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Plasma viscosity in ischemic heart disease.

Plasma viscosity was measured by the capillary method in 108 patients with ischemic heart disease. The highest value of plasma viscosity was found in 11 patients with severe unstable angina (1.66 +/- 0.068), while in 18 patients with less severe unstable angina plasma viscosity was lower (1.61 +/- 0.056; p less than 0.025). In 43 patients with acute myocardial infarction plasma viscosity was 1.53 +/- 0.10, significantly lower than in the two groups with unstable angina (p less than 0.005). In 36 patients with stable angina plasma viscosity was 1.42 +/- 0.089, similar to that found in 100 normal subjects. Plasma viscosity did not increase in 30 ischemic heart disease patients during exercise-induced myocardial ischemia. It is suggested that the elevated plasma viscosity in unstable angina demonstrated in this study compromises the oxygen delivery to the myocardium and coronary blood flow and therefore may possibly be a factor in the pathophysiology of this syndrome.

Adult↗

Adenosine, a cytoprotective autocoid: effects of adenosine on neutrophil plasma membrane viscosity and chemoattractant receptor display.

At inflammatory sites neutrophils are stimulated to produce a variety of toxic agents, yet rarely harm the endothelium across which they migrate. We have recently found that endothelium releases adenosine which, acting via receptors on the surface of human neutrophils, inhibits generation of toxic metabolites by stimulated neutrophils but, paradoxically, promotes chemotaxis. Agents which diminish plasma membrane viscosity affect neutrophil function similarly, possibly by modulating chemoattractant receptor number or affinity. We therefore determined whether adenosine receptor agonists modulate neutrophil function by decreasing membrane viscosity and/or changing the affinity of chemoattractant (N-fMet-Leu-Phe, FMLP) receptors. Surprisingly, 5'-(N-ethylcarboxamido)adenosine (NECA, 10 microM), the most potent agonist at neutrophil adenosine receptors, increased plasma membrane viscosity, as measured by fluorescence anisotropy of the plasma membrane specific probe 1-(4-trimethylaminophenyl)-6-diphenyl-1,3,5-hexatriene (TMA-DPH), in unstimulated neutrophils from a mean microviscosity of 1.67 +/- 0.02 (S.E.) to 1.80 +/- 0.02 (p less than 0.001) while inosine (10 microM), a poor adenosine receptor agonist, had no effect (1.73 +/- 0.04, p = n.s. vs. control, p less than 0.01 vs. NECA). Adenosine receptor agonists increased plasma membrane viscosity in neutrophils with the same order of potency previously seen for inhibition of superoxide anion generation and enhancement of chemotaxis (NECA greater than adenosine = N6-phenylisopropyladenosine). The adenosine receptor antagonist 8-(p-sulfophenyl)theophylline reversed the effect of NECA on plasma membrane viscosity. Unlike other agents which modulate plasma membrane viscosity, NECA (10 microM) did not significantly change the number or affinity of [3H]FMLP binding sites on neutrophils. In contrast to the hypothesis of Yuli et al. these results indicate that occupancy of adenosine receptors on neutrophils increases plasma membrane viscosity without affecting chemoattractant receptor display.

Adenosine↗

Effect of lipids and proteins on the viscosity of gastric mucus glycoprotein.

The effect of associated lipids and covalently bound fatty acids, and the contribution of serum albumin and secretory IgA to the viscosity of dog gastric mucus glycoprotein was investigated. Using a cone/plate viscometer at shear rates between 1.15 - 230s -1, it was found that extraction of associated lipids from the glycoprotein lead to 80-85% decrease in the viscosity. Further loss (39%) in viscosity of the delipidated glycoprotein occurred following removal of covalently bound fatty acids. Reassociation of the delipidated glycoprotein with its neutral lipids increased the viscosity 3-fold, a 2.5-fold increase was obtained with glycolipids, and 2-fold with phospholipids. Preincubation of purified mucus glycoprotein with albumin or IgA resulted in the increase in viscosity. This increase in viscosity was proportional to albumin concentration up to 10%, and to IgA concentration up to 5%. The results show that interaction of lipids and proteins with mucus glycoprotein contributes significantly to the viscosity of gastric mucus.

Animals↗

Effect of low-dose oral triphasic contraceptives on blood viscosity, coagulation and lipid metabolism.

