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At least 901 records · Page 50Linked to original sources
PubMed1965

The relation between skeletal and extracellular-fluid magnesium in vitro.

1. Femora from control and magnesium-deficient rats were incubated in media of different magnesium concentrations. 2. Magnesium was lost at the same rate from fresh and boiled bones to a magnesium-free medium. 3. The equilibrium established was dependent on the magnesium concentrations in both the bone and the medium. 4. Parathyroid extract increased the rate of magnesium loss from bone to a magnesium-low medium containing bovine serum (50%), but had no effect in a protein-free medium.

Journal Article↗
PubMed1982

Superoxide-dependent formation of hydroxyl radicals and lipid peroxidation in the presence of iron salts. Detection of 'catalytic' iron and anti-oxidant activity in extracellular fluids.

Synovial fluid from rheumatoid patients and normal cerebrospinal fluid contains micromolar concentrations of non-protein-bound iron salts that can promote lipid peroxidation and also the superoxide-dependent formation of hydroxyl radicals from hydrogen peroxide. These iron catalysts of oxygen radical reactions cannot be detected by conventional assays unless interfering high-molecular-weight substances, probably proteins, are removed by ultrafiltration or inactivated by exposure to low pH values. The bleomycin assay for ;catalytic' iron [Gutteridge, Rowley & Halliwell (1981) Biochem. J.199, 263-265] does not suffer from these artifacts.

Animals↗
PubMed1987

The antioxidant action of human extracellular fluids. Effect of human serum and its protein components on the inactivation of alpha 1-antiproteinase by hypochlorous acid and by hydrogen peroxide.

The elastase-inhibitory capacity of purified human alpha 1-antiproteinase is inactivated by low concentrations of the myeloperoxidase-derived oxidant hypochlorous acid, but much higher concentrations are required to inhibit the elastase-inhibitory capacity of serum samples. The protective effect of serum appears to be largely due to albumin. High concentrations of H2O2 also inactivate the elastase-inhibitory capacity of alpha 1-antiproteinase, by a mechanism not involving formation of hydroxyl radicals. Serum offers protection against H2O2 inactivation of alpha 1-antiproteinase. The relevance of these results to the tissue damage produced by activated phagocytes is discussed.

Blood↗
PubMed1998

A dynamic model of outer hair cell motility including intracellular and extracellular fluid viscosity.

The deformation response of a guinea pig outer hair cell is modeled for mechanical and electrical stimulation up to 25 kHz. The analysis uses a Fourier series technique for a finite length cell surrounded internally and externally by a much larger continuum of viscous fluid. The analytical solution predicts that outer hair cell length changes occur due to applied mechanical or electrical stimulation without significant resonance, characteristic of a highly damped system. The deformation is found to have little attenuation up to a corner frequency of about 2 kHz for long cells and 10 kHz for short cells, in agreement with published experimental results. For electrical loading of 1 mV across the lateral cell wall, deformation for short cells is calculated to be greater than 1 nm for frequencies up to 20 kHz. These results support the proposition that in vivo the outer hair cell modifies the character of basilar membrane deformation on a cycle-by-cycle basis. An estimate of the capability of the cell to supply energy to the basilar membrane is given based on published values of outer hair cell material properties.

Animals↗
PubMed1979

Metallothionein in the extracellular fluids as an index of cadmium toxicity.

In rats injected with 5 micron mole CdCl2/kg, 5 days/week, metallothionein was detected in plasma by gel filtration chromatography as early as four weeks. The mean renal concentration of cadmium was 80 microgram/g. The excretion of cadmium in urine at this time was rather low and amounted to 0.01% of the total dose. The amount of metallothionein in plasma, as determined by 109Cd-binding to the 10,000 molecular weight fraction, increased markedly during week 14. Its excretion in urine, however, did not start until about 10 weeks, when the cadmium concentration in kidney approached a mean value of 212 microgram/g. Signs of renal toxicity were evident from glucosuria and proteinuria which became severe during the next four weeks. The excretion of cadmium in urine increased markedly and the majority of it was in the form of metallothionein. It is suggested that the appearance of metallothionein in plasma and urine can be used as specific indices of cadmium poisoning and that the assay of the protein in these fluids may be useful in screening for excessive cadmium exposure.

Animals↗