Results 251 to 260 of about 645,590 (301)
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Effects of Cobalt on Mitochondrial Respiration
Nature, 1963Dingle, Heath, Webb, and Daniel have suggested that the toxicity of cobalt (II) is due to inhibition of keto-acid oxidation1. This hypothesis was supported by the finding that cobalt (II) inhibited oxidation of α-ketoglutarate and pyruvate by rat liver mitochondria during a prolonged incubation without the addition of phosphate acceptor1.
E H, STRICKLAND, C R, GOUCHER
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Regulation of Mitochondrial Respiration in Liver
1986In studies on the control of mitochondrial respiration carried out in the past 10 years, particular attention has been focussed on cytochrome c oxidase and the adenine nucleotide translocator as rate-controlling steps. On the basis of the observation that the first two phosphorylation sites of the respiratory chain are in near equilibrium with the ...
Verhoeven, A. J. +5 more
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Ochratoxin A: Inhibition of Mitochondrial Respiration
Science, 1970Ochratoxin A is a fungal metabolite which induces pathological changes in animals. The toxin was isolated from cultures of Aspergillus ochraceus and purified by thin-layer chromatography. Ochratoxin A and one of its hydrolysis products, dihydroisocoumarin, severely inhibited coupled respiration when applied at low ...
J H, Moore, B, Truelove
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Mitochondrial regulation of tissue respiration
American Journal of Physiology-Legacy Content, 1959Mitochondrial and nuclear counts and homogenate and washed mitochondrial qO2 determinations were made on kidney cortex, liver and brain of albino rats. Homogenate qO2 was inversely related to mitochondrial count in the three tissues, but directly related to cellularity and to O2 uptake per mitochondrion.
A T, MILLER +3 more
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Lactate as a fuel for mitochondrial respiration
Acta Physiologica Scandinavica, 2000Lactate production in skeletal muscle has now been studied for nearly two centuries and still its production and functional role at rest and during muscle contraction is a subject of debate. Historically, skeletal muscle was seen mainly as the site of lactate production during contraction and lactate production associated with a lack of muscle ...
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Effect of Ryanodine on Mitochondrial Respiration
Pharmacology, 2008Ryanodine is a pharmacological agent that stimulates calcium leakage into the cytoplasm resulting in an increase in tension. In skeletal muscle, ryanodine acts primarily on the sarcoplasmic reticulum whereas in smooth muscle, the sites of action are less clear.
R M, Levin +4 more
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The effect of acetaldehyde on mitochondrial respiration
Experimental Cell Research, 1963Abstract The inhibiting effect of acetaldehyde on the pyruvate oxidation in mitochondria from various tissues has been investigated. The following sequence was found as to the degree of aldehyde inhibition: liver Liver and kidney mitochondria oxidize acetaldehyde rapidly compared with muscle and brain mitochondria.
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Regulation of mitochondrial respiration in senescence
Journal of Cellular Physiology, 1972AbstractThe ADP‐stimulated (State 3) respiration of myocardial mitochondria with glutamate‐malate, glutamate‐pyruvate, palmitylcarnitine and β‐hydroxybutyrate as substrates declined in rats after the age of 20 months. There was no significant decline in pyruvate‐malate, α‐oxoglutarate, palmityl‐CoA, succinate and ascorbate cytochrome c oxidation ...
J C, Chen, J B, Warshaw, D R, Sanadi
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Control of mitochondrial respiration in muscle
Molecular and Cellular Biochemistry, 1988Control of mitochondrial respiration depends on ADP availability to the F1-ATPase. An electrochemical gradient of ADP and ATP across the mitochondrial inner membrane is maintained by the adenine nucleotide translocase which provides ADP to the matrix for ATP synthesis and ATP for energy-dependent processes in the cytosol.
J B, McMillin, D F, Pauly
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Uncoupling Mitochondrial Respiration for Diabesity
Rejuvenation Research, 2016Until recently, the mechanism of adaptive thermogenesis was ascribed to the expression of uncoupling protein 1 (UCP1) in brown and beige adipocytes. UCP1 is known to catalyze a proton leak of the inner mitochondrial membrane, resulting in uncoupled oxidative metabolism with no production of adenosine triphosphate and increased energy expenditure.
James W, Larrick +2 more
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