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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the previous paper [ramos, S., and Kaback, H.R. (1977), Biochemistry 16 (preceding paper in this issue)], it was demonstrated that Escherichia coli membrane vesicles generate a large electrochemical proton gradient (delta-muH+) under appropriate conditions, and some of the properties of delta-muH+ and its component forces [i.e., the membrane potential (delta psi) and the chemical gradient of protons (deltapH)] were described. In this paper, the relationship between delta-muH+, delta psi, and deltapH and the active transport of specific solutes is examined. Addition of lactose or glucose 6-phosphate to membrane vesicles containing the appropriate transport systems results in partial collapse of deltapH, providing direct evidence for the suggestion that respiratory energy can drive active transport via the pH gradient across the membrane. Titration studies with valinomycin and nigericin lead to the conclusion that, at pH 5.5, there are two general classes of transport systems: those that are driven primarily by delta-muH+ (lactose, proline, serine, glycine, tyrosine, glutamate, leucine, lysine, cysteine, and succinate) and those that are driven primarily by deltapH (glucose 6-phosphate, D-lactate, glucuronate, and gluconate). Importantly, however, it is also demonstrated that at pH 7.5, all of these transport systems are driven by delta psi which comprises the only component of delta-muH+ at this external pH. In addition, the effect of external pH on the steady-state levels of accumulation of different solutes is examined, and it is shown that none of the pH profiles correspond to those observed for delta-muH+, delta psi, or deltapH. Moreover, at external pH values above 6.0-6.5, delta-muH+ is insufficient to account for the concentration gradients established for each substrate unless the stoichiometry between protons and accumulated solutes is greater than unity. The results confirm many facets of the chemiosmotic hypothesis, but they also extend the concept in certain important respects and allow explanations for some earlier observations which seemed to preclude the involvement of chemiosmotic phenomena in active transport.
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PMID:The relationship between the electrochemical proton gradient and active transport in Escherichia coli membrane vesicles. 1 65

The role of biotin-dependent enzymes in the fatty liver and kidney syndrome of young chicks was studied. Under conditions of a marginal deficiency of dietary biotin, the level of biotin in the liver has differing effects on the activities of two biotin-dependent enzymes, pyruvate carboxylase and acetyl-CoA carboxylase. The activity of acetyl-CoA carboxylase is increased, but when the dietary deficiency of biotin produces biotin levels which are below 0-8 mug/g of liver, the activity of pyruvate carboxylase may be insufficient to completely metabolize pyruvate via gluconeogenesis. There is an increase in liver size and in the activities of enzymes involved in alternate pathways for the removal of pyruvate. Blood lactate accumulates and there is increased synthesis of fatty acids, and an accumulation of palmitoleic acid; these steps are accomplished by increased activities of at least the following enzymes: acetyl-CoA carboxylase, malate dehydrogenase (decarboxylating) (NADP+) and the desaturase enzyme. When the biotin level is below 0-35 mug/g of liver and the chick is subjected to a stress, physiological defence mechanisms of the chick may be inadequate to maintain homeostasis and they finally collapse, resulting in accumulation of triacylglycerol in the liver and blood; the chick is unable to maintain blood glucose levels and death occurs, often only a few hours after the imposition of the stress.
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PMID:Fatty liver and kidney syndrome in chicks. II. Biochemical role of biotin. 1 36

Colicins Ia and E1 are shown to inhibit the formation and bring about the collapse of a potassium diffusion potential imposed across the membrane of liposomes prepared from soybean or Escherichia coli phospholipids. Such depolarization results from a colicin-induced increase in membrane ion permeability. Colicins E2 and E3 do not depolarize such membranes. In addition to the colicin Ia-induced rapid efflux of preloaded rubidium, sodium, phosphate, or choline from liposomes, a slower efflux of preloaded sucrose or glucose 6-phosphate occurs. However, treated liposomes do not leak inulin or dextran, demonstrating that the effects of E1 and Ia are not due to a general disruption of membrane structure. The fact that colicin-induced ion efflux is observed in the complete absence of a membrane potential shows that the action of these colicins on liposomes is not voltage dependent. These results provide strong evidence that the depolarization of E. coli cells by colicins Ia and E1 results from a colicin-induced increase in membrane permeability to ions. It is proposed that this is brought about by the direct interaction of the colicin molecules with the bacterial cytoplasmic membrane.
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PMID:Effect of colicins Ia and E1 on ion permeability of liposomes. 9 88