The purpose of the study was to determine the relationship between hemorheological profile, i.e. blood viscosity, and other risk factors for cardiovascular and thrombotic diseases in women taking oral contraceptives and if blood viscosity may be considered a marker of cardiovascular risk in OC users. Plasma levels of coagulation parameters, serum lipids, blood viscosity and RBC deformability were determined in a group of 10 women taking OC vs. 10 controls. The blood parameters were evaluated before OC use and thereafter at 3 and 6 months. A significant change in the partial thromboplastin time, fibrinogen, HDL and apolipoprotein A-I was observed, while the other parameters remained unchanged. Plasma viscosity was significantly increased during OC treatment; whole blood viscosity and RBC deformability remained unchanged. However, although some parameters were significantly modified during OC treatment, all alterations remained within the normal range of laboratory values. The data confirm that low-dose triphasic OC therapy does not affect significantly the coagulation system, serum lipid metabolism and blood viscosity. Plasma viscosity measurement may be considered as a marker for monitoring women using OC because it is apparently the most sensitive parameter.

Adolescent↗

Effects of viscosity and oxygen content on cerebral blood flow in ischemic and normal rat brain.

The mechanism of hemodilution-induced increases in cerebral blood flow (CBF) was investigated. Hemodilution was achieved with a molecular hemoglobin solution (DCLHb) and albumin which have similar viscosities but different oxygen carrying capacities. Part A: CBF was assessed in rats after one of the following regimens: (1) control-hematocrit not manipulated, (2) 30/Alb-hematocrit decreased to 30% with albumin, (3) 30/DCLHb-hematocrit decreased to 30% with DCLHb, or (4) 16/Alb/DCLHb-hematocrit decreased to 30% with albumin and then 16% with DCLHb. For viscosity matched groups (30/Alb and 30/DCLHb), CBF was greater in animals with decreased oxygen content (30/Alb); while in oxygen content matched groups (30/Alb and 16/Alb/DCLHb), CBF was greater in animals with decreased viscosity (16/Alb/DCLHb) (p < 0.05). Part B: Middle cerebral artery occlusion was performed, hemodilution achieved as in Part A, and CBF determined. For viscosity matched groups (30/Alb and 30/DCLHb), CBF was less in rats with decreased oxygen content (30/Alb); while in oxygen content matched groups (30/Alb and 16/Alb/DCLHb), CBF was greater in animals with decreased viscosity (16/Alb/DCLHb) (p < 0.05). This data supports the premise, that in normal brain, both viscosity and oxygen content effect CBF; while in ischemic brain, a decrease in viscosity but not oxygen content increases CBF.

Animals↗

Further observations on serum viscosity changes in diabetes mellitus.

The 8% increase in serum viscosity in diabetes mellitus, more striking in diabetics with evidence of microangiopathy, has been further investigated. Methodology has been developed to eliminate the effect of fluctuating levels of glucose, lipids and protein. This was accomplished first by dialysis of fresh serum and later by ultracentrifugation to remove lipoprotein followed by dialysis. The distinction between diabetic and nondiabetic viscosity levels was improved by removing glucose and correcting for fluctuations in serum protein level, principally because variation between observations on the same subject was substantially reduced. Two methods were utilized to adjust for protein concentration differences. Ether technique increased the statistical significance of the viscosity increase in diabetes. Without lipoprotein removal the regression of specific fluidity (1-1/relative viscosity) with concentration differed between the sexes. When lipoprotein was removed the sex difference disappeared and the regression line passed through the origin. Removal of lipoprotein also further increased the discrimination between diabetic and normal serum. Even without lipoprotein removal elevated serum viscosity was readily detected in advanced glucose intolerance. In both studies, viscosity was higher in diabetics with microangiopathic sequelae, increasing progressively with more evidence of microangiopathy. No effect of severity of hyperglycemia or duration of diabetes could be demonstrated. Increased serum viscosity' association with microvascular sequelae and its presence early in the disorder suggest that the protein changes responsible for its elevation may play a role in the development of diabetic microangiopathy.

Adolescent↗

Viscosity modulates blood glucose response to nutrient solutions in dogs.

