Calcium-induced damage of rat heart mitochondria.

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.

Growth and Sucrose Metabolism of Carrot Callus Strains with Normal and Low Acid Invertase Activity.

The properties of two strains of carrot (Daucus carota) callus are presented. One has a very low acid invertase activity which is accompanied by differences in morphology and metabolic rate, but not in growth rate. We conclude that one of the main functions of plant acid invertases is in controlling the levels of sugars which, by interaction with hormones, affect differentiation, both morphological and biochemical. The effect of tris on sucrose metabolizing enzymes, and the cause of the "sucrose effect" are considered.

Release of hydrolytic enzymes from the cell walls of intact and disrupted carrot callus tissue.

The effect of ionic strength and pH on the solubility of acid invertase (E.C. 3.2.1.26.) and α-glucosidase (E.C. 3.2.1.20.) from carrot Daucus carota L. tissue cultures is presented. The action of these two factors on disrupted tissue is contrasted with the effects of the same treatment on the solubility of these enzymes from intact tissue. The results are discussed in terms of a unified theory on the solubility behaviour of acid invertase and other hydrolytic enzymes in plant cells.

The effect of lead on the calcium-handling capacity of rat heart mitochondria.

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.