steinkopff, Heidelberg
Print ISBN: 978-3-662-08392-5
Online ISBN: 978-3-662-08390-1
eBook Packages: Springer Book Archive