Mitochondrial calcium efflux and porcine stress-susceptibility

Summary Mitochondrial Ca²⁺ efflux rates ofM. longissimus dorsi correlate very closely with parameters associated with porcine stress-susceptibility. Experimental data support the measurement of mitochondrial Ca²⁺ efflux to be a very sensitive and reliable method for differentiating porcine stress-susceptibility.Acknowledgments. The autors are grateful to Dr Webb (Edinburgh) and to Dr Monin (Theix) for supplying halothanescreened pigs, to Mr C.C. Ketteridge for technical assistance and to Mr N. F. Doun for drip measurements.     

Na-Activated calcium efflux in rabbit vagus nerve fibres

Zusammenfassung Die vorliegenden Resultate deuten darauf hin, dass aus marklosen Nervenfasern ein passiver Austausch von intrazellulärem Kalzium gegen extrazelluläres Natrium erfolgt, und zwar mittels eines überträgersystems, das von dem für die Erregung notwendigen Na-übertragenden System verschieden ist.     

Stimulation by caffeine of the calcium efflux in barnacle muscle fibers

Zusammenfassung Die Befunde ergeben, dass einzelne Muskelfasern der Entenmuschel durch Mikroinjektion mit⁴⁵Ca aufgeladen werden können. Eine Umspülung der Muskelfasern mit einer coffeinhaltigen Lösung bewirkt ein stärkeres Ausströmen des Calciums als eine Mikroinjektion des Coffeins in die Fasern direkt.     

Sensitivity of sodium efflux in barnacle muscle fibers to the microinjection of calcium chloride

Zusammenfassung Nachweis, dass der Auswärtsstrom von Natrium aus Muskelfasern der ArthropodenBalanus nubilus undBalanus aquila in künstlichem, kaliumfreiem Meerwasser durch Mikroinjektion von Kalziumchlorid aktiviert wird.

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Postdoctoral Fellow of the Wisconsin Heart Association.     

Hypoxia increases potassium efflux from mammalian myocardium.

Hypoxia with or without simultaneous depletion of extracellular glucose increases 42K-efflux in cat and guinea-pig papillary muscles and bovine Purkinje fibres. The change observed in K efflux may be the result of an increase in K conductance at rest.     

Mitochondrial distribution and inheritance

Mechanisms mediating the inheritance of mitochondria are poorly understood, but recent studies with the yeastsSaccharomyces cerevisiae andSchizosaccharomyces pombe have begun to identify components that facilitate this essential process. These components have been identified through the analysis of conditional yeast mutants that display aberrant mitochondrial distribution at restrictive conditions. The analysis of these mutants has uncovered several novel proteins that are localized either to cytoskeletal structures or to the mitochondria themselves. Many mitochondrial inheritance mutants also show altered mitochondrial morphology and defects in maintenance of the mitochondrial genome. Although some inheritance components and mechanisms appear to function specifically in certain types of cells, other conserved proteins are likely to mediate mitochondrial behavior in all eukaryotic cells.     

Mitochondrial defects and hearing loss

The techniques of human molecular genetics have been rapidly applied to the study of hearing loss. These studies have implicated more than 60 loci as causes of nonsyndromic hearing loss. Mutations at more than a dozen nuclear genes have been demonstrated to cause hearing loss, and these have been covered in recent reviews. However, a perhaps unexpected feature of the molecular characterization of human hearing loss has been the occurrence of mutations in the mitochondrial DNA (mtDNA). The importance of mitochondrial function in hearing is emphasized by the recent discovery of mutations in a nuclear-encoded mitochondrial protein which results in hearing loss. This article reviews the current status of our knowledge of mtDNA mutations that have been shown to cause hearing loss, and the suggestion of potential molecular, cellular and tissue-specific pathophysiological mechanisms by which dysfunction of mitochondria may lead to a loss of hearing.     

Rapid isolation of mitochondrial DNA. Mitochondrial DNA from Drosophila serrata.

A simple and rapid method for isolation of high quality mitochondrial DNA (mtDNA) is presented in this report. Using this method, isolation and restriction site maps for 10 enzymes of the mtDNA of Drosophila serrata were established.     

Rapid isolation of mitochondrial DNA. Mitochondrial DNA fromDrosophila serrata

A simple and rapid method for isolation of high quality mitochondrial DNA (mtDNA) is presented in this report. Using this method, isolation and restriction site maps for 10 enzymes of the mtDNA ofDrosophila serrata were established.     

