Effect of hypoxia on degradation of mitochondrial components in rat cardiac muscle

Aschenbrenner, V.; Zak, Roksana; Af, Cutilletta; Rabinowitz, Murray

doi:10.1152/ajplegacy.1971.221.5.1418

Cited by 38 publications

(19 citation statements)

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“…Caloric restriction induces mitochondrial biogenesis and bioenergetic efficiency [3]. Hypoxia accelerates mitochondrial protein turnover, reflecting increased destruction and biogenesis [4]. Like hypoxia, ischemic preconditioning is expected to accelerate mitochondrial turnover, as it was shown that many mitochondrial inner membrane proteins and heme groups turn over with the same kinetics, reflecting destruction of the entire organelle [5], which has subsequently been shown to be mediated by autophagy.…”

Section: Overviewmentioning

confidence: 99%

Mitochondrial turnover in the heart

Gottlieb

Gustafsson

2011

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

115

100

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Mitochondrial quality control is increasingly recognized as an essential element in maintaining optimally functioning tissues. Mitochondrial quality control depends upon a balance between biogenesis and autophagic destruction. Mitochondrial dynamics (fusion and fission) allows for the redistribution of mitochondrial components. We speculate that this permits sorting of highly functional components into one end of a mitochondrion, while damaged components are segregated at the other end, to be jettisoned by asymmetric fission followed by selective mitophagy. Ischemic preconditioning requires autophagy/mitophagy, resulting in selective elimination of damaged mitochondria, leaving behind a population of robust mitochondria with a higher threshold for opening of the mitochondrial permeability transition pore. In this review we will consider the factors that regulate mitochondrial biogenesis and destruction, the machinery involved in both processes, and the biomedical consequences associated with altered mitochondrial turnover.

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Section: Overviewmentioning

confidence: 99%

Mitochondrial turnover in the heart

Gottlieb

Gustafsson

2011

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

115

100

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“…This relatively great synthetic capacity allows the heart to meet augmented mechanical demands, in response to which the myo cardial mass may reversibly increase up to 50% within 36 h. After a myo cardial infarction reparative processes are promptly and maximally stim ulated, and the surrounding muscle may hypertrophy as a result. Ischemia and hypoxia, insufficient to produce massive heart muscle necrosis, may themselves be potent stimuli for considerable protein synthesis [1],…”

Section: Amino Acid Transportmentioning

confidence: 99%

Insulin: Fundamental Mechanism of Action and the Heart

Kones¹,

Phillips²

1975

Cardiology

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Insulin accelerates the entry of glucose and amino acids into muscle cells by acting upon the ‘carrier-facilitated’ transport mechanism. For glucose this process is passive and leads to equilibration of intracellular and extracellular concentrations. In heart muscle, glucose transport is a rate-limiting step for glucose uptake. During hypoxia and ischemia the heart turns to anaerobic glycolysis for energy production and therefore, maximal glucose transport becomes important. Insulin is necessary to insure proper protein synthesis, probably at the level of membrane-bound polyribosomes. However, during myocardial hypoxia, insulin alone cannot restore the associated depression in protein synthesis. Although insulin hyperpolarizes the cell, a change in the ratio of intracellular to extracellular activities of potassium is not its primary mode of action. An insulin-induced configurational change in the plasma membrane could simultaneously account for the effects of insulin on sodium and potassium permeability and the action on facilitated transport. Intracellular levels of cyclic adenylate may be reduced by insulin in adipose tissue because of inhibition of adenyl cyclase or stimulation of phosphodiesterase. However, at this time there is little evidence that insulin alters cyclic AMP levels in the heart. Insulin secretion is depressed in patients with heart disease in proportion to the reduction of cardiac index sustained. Since the ischemic heart is dependent upon glucose as the major fuel, insulin lack may deprive the heart of adequate substrate.

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“…Thus, induction of adaptive heart growth by pressure overload produces differences in relative magnitude depending upon the existing status of myocardial growth at the time an adaptive stimulus is encountered. Rapidly enlarging hearts of weanling rats are more responsive in terms of adaptive growth than the less rapidly enlarging hearts of adult rats (17).…”

Section: Table VI Malate Dehydr~genase Enzyme Activity In Whole-hearmentioning

confidence: 86%

“…Tissue was homogenized in 250 Msucrose buffered with 10 mMTris, pH 7.4, using a Brinkmann Polytron. Mitochondria were isolated by differential centrifugation as outlined by Aschenbrenner et al ( 17). Isolated mitochondria were suspended in 100 Mphosphate buffer containing 5 mM reduced glutathione.…”

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confidence: 99%

Metabolic Enzyme Response in the Pressure-Overloaded Heart of Weanling and Adult Rats

Dowell

Haithcoat

Hasser

1983

Experimental Biology and Medicine

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Absfrad.Weanling and adult rats were subjected to left ventricular pressure overload induced by abdominal aortic constriction. At 5 days or 5 weeks postsurgery, the left ventricle (LV) was dissected, weighed, and metabolic marker enzyme activities (pmole/g/min) of tissue homogenates were measured. Enzymes representing glycolytic (phosphofructokinase (PFK)) and mitochondria1 (citrate synthase (CS) and malate dehydrogenase (MDH)) metabolisms were evaluated. Five days of pressure overload had detectable, but statistically nonsignificant effects on left ventricles of both weanling and adult rats. Sustained pressure overload ( 5 weeks) increased LV weight by 52 and 3990 in weanling and adult rats, respectively. PFK activity was 24 f 1 (mean 2 SE) in control weanlings and was unaltered in any of the other groups. LDH isoenzyme composition was estimated by substrate inhibition (ratio 0.33/10 mM pyruvate). With normal heart development, the LDH ratio increased from 1.89 * 0.06 to 2.03 k 0.08. Pressure overload had no influence on the adult LDH ratio. Developmental LDH responses were not observed in weanling LV after 5 weeks of aortic constriction ( 1.74 * 0.06). The product of CS activity and LV weight was used to estimate mitochondrial mass in the ventricle. Mitochondria accumulated at a rate of about 5% increase per day over the intervening 5-week period of normal heart growth. Pressure overload for 5 weeks in weanling rats elicited net accumulation of mitochondria at a rate of about 9% increase per day. Mitochondria1 accumulation in the adapting adult rat heart amounted to less than 1% increase per day. The results indicate that qualitative and quantitative differences exist between young and adult animals in their heart enzyme adaptive responses to pressure overloading. Divergent metabolic adaptations may contribute to heart functional differences in the enlarged heart of weanlings and adults.368

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Effect of hypoxia on degradation of mitochondrial components in rat cardiac muscle

Cited by 38 publications

References 0 publications

Mitochondrial turnover in the heart

Mitochondrial turnover in the heart

Insulin: Fundamental Mechanism of Action and the Heart

Metabolic Enzyme Response in the Pressure-Overloaded Heart of Weanling and Adult Rats

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