Sugars such as glucose are transported into Escherichia coli by a coupled phosphorylation mechanism (the phosphoenolpyruvate:sugar phosphotransferase system, PTS). Transport of sugars through the PTS results in inhibition of adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] activity by a mechanism involving a change in the state of phosphorylation of PTS proteins. Other sugars (e.g., lactose) are transported without modification by a mechanism involving proton cotransport, which requires a proton motive force across the cell membrane. We show here that uptake of sugars through the lactose transport system results in inhibition of adenylate cyclase activity if the proton symport mechanism is also active. The protonophore carbonyl cyanide m-chlorophenylhydrazone also inhibits adenylate cyclase activity. These data suggest that the steady-state electrochemical proton gradient regulates the activity of adenylate cyclase. We propose that sugar-dependent inhibition of adenylate cyclase activity may occur by either of two mechanisms. Sugars transported by the PTS inhibited adenylate cyclase activity by dephosphorylation of a regulatory protein, while sugars transported by the proton motive force system inhibit adenylate cyclase activity as a result of collapse of the proton electrochemical gradient.
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PMID:Escherichia coli adenylate cyclase complex: regulation by the proton electrochemical gradient. 10 76

In order to evaluate the manner by which fumarate enhances contractility in the anaerobic heart, we examined Ca++ movements in isolated heart mitochondria and in the isolated perfused heart. Our experiments showed that in isolated antimycin A plus cyanide treated mitochondria: (a) Ca++ uptake was promoted by electron transport generated by fumarate-dependent oxidation of NADH, (b) Ca++ stimulated fumarate-dependent oxidation of NADH, (c) the ratio of Ca++ uptake:NADH oxidized was 1.7 and (d) the Ca++ sequestered is transiently highly mobile and is rapidly released upon collapse of the membrane potential. In anaerobic hearts perfused with glucose plus fumarate, malate and glutamate Ca++ levels were the same as those in oxygenated hearts while in anaerobic organs perfused with or without glucose Ca++ content was appreciably lower. Succinate production in anaerobic heart perfusions was related to: (a) an increased retention of Ca++ by the heart, (b) a diminution in peak aortic pressure generated by cardiac contractions and (c) an increase in heart rate. The information obtained indicates that mitochondria have a capability for Ca++ movement which be used physiologically, particularly in fumarate perfused anaerobic hearts, to assist the mechanism for contraction and relaxation of the heart.
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PMID:Anaerobic rat heart: mitochondrial role in calcium uptake and contractility. 22 34

The incorporation of cholesterol into unilamellar liposomes greatly increased the transmembranous movement of hydrophobic ionophores such as nigericin. In reconstituted liposomes containing rhodopsin as the only protein, the presence of cholesterol lowers by 10-fold or more the amount of negericin required to eliminate the light-driven proton gradient. These effects are seen both above and below the transition temperature of the phospholipid used for reconstitution. Cholesterol similarly increases the ability of A-23187, 1799, or NH4SCN to collapse the proton gradient of bacteriorhodopsin vesicles. Cholesterol also lowers the concentration of nigericin or valinomycin required for a rapid translocation of Rb+ into protein-free liposomes. It also lowers the concentration of A-23187 required for the release of Ca45 trapped in protein-free liposomes. In contrast to these observations and in confirmation of previous findings, we observed that cholesterol decreased the permeability of liposomes for glucose. Thus the effects of cholesterol on the permeability of the membrane vary with the chemical nature of the permeating compounds. We have also confirmed that in multilamellar liposomes cholesterol decreases the permeability of Rb+ in the presence of valinomycin. It therefore appears that the effect of cholesterol changes with the size and structural features of the model membranes.
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PMID:Cholesterol Stimulation of Penetration of Unilamellar Liposomes by Hydrophobic Compounds. 32 87

