Hemolysis by asbestos

Harington, J. S.; Miller, K.; Macnab, G M

doi:10.1016/0013-9351(71)90038-7

Cited by 180 publications

(45 citation statements)

References 25 publications

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“…Amphiboles and chrysotile differ in their ability to impair the integrity ofisolated membranes, the former being much less hemolytic than the latter, whose magnesium but not silicon content bore a linear relationship with the degree of lysis (27). The activity ofchrysotile evidently depended at least in part on its outer layer ofmagnesium hydroxide, since removal by acid leaching exerted a depressive effect (174), as did nonspecific chelation of metal ions by sodium ethylenediaminetetraacetate (27), though silica does not require magnesium for lysis. Because it lacks a hydrogen bond, PNO afforded minimal protection.…”

Section: Mechanisms Of Fibrogenesismentioning

confidence: 99%

“…In consequence clustering of surface proteins occurred with the formation of ionic-sized gaps (as with silica), which led to disturbance of Na and K balance and osmotic rupture (177). Removal of red cell sialic acid residues by neuraminidase reduced the lytic effect ofchrysotile (27), but though crocidolite also bound to red cells its distorting effect was not thereby abolished and the fiber's negative charge could instead become attached to oppositely charged groups on phospholipids or proteins (177).…”

Section: Mechanisms Of Fibrogenesismentioning

confidence: 99%

“…The formation ofH-bonded complexes, notably with phospholipids ofcell membranes, through hydrogen donation by polymeric silicic acid, was considered to mediate silica toxicity (26). Hemolysis was much reduced by the polymer polyvinylpyridine-N-oxide (PNO) (27), which was known to inhibit both cell damage by quartz in culture and experimental silicosis. PNO might thus establish H-bonds preferentially with silicic acid and so preserve cell membranes, but the polymer may also accumulate on the surface of quartz particles to present a simple barrier (28).…”

Section: Introductionmentioning

confidence: 99%

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Minerals, Fibrosis, and the Lung

Heppleston¹

1991

Environmental Health Perspectives

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Section: Mechanisms Of Fibrogenesismentioning

confidence: 99%

Section: Mechanisms Of Fibrogenesismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Minerals, Fibrosis, and the Lung

Heppleston¹

1991

Environmental Health Perspectives

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“…The mechanisms of asbestos-induced cytotoxicity were first explored in red blood cells (5) and later in cell cultures and tissues from the respiratory tract maintained in culture. A recent volume addresses toxicity of asbestos in detail (6).…”

Section: Studies On Cytotoxicity Of Asbestos and Nonasbestos Fibersmentioning

confidence: 99%

In vitro studies on the biologic effects of fibers: correlation with in vivo bioassays.

Mossman

1990

Environ Health Perspect

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In vitro studies employing organ cultures, primary cell cultures, cell lines, and bacterial systems have been used to assess the toxicity, mutagenicity, and carcinogenic potential of asbestos and nonasbestos fibers. These experiments have been useful in defining mechanisms contributing to the causation of fiber-associated lung diseases. Long (greater than 8 microns), thin asbestos fibers are more active in vitro than short (less than or equal to 2 microns) fibers or nonfibrous particles, an observation supporting the importance of fiber dimension in disease. Although in vitro bioassays cannot evaluate characteristics such as clearance and/or durability of fibers which may be critical determinants of fiber toxicity in lung, they can be used both to address dosimetry at the cellular level (i.e., number of fibers per cell that elicit a measurable biologic end point) and to evaluate preventive approaches to fiber-induced cell injury. Development of in vitro models employing target cells of the lung, i.e., mesothelial cells, tracheobronchial epithelial cells, and lung fibroblasts, as well as carefully characterized preparations of fibers and particles, will be necessary to evaluate whether in vitro bioassays are amenable to predicting the pathogenic potential of synthetic and naturally occurring fibers comparatively.

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“…It is known through the work of Harington et al (2)(3)(4) that the lytic property of chrysotile can be inhibited by serum proteins, phosphate ions, and the chelating action of ethylenediaminetetraacetic acid (ED-TA). Schnitzer and Pundsack (5) first showed the marked antagonism of polyanions in chrysotile hemolysis and pointed out the specificity of this reaction, which is generally limited to asbestos.…”

Section: Introductionmentioning

confidence: 99%

Modification of biological surface activity of particles

Schnitzer¹

1974

Environ Health Perspect

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The hemolytic activity of fibrous asbestos varieties and of fibrous or granular silica dust can be markedly reduced by adsorption of polymers. Polyanions exert a specific action on asbestos, particularly chrysotile, whereas silica is inactivated by nonionic polymers. A high degree of reduction of the lytic action by comparatively small amounts of the antagonistic polymers can be demonstrated after short exposure to concentrations of 0.1-0.4 mg/ml of appropriate polymers. Inactivation is based on stable adsorption. Repeated washings of inactivated mineral sediments or exposure to elevated temperatures (80-1200C) produced no essential loss of the reduction of lytic potency. In one example, inactivation of chrysotile by sodium alginate, depolymerization by ascorbic acid was also ineffective.

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Hemolysis by asbestos

Cited by 180 publications

References 25 publications

Minerals, Fibrosis, and the Lung

Minerals, Fibrosis, and the Lung

In vitro studies on the biologic effects of fibers: correlation with in vivo bioassays.

Modification of biological surface activity of particles

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