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At least 523 records · Page 29Linked to original sources
PubMed1983

Human NADH-cytochrome b5 reductases: comparison among those of erythrocyte membrane, erythrocyte cytosol, and liver microsomes.

NADH-cytochrome b5 reductases purified from human red cell membranes and cytosol were compared with those prepared from human liver microsomes. Minimal molecular weights of the membrane and the cytosol enzymes as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) were 36,000 and 32,000 daltons, respectively, which are comparable to those of the detergent-solubilized reductase (dfp) and the protease-solubilized one (tfp) of liver microsomes, respectively. All the enzymes contained FAD and had essentially the same turnover numbers and apparent Km values for NADH and protease-solubilized cytochrome b5. The membrane enzyme and liver dfp reduced cytochrome c in the presence of detergent-solubilized cytochrome b5 70-80 times faster than in the presence of trypsin-solubilized cytochrome b5, whereas the cytosol enzyme and liver tfp showed essentially the same low activities with both preparations of cytochrome b5. SDS-PAGE mapping of the limited proteolytic products of the reductases obtained by digestion with staphylococcal protease or a-chymotrypsin showed essentially the same patterns of peptides between the red cell membrane enzyme and liver dfp and between the red cell cytosol enzyme and liver tfp. These results suggest that the NADH-cytochrome b5 reductase of human red cell membranes is identical with that of liver microsomes and that the enzyme of red cell cytosol is a proteolytic product of the membrane enzyme.

Cytochrome Reductases↗
PubMed2003

Endotoxin binding to erythrocyte membrane and erythrocyte deformability in human sepsis and in vitro.

OBJECTIVE: Several studies have shown that lipopolysaccharide and lipid A impair red blood cell deformability and. However, it is unclear whether impaired red blood cell deformability is associated with binding of lipopolysaccharide to the red blood cell membrane. DESIGN: Analysis of hydroxymyristic acid content in red blood cell membranes and red blood cell deformation in patients with Gram-negative septicemia and after incubation of red blood cells from healthy adults with 100 microg of lipid A or 1 mg of lipopolysaccharide per milliliter of red blood cell in buffer solution and in whole blood. Hydroxymyristic acid is a fatty acid of the lipid A part of lipopolysaccharide in most Gram-negative bacteria. SETTING: University research laboratories. SUBJECTS: Ten healthy adults and four patients with clinical and laboratory signs of septicemia. INTERVENTIONS: Blood sampling. MEASUREMENTS AND MAIN RESULTS: Red blood cell deformation was measured with a laser-diffraction shearing device (Rheodyn) and a computerized micropore filtration system (CTA). Lipopolysaccharide and lipid A binding to red blood cell membranes was studied by measuring the amide-linked hydroxymyristic acid by gas chromatography. The detection rates of hydroxymyristic acid were 82% for lipopolysaccharide and 79% for lipid A in buffer solution. In membranes of washed red blood cell, the detection rates of lipopolysaccharide and lipid A were 0.26 +/- 0.03% (2.6 +/- 0.3 microg/mL) and 1.3 +/- 0.5% (1.3 +/- 0.5 microg/mL), and in red blood cell membranes of whole blood the detection rates were 2.6% (25.5 microg/mL) and 4.1% (4.1 microg/mL), respectively. The lipopolysaccharide content in red blood cell membranes of septic patients ranged from 47 to 103 microg/mL of red blood cell. Red blood cell deformation in the Rheodyn and in the CTA were not influenced by lipopolysaccharide incubated with washed red blood cells. In the Rheodyn, red blood cell deformation was significantly decreased by 18% after lipid A incubation in washed red blood cells, by 26% after lipopolysaccharide incubation in whole blood, and by 31% in septic patients. Similar effects were observed when we used the CTA. CONCLUSIONS: Red blood cell deformation is decreased in septic patients, after incubation of washed red blood cells with lipid A and of whole blood with lipopolysaccharide. Lipopolysaccharide did not influence red blood cell deformation after incubation with washed red blood cells. The decrease of red blood cell deformation was related to the amount of hydroxymyristic acid measured in red blood cell membranes, suggesting that endotoxin binding directly affects mechanical properties of red blood cells.

Adult↗
PubMed2006

Erythrocytes and the regulation of human skeletal muscle blood flow and oxygen delivery: role of erythrocyte count and oxygenation state of haemoglobin.

Blood flow to dynamically contracting myocytes is regulated to match O(2) delivery to metabolic demand. The red blood cell (RBC) itself functions as an O(2) sensor, contributing to the control of O(2) delivery by releasing the vasodilators ATP and S-nitrosohaemoglobin with the offloading of O(2) from the haemoglobin molecule. Whether RBC number is sensed remains unknown. To investigate the role of RBC number, in isolation and in combination with alterations in blood oxygenation, on muscle and systemic perfusion, we measured local and central haemodynamics during one-legged knee-extensor exercise ( approximately 50% peak power) in 10 healthy males under conditions of normocythaemia (control), anaemia, anaemia + plasma volume expansion (PVX), anaemia + PVX + hypoxia, polycythaemia, polycythaemia + hyperoxia and polycythaemia + hypoxia, which changed either RBC count alone or both RBC count and oxyhaemoglobin. Leg blood flow (LBF), cardiac output (Q) and vascular conductance did not change with either anaemia or polycythaemia alone. However, LBF increased with anaemia + PVX (28 +/- 4%) and anaemia + PVX + hypoxia (46 +/- 6%) and decreased with polycythaemia + hyperoxia (18 +/- 5%). LBF and Q with anaemia + PVX + hypoxia (8.0 +/- 0.5 and 15.8 +/- 0.7 l min(-1), respectively) equalled those during maximal knee-extensor exercise. Collectively, LBF and vascular conductance were intimately related to leg arterial-venous (a-v) O(2) difference (r(2)= 0.89-0.93; P < 0.001), suggesting a pivotal role of blood O(2) gradients in muscle microcirculatory control. The systemic circulation accommodated to the changes in muscle perfusion. Our results indicate that, when coping with severe haematological challenges, local regulation of skeletal muscle blood flow and O(2) delivery primarily senses alterations in the oxygenation state of haemoglobin and, to a lesser extent, alterations in the number of RBCs and haemoglobin molecules.

Adaptation, Physiological↗