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Biomedical subjects

M Lundborg

Publications and source records attributed to M Lundborg.

At least 37 records · Page 2Linked to original sources
PubMed1988

Alveolar macrophages in rabbits after combined exposure to nickel and trivalent chromium.

Rabbits were exposed to a combination of 0.7 mg/m3 Ni2+ as NiCl2 and 1.2 mg/m3 of Cr3+ as Cr(NO3)3, to 0.6 mg/m3 of Ni2+ as NiCl2, or to filtered air for about 4 months, 5 days/week and 6 hr/day. Alveolar macrophages were recovered by lung lavage and studied by light and electron microscopy. Metabolic activity, phagocytic capacity and lysozyme activity in the macrophages were studied. After the combined exposure, the effects on lung weight, number of macrophages, and appearance of surface and number of intracellular laminated inclusions in these cells were more than additive. These effects might be explained by a combination of increased production by Ni2+ and impaired catabolism of surfactant by Cr3+. Because the metal concentrations used were not far above occupational threshold limit values, combined exposures to nickel and trivalent chromium should be considered more seriously.

Animals↗
PubMed1987

Dissolution of two arsenic compounds by rabbit alveolar macrophages in vitro.

The ability of rabbit alveolar macrophages to dissolve two arsenic compounds, 74As-labeled lead arsenate and arsenic trisulfide, was studied in vitro. The solubilities in water of these two compounds are related differently to pH. The solubility of lead arsenate increases and that of arsenic trisulfide decreases with decreasing pH. The radiolabeled particles were incubated with and without macrophages for up to 3 days, whereafter the amount of 74As in soluble form and the amount in particle form and/or bound to macrophages were determined. The results strongly support the hypothesis that the dissolution of particles by macrophages is influenced by the acid milieu in the phagosomes. About 14% of the 74As-labeled lead arsenate particles incubated for 3 days with the macrophages was released into the culture medium, compared with about 2% of the particles incubated with the culture medium without macrophages. With the arsenic trisulfide particles, less soluble 74As was released into the medium in samples with macrophages than in samples without macrophages, although the solubility in all incubations was considerably greater than that for lead arsenate. The results indicate that dissolution in the phagosomes of the macrophages may be of great importance for the clearance of particles such as lead arsenate, which are more soluble at pH 4 than at pH 7.

Animals↗
PubMed1987

Fibronectin concentrations in lung lavage fluid after inhalation exposure to low levels of metals.

Groups of rabbits were exposed by inhalation to chlorides of cobalt, nickel, and manganese as well as to tri- and hexavalent chromium at metal concentrations ranging from 0.4 to 3.9 mg/m3 for 1-4 months (5 days/week, 6 hr/day). Fibronectin content and lysozyme (muramidase) activity in lavage fluid were measured after all treatments and in alveolar macrophages after treatment with nickel chloride. In the lavage fluid no marked changes were seen in fibronectin content and lysozyme activity after exposure to tri- or hexavalent chromium or manganese. Nickel exposure significantly decreased the lysozyme activity in the lavage fluid and in the macrophages whereas the fibronectin content was unchanged in the lavage fluid and significantly increased in the macrophages. Both fibronectin content and lysozyme activity were increased markedly in the lavage fluid after cobalt exposure.

Administration, Inhalation↗
PubMed1987

Lysozyme activity in ultrastructurally defined fractions of alveolar macrophages after inhalation exposure to nickel.

Rabbits were exposed to 0.6 mg/m3 of nickel as NiCl2 for about one month. After exposure, alveolar macrophages were lavaged from the lung and divided into three fractions by elutriation. Laminated structures in the macrophages were related to fraction number so that the fractions with the largest cells contained the highest number of structures. The lysozyme activity decreased in unfractionated as well as in fractionated macrophages from nickel exposed rabbits. The decrease was most pronounced in the fraction with the smallest macrophages and smallest number of laminated structures. Therefore the pronounced decrease in lysozyme activity seen in this and earlier studies is not caused by the increased amount of surfactant material. Increased amount of surfactant is a hallmark of nickel inhalation exposure and the surfactant material is responsible for the morphological and metabolic effects of the macrophages. The decreased lysozyme activity is probably a direct effect of nickel on the macrophages.

