			Home About us Contact

Electrochemical Gradient (electrochemical + gradient)

Distribution by Scientific Domains

Life Sciences	66%

Selected Abstracts

PfCRT and the trans -vacuolar proton electrochemical gradient: regulating the access of chloroquine to ferriprotoporphyrin IX

MOLECULAR MICROBIOLOGY, Issue 1 2006
Patrick G. Bray
Summary It is accepted that resistance of Plasmodium falciparum to chloroquine (CQ) is caused primarily by mutations in the pfcrt gene. However, a consensus has not yet been reached on the mechanism by which resistance is achieved. CQ-resistant (CQR) parasite lines accumulate less CQ than do CQ-sensitive (CQS) parasites. The CQR phenotype is complex with a component of reduced energy-dependent CQ uptake and an additional component that resembles energy-dependent CQ efflux. Here we show that the required energy input is in the form of the proton electrochemical gradient across the digestive vacuole (DV) membrane. Collapsing the DV proton gradient (or starving the parasites of glucose) results in similar levels of CQ accumulation in CQS and CQR lines. Under these conditions the accumulation of CQ is stimulated in CQR parasite lines but is reduced in CQS lines. Energy deprivation has no effect on the rate of CQ efflux from CQR lines implying that mutant PfCRT does not function as an efflux pump or active carrier. Using pfcrt -modified parasite lines we show that the entire CQ susceptibility phenotype is switched by the single K76T amino acid change in PfCRT. The efflux of CQ in CQR lines is not directly coupled to the energy supply, consistent with a model in which mutant PfCRT functions as a gated channel or pore, allowing charged CQ species to leak out of the DV. [source]

Cystic fibrosis transmembrane conductance regulator in human muscle: Dysfunction causes abnormal metabolic recovery in exercise

ANNALS OF NEUROLOGY, Issue 6 2010
Anne-Marie Lamhonwah PhD
Objective Individuals with cystic fibrosis (CF) have exercise intolerance and skeletal muscle weakness not solely attributable to physical inactivity or pulmonary function abnormalities. CF transmembrane conductance regulator (CFTR) has been demonstrated in human bronchial smooth and cardiac muscle. Using 31P-magnetic resonance spectroscopy of skeletal muscle, we showed CF patients to have lower resting muscle adenosine triphosphate and delayed phosphocreatine recovery times after high-intensity exercise, suggesting abnormal muscle aerobic metabolism; and higher end-exercise pH values, suggesting altered bicarbonate transport. Our objective was to study CFTR expression in human skeletal muscle. Methods and Results We studied CFTR expression in human skeletal muscle by Western blot with anti-CFTR antibody (Ab) L12B4 and demonstrated a single band with expected molecular weight of 168kDa. We isolated the cDNA by reverse transcription polymerase chain reaction and directly sequenced a 975bp segment (c. 3,600,4,575) that was identical to the human CFTR sequence. We showed punctate staining of CFTR in sarcoplasm and sarcolemma by immunofluorescence microscopy with L12B4 Ab and secondary Alexa 488-labeled Ab. We confirmed CFTR expression in the sarcotubular network and sarcolemma by electron microscopy, using immunogold-labeled anti-CFTR Ab. We observed activation of CFTR Cl, channels with iodide efflux, on addition of forskolin, 3-isobutyl-1-methyl-xanthine, and 8-chlorphenylthio,cyclic adenosine monophosphate, in wild-type C57BL/6J isolated muscle fibers in contrast to no efflux from mutant F508del-CFTR muscle. Interpretation We speculate that a defect in sarcoplasmic reticulum CFTR Cl, channels could alter the electrochemical gradient, causing dysregulation of Ca2+ homeostasis, for example, ryanodine receptor or sarco(endo)plasmic reticulum Ca2+ adenosine triphosphatases essential to excitation-contraction coupling leading to exercise intolerance and muscle weakness in CF. ANN NEUROL 2010 [source]

Chloride ATPase pumps in nature: do they exist?

BIOLOGICAL REVIEWS, Issue 2 2003
GEORGE A. GERENCSER
ABSTRACT Five widely documented mechanisms for chloride transport across biological membranes are known: anioncoupled antiport, Na+ and H+ -coupled symport, Cl, channels and an electrochemical coupling process. These transport processes for chloride are either secondarily active or are driven by the electrochemical gradient for chloride. Until recently, the evidence in favour of a primary active transport mechanism for chloride has been inconclusive despite numerous reports of cellular Cl, -stimulated ATPases coexisting, in the same tissue, with uphill ATP-dependent chloride transport. Cl, -stimulated ATPase activity is a ubiquitous property of practically all cells with the major location being of mitochondrial origin. It also appears that plasma membranes are sites of Cl, -stimulated ATPase pump activity. Recent studies of Cl, -stimulated ATPase activity and ATP-dependent chloride transport in the same plasma membrane system, including liposomes, strongly suggest a mediation by the ATPase in the net movement of chloride up its electrochemical gradient across the plasma membrane structure. Contemporary evidence points to the existence of Cl, -ATPase pumps; however, these primary active transporters exist as either P-, F- or V-type ATPase pumps depending upon the tissue under study. [source]

Active Control of Epithelial Cell-Density Gradients Grown Along the Channel of an Organic Electrochemical Transistor

ADVANCED MATERIALS, Issue 43 2009
Maria H. Bolin
Complex patterning of the extracellular matrix, cells, and tissues under in situ electronic control is the aim of the technique presented here. The distribution of epithelial cells along the channel of an organic electrochemical transistor is shown to be actively controlled by the gate and drain voltages, as electrochemical gradients are formed along the transistor channel when the device is biased.. [source]

Physiological Ecology of Aquatic Overwintering in Ranid Frogs

BIOLOGICAL REVIEWS, Issue 2 2008
Glenn J. Tattersall
Abstract In cold-temperate climates, overwintering aquatic ranid frogs must survive prolonged periods of low temperature, often accompanied by low levels of dissolved oxygen. They must do so with the energy stores acquired prior to the onset of winter. Overwintering mortality is a significant factor in their life history, occasionally reaching 100% due to freezing and/or anoxia. Many species of northern ranid frogs overwinter in the tadpole stage, which increases survival during hypoxic episodes relative to adults, as well as allowing for larger sizes at metamorphosis. At temperatures below 5 °C, submerged ranid frogs are capable of acquiring adequate oxygen via cutaneous gas exchange over a wide range of ambient oxygen partial pressures (PO2), and possess numerous physiological and behavioural mechanisms that allow them to maintain normal rates of oxygen uptake across the skin at a relatively low PO2. At levels of oxygen near and below the critical PO2 that allows for aerobic metabolism, frogs must adopt biochemical mechanisms that act to minimise oxygen utilisation and assist in maintaining an aerobic state to survive overwintering. These mechanisms include alterations in mitochondrial metabolism and affinity, changes in membrane permeability, alterations in water balance, and reduction in cellular electrochemical gradients, all of which lead to an overall reduction in whole-animal metabolism. Winter energetic requirements are fueled by the energy stores in liver, muscle, and fat depots, which are likely to be sufficient when the water is cold and well oxygenated. However, under hypoxic conditions fat stores cannot be utilised efficiently and glycogen stores are used up rapidly due to recruitment of anaerobiosis. Since ranid frogs have minimal tolerance to anoxia, it is untenable to suggest that they spend a significant portion of the winter buried in anoxic mud, but instead utilise a suite of behavioural and physiological mechanisms geared to optimal survival in cold, hypoxic conditions. [source]