The relationship between postprandial blood glucose levels and meal viscosity was studied by adding various combinations of hydroxypropylmethylcellulose to glucose solutions and administering them to female mongrel dogs. Glucose was administered as 5% or 20% solutions in water. Hydroxypropyl-methylcellulose was dissolved in the glucose solutions to yield low (5000 cP measured at 37 degrees C and 1 s-1), medium (15,000 cP) or high (30,000 cP) viscosities. High viscosity hydroxypropylmethylcellulose significantly reduced the maximum blood glucose concentration, Cmax, by 60% (5% glucose meal) and 40% (20% glucose meal) while reducing the area under the blood level vs. time curve (AUC0-3 h) by 40-50%. Medium viscosity hydroxypropylmethylcellulose reduced the Cmax at both glucose levels, but reduced the AUC only for the 5% glucose meal. Low viscosity HPMC lowered the Cmax only after the 5% glucose meal, and had no significant effect on the AUC at either glucose level. The average time to reach maximum concentration, Tmax, was prolonged two- to three-fold at all viscosity levels for the 5% glucose solutions, but was not affected when 20% glucose solutions were administered. It was concluded that hydroxypropylmethylcellulose can effectively retard the absorption of glucose from the gastrointestinal tract, and that the extent of this effect is related to the viscosity of the solution administered.

Animal Nutritional Physiological Phenomena↗

Effect of viscosity on neurite outgrowth and fractal dimension.

The growth mechanism by which neurons achieve their characteristic ramified morphology has long been of interest, but determining whether physical parameters, such as viscosity, are important has been difficult due to a lack of useful hypotheses and standard reproducible techniques. We have recently shown that neurons exhibit fractal behavior and that their fractal dimension (df) is consistent with a physical process called diffusion-limited aggregation (DLA). We suggested that this DLA behavior might stem from viscosity differences, chemical gradients or electrical fields (Caserta et al., Phys. Rev. Lett., 64 (1990) 95-98). DLA is a model for a large family of growth processes. In order for a process to fit the DLA model, the growth rate must be proportional to the gradient of a field at a point on the growing structure (Feder, Plenum, New York, 1988, Ch. 4). Chemical, electrical, or fluid pressure fields can fit the model depending on the particular physical system under study. Here, we studied growth of retinal neurons from chick embryos in culture media of various fluid viscosities. Thus, we test whether DLA in this system was based on a fluid pressure field. As viscosity was increased from 1 to 4.3 cps, the number of neurite branches decreased 98%. However, there was no effect on df. Over this range of viscosities, total cellular protein synthesis decreased only 17%. The results indicate that, while differences in viscosity between the interior and exterior of the cell affect neurite outgrowth, they do not affect the fractal behavior of neurons. Thus, viscosity differences are not the basis for the DLA pattern of neuronal arborization.

Algorithms↗

Viscous properties of pig cecal contents and the contribution of solid particles to viscosity.

OBJECTIVE: It is believed that solid particles are not responsible for digesta viscosity. However, solid particles are responsible for the viscosity of whole blood and fiber suspension such as wood pulp. Therefore, we measured viscosity of gut contents with and without solid particles. We also determined the contribution of solid particles to viscoelastic characters of gut contents. METHODS: We measured the coefficient of viscosity, shear rate, and shear stress of pig cecal contents by using a tube-flow viscometer before and after removal of particles. RESULTS: The coefficient of viscosity of intact pig cecal contents was negatively correlated with shear rate, a typical character of non-Newtonian fluids. The removal of solid particles from the contents resulted in a Newtonian fluid with very low viscosity. CONCLUSION: Solid particles were mainly responsible for the viscoelastic character of pig cecal contents. Accordingly, the contribution of indigestible solid food components, sloughed epithelial cells, and bacterial cell bodies to the viscosity of gut contents should be re-evaluated.

Animals↗

Viscosity regulates apolipoprotein A-1 gene expression in experimental models of secondary hyperlipidemia and in cultured hepatocytes.

This study analyzes the relationship of plasmatic colloid osmotic pressure (PCO) and viscosity with the different hyperlipidemic stages observed in rats with acute liver damage induced by carbon tetrachloride (CCl4) and in rats with nephrotic syndrome induced by puromycin amino nucleoside (PAN). In both animal models viscosity increases were associated with the induction of the hyperlipidemic stage characterized by an increase of high density lipoproteins (HDL) and steady-state levels (SSL) of apo A-1 mRNA. In both animal models PCO decreased at early stages of the disease when hyperlipidemia was characterized principally by an increase of total cholesterol and triacylglycerols, but was not associated with the induction of HDL and apo A-1 mRNA. To confirm the in vivo findings, we studied the effect of viscosity on apo A-1 gene expression in an in vitro model using cultured hepatocytes. When medium viscosity was maintained below physiological values, an induction of the SSL of apo A-1 mRNA was observed. By contrast, when medium viscosity was raised to values similar or higher than the physiological range, the SSL of apo A-1 mRNA decreased steadily and after 24 h incubation an almost total inhibition was observed. These results suggest that in both experimental animal models of secondary hyperlipidemia, small viscosity changes below the physiological range, most probably in the interstitial fluid, can induce apo A-1 gene expression at the mRNA level, and that when viscosity reaches physiological values, apo A-1 gene expression is inhibited. Both effects were shown in cultured hepatocytes.

