Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sonicated vesicles of phosphatidylserine and phosphatidylserine/phosphatidylcholine mixtures were recombined with spectrin-actin from human erythrocyte ghosts. Morphological properties and physicochemical characteristics of the recombinates were studied with freeze etch electron microscopy, 31P NMR and differential scanning calorimetry. Sonicated dimyristoyl phosphatidylserine vesicles show a decrease in enthalpy change of the lipid phase transition upon addition of spectrin-actin. These vesicles collapse and fuse, into multilamellar structures in the presence of spectrin-actin, as demonstrated by freeze fracturing and NMR. Spectrin-actin cannot prevent the salt formation between phosphatidylserine and Ca2+, all phosphatidylserine is withdrawn from the lipid phase transition. In contrast a protection against the action of Mg2+ could be observed. Mixed bilayers of dimyristoyl phosphatidylserine/dimyristoyl phosphatidylcholine show phase separations at molar ratios above 1/1 (van Dijck, P.W.M., de Kruijff, B., Verkleij, A.J., van Deenen, L.L.M. and de Gier, J. (1978) Biochim. Biophys. Acta 512, 84--96). These phase spearations can be prevented by spectrin-actin. Ca2+-induced lateral phase separations in cocrystallizing phosphatidylserine/phosphatidylcholine mixtures, can be reduced by spectrin-actin. Formation of the Ca2+-phosphatidylserine salt, occurring in addition to lateral phase separation when mixtures contain more than 30 mol % phosphatidylserine, cannot be prevented by spectrin-actin.
 ...
PMID:The interaction of spectrin-actin and synthetic phospholipids. II. The interaction with phosphatidylserine. 42 Aug 34

The addition of the trivalent or tetravalent cations spermidine or spermine to a solution of T7 DNA in aqueous solution causes an alteration of the DNA from its extended coil form to a condensed form. If performed at low DNA concentration and at low ionic strengths, this transformation results in a monomolecular collapse to form a particle with a hydrodynamic radius of about 500 A. We have monitored this change using quasielastic and total intensity light scattering. In a solution of 50% methanol in water, the divalent cations Mg2+ and putrescine also can cause the condensation of DNA. Using Manning's (1978) counterion condensation theory, we calculate a striking unity among these disparate ions: the collapse occurs in each case when from 89 to 90% of the DNA phosphate charges are neutralized by condensed counterions.
 ...
PMID:Counterion-induced condesation of deoxyribonucleic acid. a light-scattering study. 44 48

Magnesium-deficient fetuses exhibited malformations (44%), anemia, and edema. Maternal plasma magnesium levels at day 21 of pregnancy reflected the level of dietary magnesium (2.43 +/- 0.09 mg Mg/100 ml, control; 0.74 +/- 0.02 mg Mg/100 ml, deficient). Plasma magnesium levels of deficient fetuses showed similar decreases although all fetal magnesium values at term were hihger than maternal values from the same group (3.29 +/- 0.22 mg Mg/100 ml, control; 1.78 +/- 0.07 mg Mg/100 ml, deficient). Magnesium deficiency did not appear to affect the maternal blood parameters. However, when fetal blood was examined, all of the parameters measured were altered in magnesum-deficient fetuses (Table 2). No abnormalities in hemoglobin bands or plasma proteins were seen between any groups by electrophoresis. Measurement of total protein contents showed no differences between maternal blood protein contents, but total plasma protein from magnesium-deficient fetuses was significantly lower than controls (2.00 +/- 0.14 versus 2.62 +/- 0.13 g/100 ml), thus establishing a factor in fetal edema production. Morphologic data showed that in magnesium-deficient fetuses, fetal erythropoiesis was significantly greater in liver, adrenal glands, and spleen than in controls and that maturation was normoblastic. Stained and unstained peripheral blood smears of magnesium-deficient fetuses showed and obvious macrocytosis and at least 50% of the red cells stained abnormally, exhibiting pale areas. Erythrocytic morphology seen in fetal magnesium deficiency is consistent with inadequate filling of the cell by hemoglobin as suggested by Cohlan et al. (5), a probable cause of membrane collapse. The inadequate filling of magnesium-deficient red blood cells (RBC) with hemoglobin might be explained by a reduction in hemoglobin synthesis which is consistent with the reduced mean corpuscular hemoglobin (MCH) and MCH concentration (MCHC) of the deficient fetal red cells. The role of magnesium in protein synthesis is also compatible with a reduction in hemoglobin synthesis, yet may not completely explain the abnormalities and resultant shortened lifespan of the red cells.
 ...
PMID:Magnesium deficiency anemia in the rat fetus. 86 20

1. The effect of gossypol in the presence of K+ or Mg2+, or both, was studied on ATPase activity and respiration of rat liver mitochondria. 2. Respiration was uncoupled in the presence of gossypol, Mg2+, and K+, whereas in the presence of gossypol and Mg2+ a partial inhibition was observed. 3. Gossypol stimulated ATPase activity in the presence of K+ or Mg2+, but maximal activity was observed when both cations were in the incubation medium. 4. Stimulation of ATPase activity in the presence of Mg2+ was dose related. 5. EDTA reverted the stimulation produced by gossypol on ATPase activity. 6. Gossypol had no effect on the ATPase activity of submitochondrial particles, which suggests an indirect action of gossypol on the enzyme. 7. Mitochondrial membrane potential showed a higher collapse in the presence of gossypol and 1 mM MgCl2. 8. The observed effects of gossypol could be explained by the collapse of the mitochondrial membrane potential.
 ...
PMID:The antifertility agent, gossypol, changes several mitochondrial functions in the presence of Mg2+. 136 Mar 78