Animals↗
PubMed1986

Rabbit alveolar macrophages after long-term inhalation of soluble cobalt.

Rabbits were exposed to 2 or 0.4 mg/m3 of cobalt as CoCl2 for 14-16 weeks (5 days/week and 6 hr/day). More macrophages were lavaged from the lungs of rabbits exposed to the higher Co2+ concentration, and the diameter and variation of the diameter of the macrophages were significantly larger than in controls. The activity of lysozyme in the lavage fluid and in the macrophages was increased in the two exposed groups. Some macrophages in the exposed animals were large and engorged with intracellular lamellar inclusions and lipid droplets. Most of these cells had a smooth surface. The oxidative metabolic activity measured by reduction of nitroblue tetrazolium was increased in the exposed groups. The number of yeast cell particles attached to the surface of the macrophages was increased in the group exposed to the high concentration, but the number of ingested particles was not affected by cobalt exposure. Apart from the fact cobalt increased lysozyme activity whereas nickel decreased it, cobalt produced the same type of effects on macrophages as nickel did in earlier studies. Cobalt affected only a minor proportion whereas nickel affected most macrophages. This can be explained by the fact nickel produced a general increase in the volume density of the type II cells while cobalt affected the type II cells only in some areas of the lungs.

Administration, Inhalation↗
PubMed1985

Dissolution of metals by human and rabbit alveolar macrophages.

The ability of human and rabbit alveolar macrophages to dissolve 0.1-0.5 micron MnO2 particles in vitro was compared. The amount of Mn added and dissolved from the particles over periods of nought, one, and three days was determined by flame atomic absorption spectrophotometry. The amount dissolved by human and rabbit macrophages was similar; on average 43.1% and 43.9%, respectively, were dissolved within three days. But rabbit and human macrophages dissolved significantly more Mn than was dissolved in the respective culture medium without macrophages after one and three days. It is suggested that the dissolution of particles by alveolar macrophages should be one basic component in any model of alveolar clearance of inorganic particles.

Adult↗
PubMed1984

Lysozyme levels in rabbit lung after inhalation of nickel, cadmium, cobalt, and copper chlorides.

Groups of rabbits were exposed to chlorides of nickel, cadmium, copper, and cobalt at concentrations ranging from 0.2 to 0.6 mg/m3 (as metal) for 4-6 weeks (5 days/week, 6 hr/day). Activity of lysozyme (muramidase) in lavage fluid, in alveolar macrophages, and in culture medium from macrophages incubated at 37 degrees C for 1 and 20 hr was estimated using the lyso-plate technique, agar plates with heat-killed Micrococcus lysodeikticus. In the nickel-exposed rabbits lysozyme activity in the mucous membrane from the left main bronchus was also estimated. Following nickel exposure the lysozyme level was significantly decreased in lavage fluid, macrophages, and in culture medium from incubated macrophages but remained unchanged in the mucous membrane. After exposure to cadmium, copper, and cobalt, lysozyme levels increased or were unchanged.

Animals↗
PubMed1984

Ability of rabbit alveolar macrophages to dissolve metals.

Manganese dioxide particles, 0.1-0.5 micron, were added to samples of 2-3 X 10(6) rabbit alveolar macrophages. The amount of manganese added and dissolved from the particles, over periods of 0, 1, 3, and 5 days, was determined by flame atomic absorption spectrophotometry. Macrophages from six rabbits received about 10 micrograms of Mn, macrophages from two rabbits about 30 micrograms, and macrophages from another two rabbits about 100 micrograms. Over periods of 1, 3, and 5 days the macrophages in all three dose groups dissolved two to three times more Mn than was dissolved in control experiments. In control experiments solubility was studied in the medium without macrophages. Macrophages cultivated 3 days before the addition of MnO2 dissolved the particles within another 2 days to an extent similar to that in the control experiments. The ability of the macrophages to dissolve MnO2 particles might be related to the low pH values in the phagosomes. Studies of the ability of macrophages from various species to dissolve metal particles as well as of pH values in their phagosomes might lead to a better understanding of alveolar clearance of metal particles.

Animals↗
PubMed1984

Toxicology of nickel.