Animals↗

Temperature dependence of the yield shear resultant and the plastic viscosity coefficient of erythrocyte membrane. Implications about molecular events during membrane failure.

Structural failure of the erythrocyte membrane in shear deformation occurs when the maximum shear resultant (force/length) exceeds a critical value, the yield shear resultant. When the yield shear resultant is exceeded, the membrane flows with a rate of deformation characterized by the plastic viscosity coefficient. The temperature dependence of the yield shear resultant and the plastic viscosity coefficient have been measured over the temperature range 10-40 degrees C. Over this range the yield shear resultant does not change significantly (+/- 15%), but the plastic viscosity coefficient changes exponentially from a value of 1.3 X 10(-2) surface poise (dyn s/cm) at 10 degrees C to a value of 6.2 X 10(-4) surface poise (SP) at 40 degrees C. The different temperature dependence of these two parameters is not surprising, inasmuch as they characterize different molecular events. The yield shear resultant depends on the number and strength of intermolecular connections within the membrane skeleton, whereas the plastic viscosity depends on the frictional interactions between molecular segments as they move past one another in the flowing surface. From the temperature dependence of the plastic viscosity, a temperature-viscosity coefficient, E, can be calculated: eta p = constant X exp(--E/RT). This quantity (E) is related to the probability that a molecular segment can "jump" to its next location in the flowing network. The temperature-viscosity coefficient for erythrocyte membrane above the elastic limit is calculated to be 18 kcal/mol, which is similar to coefficients for other polymeric materials.

Erythrocyte Membrane↗

A novel fluorescence ratiometric method confirms the low solvent viscosity of the cytoplasm.

Two homologous indocyanine dyes, Cy3.18 and Cy5.18, can be used as a ratio pair for fluorometric determination of solvent viscosity. Succinimidyl ester derivatives of these dyes can be attached to inert carrier macromolecules, such as Ficoll 70, for measurement of intracellular or intravesicular solvent viscosity. When the viscosity of the solvent was varied by various methods, the fluorescence intensity ratio (Cy3/Cy5) in a mixture of Cy3.18-Ficoll 70 (Cy3F70) and Cy5.18-Ficoll 70 (Cy5F70) in solution was found to be solely a function of solvent viscosity and was insensitive to other solvent parameters such as dielectric constant, temperature, and the ability of the solvent to form hydrogen bonds. Most important, it was insensitive to the presence of large macromolecules, such as proteins, which increase the shear viscosity but have little effect on solvent viscosity. Following microinjection into the cytoplasm of living tissue culture cells, no binding of Cy3F70 or Cy5F70 to intracellular components was detected by fluorescence recovery after photobleaching. Fluorescence intensity ratio imaging of Cy3F70 and Cy5F70 in non-motile interphase CV1 and PtK1 cells showed that the solvent viscosity of cytoplasm was not significantly different from water and showed no spatial variation.

Biophysical Phenomena↗

Increased plasma viscosity during an air pollution episode: a link to mortality?