Single and double strand breaks (SSB and DSB) are induced by fast neutrons in plasmid (pBR322) DNA in 1 mM potassium phosphate buffer (pH 7.25). Increasing the concentration of monovalent (Na+, Cs+, Li+), divalent (Mg2+, Ca2+) and trivalent (Al3+, Co3+ (NH3)6) metal cations strongly decreases the yield of DSB. The extent of the observed protection depends on the valence of the cation. The production of SSB is only slightly decreased, except for Al3+ and Co3+ (NH3)6, whose effects are particularly large (complete protection at 1 and 0.1 mM respectively). Circular dichroism spectra show that Al3+ induces an important structural change of DNA at the ion concentration where the protection becomes total. This change is probably a condensation (collapse), as in the well-known case of Co3+ (NH3)6. Our results suggest two mechanisms of protection by metal ions: (i) the induction of structural changes of DNA, that render less accessible the critical sites of attack by OH. radicals; and (ii) the stabilization of the double helical regions between two close-set nicks on opposite strands, that hinders the effective double strand breakage of DNA.
 ...
PMID:Metal ions protect DNA against strand breakage induced by fast neutrons. 136 58

1. Addition of fluorescamine (75 microM) to mitochondria induced an increase in membrane permeability. 2. The leakiness of the inner mitochondrial membrane is characterized by extensive release of accumulated Ca2+, collapse of the transmembrane potential, mitochondrial swelling and efflux of matrix proteins, among them, malate dehydrogenase. 3. These effects were diminished by supplementing the media with 1 mM phosphate, and partially prevented by Mg2+. 4. These results indicate that the primary amino groups of membrane components contribute, partially, to the maintenance of the permeability barrier in mitochondria.
 ...
PMID:Fluorescamine-induced membrane permeability in mitochondria. 145 13

Swelling of isolated rat liver mitochondria is shown to be induced by metal-catalyzed 5-aminolevulinic acid (ALA) aerobic oxidation, a putative endogenous source of reactive oxygen species (ROS), at concentrations as low as 50-100 microM. In this concentration range, ALA is estimated to occur in the liver of acute intermittent porphyria patients. Removal of Ca2+ (10 microM) from the suspension of isolated rat liver mitochondria by added EGTA abolishes both the ALA-induced transmembrane-potential collapse and mitochondrial swelling. Prevention of the ALA-induced swelling by addition of ruthenium red prior to mitochondrial energization by succinate demonstrates the deleterious involvement of internal Ca2+. Addition of MgCl2 at concentrations higher than 2.5 mM, prevents the ALA-induced mitochondrial swelling, transmembrane potential collapse and Ca2+ efflux. This indicates that Mg2+ protects against the mitochondrial damage promoted by ALA-generated ROS. The ALA-induced mitochondrial damage might be a key event in the liver mitochondrial damage of acute intermittent porphyria patients reported elsewhere.
 ...
PMID:Calcium-dependent mitochondrial oxidative damage promoted by 5-aminolevulinic acid. 146 71

Linolenic, linoleic, oleic, palmitic and stearic acids (FFA) collapse the electrical potential of pea stem mitochondria in the absence or in the presence of 0.5 mM Mg2+. Higher concentrations of this cation (5 mM) lower the rate of dissipation caused by linoleic, oleic and palmitic acids, while abolishing that induced by stearic acid. Carboxyatractyloside and ADP do not reverse the FFA-induced collapse both in the presence or absence of Mg2+. EDTA, EGTA or BHT do not influence the dissipation caused by FFA that, in addition, is not linked to lipid peroxidation evaluated as malondialdehyde or conjugated diene formation. Only linolenic acid sustains a peroxidation which, however, appears to be caused by its own oxidation catalysed by lipoxygenases rather than by membrane lipoperoxidation induced by this free fatty acid. These results suggest that neither the ATP/ADP exchanger nor lipid peroxidation appear to be involved in FFA-induced uncoupling in pea stem mitochondria.
 ...
PMID:Electrical potential dissipation induced by free fatty acids in pea stem mitochondria. 164 82

1. The effect of the benzodiazepines Ro5-4864, AHN 086 and clonazepam on the release of Ca2+ from rat heart and kidney mitochondria was studied. 2. The peripheral-type benzodiazepines Ro5-4864 and AHN 086 induced Ca2+ release which was blocked by Mg2+ whereas the central-type benzodiazepine clonazepam was ineffective. 3. An associated collapse of membrane potential and swelling were also induced by AHN 086 in the presence of Ca2+. 4. However, no oxidation of pyridine nucleotides or increased rate or respiration were observed. 5. Release of Sr2+ was induced by AHN 086 in the absence of inorganic phosphate but not in its presence. 6. These data are discussed in the context of the current hypotheses on the mechanism of mitochondrial Ca2+ release.
 ...
PMID:Release of Ca2+ from heart and kidney mitochondria by peripheral-type benzodiazepine receptor ligands. 184 85

The effect of n-alcohols on ATP-dependent generation of delta pH and Em across the plasma membrane vesicles of the yeast Saccharomyces carlsbergensis was investigated. The alcohols were shown to collapse delta pH and Em in the order C2 less than C3 less than C4 less than C5 less than or equal to C6 greater than or equal to C7 greater than C8 greater than C11, the dissipation of Em being more pronounced. Inhibition of the plasmalemma H(+)-ATPase was insignificant; at low alcohol concentrations its activity even increased. The basic reason for the toxic effect of the alcohols on the yeast cells was suggested to be due to the increase in the anion and proton permeability of the plasma membrane. Mg2+ partially prevented the increase in the plasmalemma ion permeability by the alcohols investigated.
 ...
PMID:Increase of the anion and proton permeability of Saccharomyces carlsbergensis plasmalemma by n-alcohols as a possible cause of its de-energization. 216 10


1 2 3 4 5 6 Next >>