Rabbits were exposed to low levels of airborne metals for 1-8 months, 5 days/week, 6 hours/day. After exposure, lung tissue was examined by light and electron microscopy. Macrophages lavaged from the left lung were examined morphologically and functionally. Phospholipids were analysed in lung tissue or lavage fluid. Metallic nickel dust, 0.1-1 mg/m3, affected alveolar macrophages, alveolar epithelial type II cells and phospholipids. In the lung tissue, nodular accumulation of macrophages was seen, and the volume density of alveolar type II cells was elevated. The amount of phospholipids was markedly increased, mainly due to an increase in disaturated phosphatidylcholines. After 1 month of exposure the macrophages appeared active. After 3 months they appeared 'overfed' and inactive. Metallic iron, chromium and cobalt did not produce the same effects as nickel. Exposure to 0.2 mg/m3 soluble nickel as nickel chloride produced almost identical effects to those of metallic nickel, indicating that the effect of the metallic nickel particles was caused by nickel ions. Exposure to cadmium chloride produced nearly all the effects produced by nickel chloride. However, cadmium chloride increased the level of lysozyme in the macrophages whereas nickel chloride decreased it. Cadmium chloride also produced interstitial alveolitis and cytoplasmic blebs on the surface of the macrophages. Cobalt chloride affected the growth of the type II cells, which formed nodules, but did not seem to affect the production of surfactant material by those cells. Copper chloride produced no effect apart from a slight increase in volume density of the type II cells. Thus, of four divalent metal ions, three (Ni2+, Cd2+ and Co2+) in similar concentrations in the inhaled air produced clear but different pathological effects in the lungs.

Animals↗
PubMed1978

Alveolar macrophage function in nickel dust exposed rabbits.

8 rabbits were exposed to metallic nickel dust (2 mg/m3, of which about half was respirable) for 4 weeks. The lungs were lavaged and the macrophages were collected. In comparison with 8 control rabbits, a significant increase was noted in the nickel exposed rabbits as concerned the weight and density of the lungs, the size variation of the lung cells, the phagocytosis of silver coated particles, and the metabolic activity as measured by NBT reduction. The last mentioned increase was recorded during basal conditions as well as during phagocytosis. The NBT reduction during phagocytosis was significantly correlated with the degree of phagocytosis of silver coated particles in both control and exposed rabbits. It is suggested that the exposure to nickel dust has unspecifically activated the macrophages perhaps by increased production of phospholipids.

Animals↗
PubMedDate not supplied

Decreased level of lysozyme in rabbit lung lavage fluid after inhalation of low nickel concentrations.

Six rabbits were exposed for 4 months (5 days/week, 6 h/day) and 6 rabbits for 8 months to approx. 0.1 mg/m3 of metallic nickel dust (U.S. threshold limit value (TLV) 1 mg/m3). Another 8 rabbits were exposed for 4-6 weeks (5 days/week, 6 h/day) to 0.3 mg/m3 (as Ni) of nickel chloride (U.S. TLV 0.1 mg/m3). After exposure lungs were lavaged. Concentration of lysozyme in the lavage fluid was estimated with the lyso-plate technique (agar plates with heat-killed Micrococcus lysodeikticus) after macrophages had been removed. All 3 exposed groups had markedly lower concentrations of lysozyme than corresponding controls. Mean values in controls and exposed rabbits were: for 4 months metallic nickel dust exposure 2.3 and less than or equal to 0.04 microgram/ml; for 8 months metallic nickel dust exposure 1.4 and less than or equal to 0.5 microgram/ml; and for nickel chloride exposure 1.9 and less than or equal to 0.4 microgram/ml.

Animals↗
PubMedDate not supplied

Lung clearance of 4-micron particles coated with silver, carbon, or beryllium.

Lung clearance in rabbits during the first week after inhalation of 4-micron teflon particles tagged with chromium-51 and coated with silver, carbon, or beryllium was studied by external measurements of the radioactivity in the lungs. Ten rabbits were exposed to silver- and carbon-coated particles on two separate occasions within 3 weeks. Clearances of the two types of particles were quite similar. Clearance in eight other rabbits that had inhaled silver-coated particles was quite similar to clearance in eight rabbits that had inhaled beryllium-coated particles. The result is regarded as evidence that alveolar macrophages do not play an active role in removing intact particles from the lung the first week after inhalation.

Animals↗