BACKGROUND: Air pollution episodes have been consistently associated with increased mortality, and most strikingly with mortality due to cardiovascular disease. One hypothesis to explain this association is that inflammation of the peripheral airways caused by pollution might increase blood coagulability. We have tested this hypothesis in a cross-sectional study by comparing measurements of plasma viscosity during a severe episode of air pollution during 1985 with those made on less polluted days. METHODS: Plasma viscosity was measured as part of the MONICA Augsburg survey during the winter of 1984-85 in 3256 randomly selected men and women aged 25-64 years. Daily mean concentrations of air pollutants and meteorological variables were measured in Augsburg as part of the automated Bavarian air-quality network. We compared measurements of plasma viscosity made in 324 people who attended for screening during the pollution episode and in 2932 people screened during the remainder of the survey period. FINDINGS: In January, 1985, high concentrations of sulphur dioxide (mean 200 micrograms/m3) and total suspended particles (mean 98 micrograms/m3) were recorded during a 13-day period in Augsburg. In men, the odds ratio for plasma viscosity above the 95th percentile of the distribution (1.38 mPa s) was 3.6 (95% CI 1.6-8.1) comparing measurements during the air pollution episode with non-episode measurements after adjustment for cardiovascular risk factors and meteorological variables. The corresponding odds ratio for women (95th percentile of plasma viscosity 1.37 mPa s) was 2.3 (1.0-5.3). High concentrations of carbon monoxide were also associated with increased plasma viscosity in women. INTERPRETATION: During the 1985 air pollution episode, an increased risk of extreme values of plasma viscosity was observed in both men and women. Altered blood rheology due to inflammatory processes in the lung that induce an acute-phase reaction might therefore be part of the pathological mechanisms linking air pollution to mortality.

Adult↗

Lipoprotein alterations in liver cirrhosis: a possible contribution to changes in plasma oncotic pressure and viscosity.

BACKGROUND/AIMS: To investigate whether physicochemical alterations in plasma lipoproteins are associated with changes in plasma oncotic pressure and viscosity in liver cirrhosis. METHODS: The study included 66 patients with cirrhosis (confirmed by liver biopsy) and 58 healthy volunteers. The constituents measured were: the concentration, density and composition of plasma lipoproteins; plasma oncotic pressure and viscosity; and the concentrations of albumin, total protein, haptoglobin, transferrin, immunoglobulin M and alpha2-macroglobulin. RESULTS: Step-wise multiple regression analysis indicated that, in the patients with cirrhosis, plasma oncotic pressure was significantly correlated with plasma albumin+viscosity (r=+0.85; p<0.001) and with plasma total protein+the density of low density lipoprotein (r=+0.74; p<0.001). The inclusion of viscosity and the density of low density lipoprotein in the regression equations significantly improved the observed correlation between albumin and plasma oncotic pressure (r=+0.70; p<0.001). Similarly, plasma viscosity was significantly correlated with the sum of plasma total protein and cholesterol (r=+0.68; p<0.001). The inclusion of cholesterol in the regression equation significantly increased the observed correlation between total protein and plasma viscosity (r=+0.59; p<0.001). CONCLUSIONS: These results suggest that lipoprotein alterations associated with liver cirrhosis may play a role in determining plasma oncotic pressure and viscosity, and thus could influence the progression of the disease.

Adult↗

Effect of renal replacement therapy on viscosity in end-stage renal disease patients.

Viscosity, an important determinant of microcirculatory hemodynamics, is related to hematocrit (HCT), and may be altered by renal failure or its treatment. To assess these factors, we studied the effect of dialysis on the viscosity of whole blood, plasma, and reconstituted 70% HCT blood of eight continuous ambulatory peritoneal dialysis (CAPD) and nine hemodialysis (HD) patients under steady shear flow conditions at different shear rates, before and after dialysis, compared with nine normal subjects. The density of the red blood cells (RBCs), a marker of cell hydration, was measured in HD patients by a nonaqueous differential floatation technique. Whole blood viscosity was higher in controls than patients, and correlated with HCT before treatment (P less than 0.05) at shear rates of 11.5 to 230 s-1) in HD patients, and 23 to 230 s-1 in all end-stage renal disease (ESRD) patients. In contrast, whole blood viscosity correlated with HCT in CAPD patients only at the lowest shear rates (2.3 and 5.75 s-1, P less than 0.05). Plasma viscosity was higher in CAPD patients than both HD patients before treatment and controls (P less than 0.05, analysis of variance [ANOVA]), despite lower plasma total protein, albumin, and similar fibrinogen concentration compared with HD patients. When all samples were reconstituted to 70% HCT, CAPD patients had higher whole blood viscosity than control subjects'. The high HCT blood viscosity of the ESRD patients was higher than control subjects' at capillary shear rates, suggesting increased RBC aggregation and decreased RBC deformability in patients with renal disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effects of interactions between powder particle size and binder viscosity on agglomerate growth mechanisms in a high shear mixer.

