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Transmembrane potential couple

Respiring, coupled mitochondria (which maintain a high transmembrane potential) release Ca2+ through two pathways that can be studied in isolated mitochondria after the addition of RR to block Ca2+ reuptake. [Pg.485]

In real cells, multiple transmembrane pumps and channels maintain and regulate the transmembrane potential. Furthermore, those processes are at best only in a quasi-steady state, not truly at equilibrium. Thus, electrophoresis of an ionic solute across a membrane may be a passive equilibrative diffusion process in itself, but is effectively an active and concentra-tive process when the cell is considered as a whole. Other factors that influence transport across membranes include pH gradients, differences in binding, and coupled reactions that convert the transported substrate into another chemical form. In each case, transport is governed by the concentration of free and permeable substrate available in each compartment. The effect of pH on transport will depend on whether the permeant species is the protonated form (e.g., acids) or the unprotonated form (e.g., bases), on the pfQ of the compound, and on the pH in each compartment. The effects can be predicted with reference to the Henderson-Hasselbach equation (Equation 14.2), which states that the ratio of acid and base forms changes by a factor of 10 for each unit change in either pH or pfCt ... [Pg.199]

Figure 28-2 Signal transduction by cell-surface receptors that are coupled to G-proteins.Two seven-transmembrane domains, coupled to different G-proteins (Gs, and G,) are shown. Activation of Gs leads to stimulation of the effector enzyme adenylate cyclase and the production of a cAMP second messenger, causing the activation of protein kinase A (PKA) and the initiation of potential phosphorylation cascades. Activation of G leads to stimulation of the effector enzyme phospholipase C p and the production of IP3 and diacylglycerol (DAG) second messengers, one effect of which is to activate protein kinase C (PKC) and Initiate a potential phosphorylation cascade. (From Conn PM.Mefmed S, eds.Textbook of endocrinolog/.Towanta Nj Humana Press 1997.)... Figure 28-2 Signal transduction by cell-surface receptors that are coupled to G-proteins.Two seven-transmembrane domains, coupled to different G-proteins (Gs, and G,) are shown. Activation of Gs leads to stimulation of the effector enzyme adenylate cyclase and the production of a cAMP second messenger, causing the activation of protein kinase A (PKA) and the initiation of potential phosphorylation cascades. Activation of G leads to stimulation of the effector enzyme phospholipase C p and the production of IP3 and diacylglycerol (DAG) second messengers, one effect of which is to activate protein kinase C (PKC) and Initiate a potential phosphorylation cascade. (From Conn PM.Mefmed S, eds.Textbook of endocrinolog/.Towanta Nj Humana Press 1997.)...
In a typical conduction experiment, alamethicin molecules are partitioned between the aqueous phase and the lipid phase. In the lipid phase, the peptide-lipid ratio is usually several orders of magnitude smaller than the observed P L, so the majority of the membrane-associated alamethicin molecules are on the membrane surface, with perhaps a small fraction of them inserted in the bilayer. When a transmembrane potential is applied, the inserted molecules (and presumably the number of channels) increase because the free energy of the inserted state is decreased by the coupling of the... [Pg.102]

Using the same approach as in analyzing chain (2), it would be of interest to trace how common is the coupling of the main redox reaction with the oxidation of membrane lipids. To this end, an investigation was made of the dark transmembrane potentials on bilayers formed from egg lecithin with cholesterol, modified by chlorophyll in the presence of such redox systems as ferri-ferrocyanide, NADP-ferrocyanide, NAD-ferrocyanide.103... [Pg.141]

Figure 12.18 Bursting behavior in (a) the transmembrane potential of a neuron in the crustacean stomatogastric ganglion (Adapted from Sharp, 1994.) (b) two coupled CSTRs, each of whose flow rates is modified according to the iodide concentration in the other reactor. Input concentrations in each reactor [ClOJo = 1 x 10 M, [I ]o = 4.2 X 10 " M. Note the similarity between the neural and chemical traces if one reverses the sign of the potential in one of the recordings. (Adapted from Dolnik and Epstein, 1993.)... Figure 12.18 Bursting behavior in (a) the transmembrane potential of a neuron in the crustacean stomatogastric ganglion (Adapted from Sharp, 1994.) (b) two coupled CSTRs, each of whose flow rates is modified according to the iodide concentration in the other reactor. Input concentrations in each reactor [ClOJo = 1 x 10 M, [I ]o = 4.2 X 10 " M. Note the similarity between the neural and chemical traces if one reverses the sign of the potential in one of the recordings. (Adapted from Dolnik and Epstein, 1993.)...
Mitochondria play a central role in response to apoptotic stimuli. There is increasing evidence that altered mitochondrial function is linked to apoptosis and a decreasing mitochondrial transmembrane potential ( Pm) is associated with mitochondria dysfunction. The MPT (mitochondria permeability transition) is a permeability increase of the mitochondria membrane coupled with depolarization of the membrane and disruption of mitochondrial membrane integrity. We measured A Pm using a fluorescent probe DiOC6(3) which specially accumulated in polarized membranes and was monitored by flow... [Pg.133]

Accumulated evidence from recent research indicates that mitochondria-derived factors, such as cytochrome c, have an important role in the apoptosis of some cells. Previous reports show that cytochrome c and caspase-9 participate in Apafl apoptosome, a complex important for caspase-3 activation. Cytochrome c was released from mitochondria of HL-60 cells during treatment with carnosic acid, carnosol or ursolic acid. Previous evidence showed that mitochondria permeability transition (MPT) coupled with depolarization of the membrane potential induces the release of cytochrome c (31-33). It also has been reported that cytochrome c released from mitochondria can precede dissipation of the voltage gradient (the mitochondrial transmembrane potential vi/ ) across the membrane, suggesting that the escape of cytochrome c from mitochondria occurs prior to permeability transition pore opening (loss of mitochondrial transmembrane potential) (34,35). Here we observed the depolarization of the mitochondrial membrane potential in HL-60 cells by treatment with carnosic acid, carnosol, or ursolic acid for Ih. Cytochrome c was released after 3h treatment of carnosic acid, carnosol, or ursolic acid. [Pg.137]


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See also in sourсe #XX -- [ Pg.141 ]

See also in sourсe #XX -- [ Pg.141 ]




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Transmembrane

Transmembrane potential

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