Fatty acid-membrane interactions in isolated cardiac mitochondria and erythrocytes

Piper, Hans Michael; Sezer, Orhan; Schwartz, Peter J.; Hütter, Joachim; Spieckermann, P. G.

doi:10.1016/0005-2736(83)90203-1

Cited by 43 publications

(20 citation statements)

References 75 publications

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“…The fatty acid binding protein from heart has been reported to bind both fatty acids equally well (9), but oleic acid and its CoA derivative are bound to biological membranes to a higher degree than palmitic acid and palmityl CoA (15,17,25,26). It might be this greater affinity of the oleyl moiety to lipid membranes together with a greater disturbing effect on the membrane structures that renders it more deleterious to mitochondria in vitro (21,22) and to the anoxic perfused myocardium. It follows from this and previous studies (21,22) that for the pathogenesis of myocardial ischemic injury not only supply or lack of exogenous fatty acids is of importance, but the nature of supplied fatty acids as well.…”

Section: Discussionmentioning

confidence: 96%

“…It might be this greater affinity of the oleyl moiety to lipid membranes together with a greater disturbing effect on the membrane structures that renders it more deleterious to mitochondria in vitro (21,22) and to the anoxic perfused myocardium. It follows from this and previous studies (21,22) that for the pathogenesis of myocardial ischemic injury not only supply or lack of exogenous fatty acids is of importance, but the nature of supplied fatty acids as well.…”

Section: Discussionmentioning

confidence: 96%

“…These interactions depend on the fatty acyl moiety (17,31). In general, the oleyl moiety being more effective than the palmityl moiety (15,21,22,31). Therefore, at equal intracellular concentrations the oleyl moiety can be expected to exert more harmful effects than the palmityl residue.…”

Section: Discussionmentioning

confidence: 98%

“…In previous studies in which isolated mitochondria were exposed to various fatty acids and acyl carnitines in vitro (21,22), marked differences between the damaging effects of various physiological fatty acid species were observed. The oleic acid residue was consistently the most harmful of the physiological long-chain fatty acyl chains.…”

Section: Introductionmentioning

confidence: 92%

“…Thereafter perfusion was continued for 60 min with an 100 % N2-equilibrated perfusate of the same composition at a constant flow rate of 0.3 ml/g fresh weight/min (oxygen tension below 1 mmHg, representing the detection threshold of the Clark-type electrode system from Yellow Springs Instruments, Yellow Springs, OH, U.S.A.). Additionally, the chamber atmosphere was changed to humidified N2 at 37 ~ The anoxic perfusate contained various concentrations of palmitic or oleic acid (0, 0.08, 0.2, 0.4 mM), complexed in 5:1 molar relationship to bovine serum albumin (22). Fatty acids (sodium salts) and bovine serum albumin (essentially fatty acid-free) were obtained from Sigma (Taufkirchen, F.R.G.…”

Section: Heart Perfusionmentioning

confidence: 99%

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The role of fatty acids in ischemic tissue injury: difference between oleic and palmitic acid

Piper

Das

1986

Basic Res Cardiol

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Guinea pig hearts were subjected to low-flow perfusion (0.3 ml/g fresh weight/min) with an oxygen depleted perfusate. Fatty acids (palmitic or oleic acid), added to the perfusate, accelerated in a dose-dependent manner the anoxic decay of creatine phosphate and ATP, impaired lactate production and augmented enzyme release (lactate dehydrogenase, malate dehydrogenase). Palmitic and oleic acid, however, differed distinctly in their deleterious effect, this being greater for oleic acid. After 60 min anoxic low-flow perfusion with 11 mM glucose and 0.2 mM of either fatty acid, complexed in 5:1 molar relationship to albumin, the creatine phosphate content with palmitate is 39% greater than with oleate, the ATP content 23%, lactate production 15% greater, and release of malate dehydrogenase 24% lower, but the elevated contents of long-chain acyl CoA and acyl carnitine are not significantly different for the two fatty acids. These results accord with earlier experiences on subcellular systems showing that the physicochemical effects of the oleyl residue are more harmful than those of the palmityl residue.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 92%

Section: Heart Perfusionmentioning

confidence: 99%

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The role of fatty acids in ischemic tissue injury: difference between oleic and palmitic acid

Piper

Das

1986

Basic Res Cardiol

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Amphiphile‐induced heart muscle‐cell (Myocyte) injury: Effects of intracellular fatty acid overload

Janero

Burghardt

Feldman

1988

Journal Cellular Physiology

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Lipid amphiphile toxicity may be an important contributor to myocardial injury, especially during ischemia/reperfusion. In order to investigate directly the potential biochemical and metabolic effects of amphiphile overload on the functioning heart muscle cell (myocyte), a novel model of nonesterified fatty acid (NEFA)-induced myocyte damage has been defined. The model uses intact, beating neonatal rat myocytes in primary monolayer culture as a study object and 5-(tetradecyloxy)-2-furoic acid (TOFA) as a nonmetabolizable fatty acid. Myocytes incubated with TOFA accumulated it as NEFA, and the consequent NEFA amphiphile overload elicited a variety of cellular defects (including decreased beating rate, depletion of high-energy stores and glycogen pools, and breakdown of myocyte membrane phospholipid) and culminated in cell death. The amphiphile-induced cellular pathology could be reversed by removing TOFA from the culture medium, which resulted in intracellular TOFA "wash-out." Although the development and severity of amphiphile-induced myocyte injury could be correlated with both the intracellular TOFA/NEFA content (i.e., the level of TOFA to which the cells were exposed) and the duration of this exposure, removal of amphiphile overload did not inevitably lead to myocyte recovery. TOFA had adverse effects on myocyte mitochondrial function in situ (decoupling of oxidative phosphorylation, impairing respiratory control) and on myocyte oxidative catabolism (transiently increasing fatty acid beta oxidation, citric acid cycle flux, and glucose oxidation). The amphiphile-induced bioenergetic abnormalities appeared to constitute a state of "metabolic anoxia" underlying the progression of myocyte injury to cell death. This anoxic state could be ameliorated to some extent, but not prevented, by carbohydrate catabolism.

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Intracellular transport of lipids

Glatz¹,

Vusse²

1989

Lipid Metabolism in Normoxic and Ischemic Heart

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Fatty acid-membrane interactions in isolated cardiac mitochondria and erythrocytes

Cited by 43 publications

References 75 publications

The role of fatty acids in ischemic tissue injury: difference between oleic and palmitic acid

The role of fatty acids in ischemic tissue injury: difference between oleic and palmitic acid

Amphiphile‐induced heart muscle‐cell (Myocyte) injury: Effects of intracellular fatty acid overload

Intracellular transport of lipids

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