Residual foot manifestations in a case of idiopathic childhood spastic hemiplegia.
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Biomedical subjects
Publications and source records attributed to E J Harris.
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The rate and extent of Cu2+ uptake by rat liver mitochondria was measured under various conditions. 1. The uptake is both greater and faster without an energy supply. 2. The uptake, when occuring in ionic media, has a biphasic character, that is it always slows down after an initial burst, and then re-accelerates. 3. Uptake of Cu2+ in the presence of energy initiates K+ uptake from K+-containing media with accompanying swelling and respiratory stimulation. Depending on the amounts of Cu2+ added and the K+ concentration, an inhibition of respiration later ensues. 4. Chelation of the Cu2+ by substrates (notably glutamate) decreases the effects. 5. Prior exposure to Cu2+ decreases or prevents energy-dependent Ca2+ uptake.
1. Very low concentrations of Pb2+ decrease the capacity of rat heart mitochondria, oxidizing pyruvate plus malate, to remove Ca2+ from the medium. 2. The primary effect is on the rate of Ca2+ sequestration; this is reflected in the overall extent of Ca2+ removal. 3. Pb2+ has at least two separate actions. Below about 0.5 nmol/mg of protein, it acts solely by competing with Ca2+ (Ki = 0.4 muM); above this concentration it also inhibits the production or use of respiratory energy, so that at 1 nmol of Pb2+/mg of protein, Ca2+ removal is almost completely abolished. 4. Pb2+ inhibits coupled and uncoupled respiratory O2 use by mitochondria oxidizing pyruvate plus malate, but at higher concentrations than those that affect Ca2+ removal; similar concentrations of Pb2+ inhibit pyruvate uptake, but not malate uptake, by the mitochondria. 5. Mg2+ only decreases Ca2+ removal by competition, and is a far-less effective competitor than Pb2+ (Ki = 0.15 mM). It is possible that the primary cause of the second effect of Pb2+ is displacement of membrane Mg2+. 6. The consequences of these results are discussed in terms of the possible involvement of heart mitochondria in excitation-contraction coupling, and the Pb2+ levels that might occur in heart tissue in vivo.
1. The metabolic response of livers to perfusion with ethanol with and without avenaciolide, has been followed by measuring the perfusate levels of glucose, lactate, pyruvate, beta-hydroxybutyrate, ethanol, amino acids, urea and lipid. 2. Analysis of the perfused livers showed changes in the activities of some of the key enzymes of glycolysis, gluconeogenesis and lipogenesis. Ethanol perfusion decreased the levels of phosphofructokinase, glucokinase and cytosolic isocitrate dehydrogenase, while avenaciolide lowered pyruvate carboxylase and phosphoenolpyruvate carboxykinase as well as glucokinase. Isocitrate dehydrogenase and phosphofructokinase were unchanged, but the ionophore increased the level of fructose-1,6-diphosphatase. Ethanol plus avenaciolide showed the same pattern as ethanol alone, together with the decrease in phosphoenolpyruvate carboxykinase found with avenaciolide. 3. Neither ethanol nor avenaciolide had any effect on kexokinase, pyruvate kinase or acetyl-CoA carboxylase. There were small changes in glucose-6-phosphatase and malic enzyme, and a tendency for citrate lyase levels to decline in avenaciolide perfusions.
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The damage which may be caused to heart mitochondria by the rapid uptake of calcium when oxygen is restored after a period of anoxia is monitored by the deterioration in phosphorylation performance. Methods of protecting mitochondria from this damage by preventing calcium uptake and by chelating cytoplasmic calcium are considered.
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The effect of alkali cations on the rate of citrate uptake of rat-liver mitochondria and on the citrate adsorption has been studied. In each set of results, as in a series of comparative respiratory studies, Cs+ is more stimulatory than the other ions. This effect might be the consequence of different electrostatic interactions between the membrane and ions in solution in the case of different cations.
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