A study was performed in order to elucidate the effects of the interactions between powder particle size and binder viscosity on the mechanisms involved in agglomerate formation and growth. Calcium carbonates having mean particle sizes in the range of 5-214 microm and polyethylene glycols having viscosities in the range of approximately 50-100000 mPas were melt agglomerated in a high shear mixer. Agglomerate growth by nucleation and coalescence was found to dominate when agglomerating small powder particles and binders with a low viscosity. Increasing the binder viscosity increased the formation of agglomerates by immersion of powder particles in the surface of the binder droplets. With a larger powder particle size, an increasing binder viscosity was necessary in order to obtain an agglomerate strength being sufficient to avoid breakage. Due to a low agglomerate strength, a satisfying agglomeration of very large particles (214 microm) could not be obtained, even with very viscous binders. The study demonstrated that the optimum agglomerate growth occurred when the agglomerates were of an intermediate strength causing an intermediate deformability of the agglomerates. In order to produce spherical agglomerates (pellets), a low viscosity binder has to be chosen when agglomerating a powder with a small particle size, and a high viscosity binder must be applied in agglomeration of powders with large particles.

Adhesiveness↗

Intrinsic viscosity of polymers and biopolymers measured by microchip.

Intrinsic viscosity provides insight to molecular structure and interactions in solution. A new microchip method is described for fast and accurate measurements of viscosity and intrinsic viscosity of polymer and biopolymer solutions. Polymer samples are diluted with solvent in the microfluidic chip by imposing pressure gradients across the channel network. The concentration and flow dilutions of the polymer sample are calculated from the fluorescent signals recorded over a range of dilutions. The viscosities at various polymer dilutions are evaluated using mass and momentum balances in the pressure-driven microchannel flow. The technique is particularly important to many chemical, biological, and medical applications where sample is available in very small quantities. The intrinsic viscosity experiments were performed for three classes of polymer solutions: (a) poly(ethylene glycol), polymers with linear hydrocarbon chains; (b) bovine serum albumin, biopolymer chains with hydrophobic and hydrophilic amino acids, and (c) DNA fragments, biological macromolecules with double-stranded polymeric chains. The measured values of intrinsic viscosity agree remarkably well with the available data obtained using different methods. The data exhibit power law behavior for molecular weight as described by the Mark-Houwink-Sakurada equation. Experiments were performed to understand the effect of solvent quality and salt concentration on molecular conformations and the intrinsic viscosity of the polymers. This method offers a new way to study the conformational changes in proteins and DNA solutions in various buffer conditions such as pH, ionic strength, and surfactants. The effects of shear rate in the microchannel and mixing time on the accuracy and limitation of the measurement method are discussed.

Animals↗

Movement of the Rieske iron-sulfur protein in the p-side bulk aqueous phase: effect of lumenal viscosity on redox reactions of the cytochrome b6f complex.

Based on the atomic structures of the mitochondrial cytochrome bc(1) complex, it has been proposed that the soluble domain of the [2Fe-2S] Rieske iron-sulfur protein (ISP) must rotate by ca. 60 degrees and translate through an appreciable distance between two binding sites, proximal to cytochrome c(1) and to the lumen-side quinol binding site. Such motional freedom implies that the electron-transfer rate should be affected by the lumenal viscosity. The flash-induced oxidation of cytochrome f, the chloroplast analogue of cytochrome c(1), was found to be inhibited reversibly by increased lumenal viscosity, as was the subsequent reduction of both cytochrome b(6) and cytochrome f. The rates of these three redox reactions correlated inversely with lumenal viscosity over a viscosity range of 1-10 cP. Reduction of cytochrome b(6) and cytochrome f was not concerted. The rate of cytochrome f reduction was observed to be approximately half that of cytochrome b(6) regardless of the actual viscosity, implying that the path length traversed by the ISP in reduction of cytochrome f is twice that of cytochrome b(6). This suggests that upon initiation of electron transfer by a light flash, cytochrome b(6) reduction requires movement of reduced ISP from an initial position predominantly proximal to cytochrome f, apparently favored by the reduced ISP, to the quinol binding site at which the oxidant-induced reduction of cytochrome b(6) is initiated. Subsequent reduction of cytochrome f requires the additional movement of the ISP back to a site proximal to cytochromef. There is no discernible viscosity dependence for cytochrome b(6) reduction under oxidizing conditions, presumably because the oxidized ISP preferentially binds proximal to the quinone binding niche. The dependence of the cytochrome redox reaction on ambient viscosity implies that the tethered diffusional motion of the ISP is part of the rate limitation for charge transfer through the b(6)f complex.

Chloroplasts↗