Protective effect of calcium against the verapamil-induced inhibition of ionophore-mediated calcium translocation.

The inhibitory effect of verapamil on A23187-mediated calcium translocation is antagonized in a competitive manner by increasing concentrations of calcium.     

A study of macromolecular diffusion through native porcine mucus.

A diffusion chamber technique based on time-lag analysis for the estimation of effective diffusion coefficients of radiolabelled macromolecules of varying molecular weights through native mucus gel is reported. For all solutes studied, a reduction in effective diffusion coefficients was observed with a retardation of solute flux in both aqueous and mucus layers. Over the molecular weight range of solutes investigated (126-186,000 Daltons), a consistent effect of molecular weight was evident with regard to the retarding effect of mucus. No apparent or absolute molecular weight cut-off for macromolecular transfer was exhibited. However, at high molecular weights (greater than 30,000 Daltons) the retardation was greatly enhanced. The results confirm that mucus can be regarded as a gel with finite pores, but that it does not constitute an absolute barrier to even high molecular weight solutes.     

Mitochondrial dynamics in cell death and neurodegeneration

Mitochondria are highly dynamic organelles that continuously undergo two opposite processes, fission and fusion. Mitochondrial dynamics influence not only mitochondrial morphology, but also mitochondrial biogenesis, mitochondrial distribution within the cell, cell bioenergetics, and cell injury or death. Drp1 mediates mitochondrial fission, whereas Mfn1/2 and Opa1 control mitochondrial fusion. Neurons require large amounts of energy to carry out their highly specialized functions. Thus, mitochondrial dysfunction is a prominent feature in a variety of neurodegenerative diseases. Mutations of Mfn2 and Opa1 lead to neuropathies such as Charcot-Marie-Tooth disease type 2A and autosomal dominant optic atrophy. Moreover, both Aβ peptide and mutant huntingtin protein induce mitochondrial fragmentation and neuronal cell death. In addition, mutants of Parkinson’s disease-related genes also show abnormal mitochondrial morphology. This review highlights our current understanding of abnormal mitochondrial dynamics relevant to neuronal synaptic loss and cell death in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and Huntington’s disease.     

Inhibition by verapamil of ionophore-mediated calcium translocation.

Verapamil and other organic calcium-antagonists inhibit the A23187-mediated translocation of calcium from an aqueous into an organic phase.     

Mitochondrial control of caspase-dependent and -independent cell death

Mitochondria control whether a cell lives or dies. The role mitochondria play in deciding the fate of a cell was first identified in the mid-1990s, because mitochondria-enriched fractions were found to be necessary for activation of death proteases, the caspases, in a cell-free model of apoptotic cell death. Mitochondrial involvement in apoptosis was subsequently shown to be regulated by Bcl-2, a protein that was known to contribute to cancer in specific circumstances. The important role of mitochondria in promoting caspase activation has therefore been a major focus of apoptosis research; however, it is also clear that mitochondria contribute to cell death by caspase-independent mechanisms. In this review, we will highlight recent findings and discuss the mechanism underlying the mitochondrial control of apoptosis and caspase-independent cell death.     

pH and calcium concentration changes in a molluscan egg during development.

During development, the egg albumen of calcified land snail eggs becomes more and more acid, correlated directly with a constant rise in the calcium concentration of this albumen. It is suggested that the developing embryo releases some acid metabolite and the subsequent change in albumen pH aids in embryonic absorption of the CaCO3 (calcite) egg shell, used for making the embryonic body shell or skeleton (CaCO3 in the form of aragonite).     

The effect of pyrophosphate and diphosphonates on calcium transport in red cells.

The effect of 0.5 mM pyrophosphate (PPi), disodium ethane-4-hydroxy-1,1-diphosphonate (EHDP) and disodium dichloromethane diphosphonate (Cl2MDP) on the ATP-dependent Ca2+ extrusion from the human red cell ghosts was studied. PPi and Cl2MDP had no effect, when introduced into the cells or added outside to the medium. EHDP slightly increased the calcium concentration in the released cells and slightly decreased the rate constant of the calcium transport, having opposite effects when it was inside or outside the cells. PPi and the 2 diphosphonates were not found to move easily across the red cell membrane.