1. In goldfish intestine (perfused unstripped segments and mucosal strips) the serosal addition of ouabain (10(-4) M) resulted in a vanishment of the transepithelial potential difference and in a continuous increase in transepithelial resistance. 2. Incubation of mucosal strips with ouabain resulted in an increase in sodium content which was greater than the decrease in potassium content. The resulting increase in cation content was accompanied by an increase in chloride content and an increase in water content. 3. Histological examination showed that exposure to ouabain resulted in a swelling of the epithelial layer as compared to the control situation. 4. The ouabain induced resistance increase is greater in the presence of glucose, 3-OMG or fructose than in the presence of mannitol. Phlorizin (10(-4) M) inhibits the extra resistance increase induced by mucosal glucose but is without effect on the fructose induced extra resistance increase. The initial velocity and the magnitude of the glucose induced extra resistance increase depends on the glucose concentration. 5. The results suggest that in goldfish intestine ouabain induces cellular swelling with a concomitant collapse of the lateral intercellular spaces, which is the cause of the increased transepithelial resistance. The additional changes in resistance induced by sugars suggest that the cell membrane is more permeable to glucose, 3-OMG and fructose than to mannitol. The resulting changes in osmotically active material within the epithelial cell influence the cross-sectional area and consequently the conductivity of the paracellular shunt pathway. The hypothesis that these sugars do not induce a resistance change in the absence of ouabain is discussed.
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PMID:Effects of glucose and ouabain on transepithelial electrical resistance and cell volume in stripped and unstripped goldfish intestine. 57 48

Twenty-seven sheep were assigned to three groups in order to study acute urea toxicity. Groups I, II and III were dosed with 0.5, 0.6 annd 0.75 g/kg of urea, respectively. The mean survival times were 165, 109 and 60 minutes, respectively. The following clinical signs such as pronounced muscle fasciculation, trembling, grinding teeth, ataxia, lateral recumbency, bloating, regurgitation, hyperesthesia, mydriasis and convulsions were observed. Anuria and lack of salivation were also present. The primary cause of death in this study was due to respiratory arrest and not cardiovascular collapse. Plasma examinations showed a marked increase in glucose, ammonia and urea levels but no change in ketone body concentration.
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PMID:Acute urea toxicity in sheep. 64 59

Four cases of hereditary fructose intolerance with an early onset are reported. The features of acute liver failure in the neonatal period include a haemorrhagic syndrome, collapse, neurological features, hypoglycaemia, disturbed bleeding and clotting studies and abnormal liver function tests. Investigations into the aetiology include a search for bacterial or viral infection but particularly for a metabolic cause: especially for hereditary fructose intolerance which may be difficult to distinguish from tyrosinosis. Finally, methods of treatment are discussed: continuous glucose infusion, exchange transfusion, assisted ventilation, and dietary measures beginning with protein exclusion. The importance of careful observation is stressed (particularly sequential studies of bloodclotting factors).
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PMID:[Hereditary fructose intolerance with early onset]. 101 80

A total of 351 single-suckled beef calves were blood sampled at twice-weekly intervals for the first two and a half weeks of life. Twenty three of them died, 13 of a syndrome characterised by acute collapse and 10 of diarrhoea which had persisted for several days before death. Those which died acutely showed a sudden terminal rise in blood levels of potassium, magnesium, inorganic phosphate and total protein. Those which died after several days of diarrhoea showed a more gradual increase in blood chloride and urea concentrations and in packed cell volume values. It is suggested that these changes indicate a difference in the pathogenesis of the two situations. Calves which died had lower blood glucose levels before the onset of clinical signs than those which survived. It is suggested that this may have been a contributory factor in their mortality.
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PMID:Biochemical studies of the "collapse syndrome" in suckled calves. 121 27


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