Formation of oxy radicals by oxygen reduction arising from the surface activity of asbestos

Zalma, Roger; Bonneau, L.; Guignard, J.; Pézerat, H.; Jaurand, Marie-Claude

doi:10.1139/v87-390

Cited by 109 publications

(54 citation statements)

References 11 publications

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“…Using cell-free systems, Weitzman and Graceffa (11) showed that a variety of asbestos types can act as catalytic substrates for hydroxyl and superoxide radical generation, apparently from hydrogen peroxide molecules. More recently, Zalma et al (12) published similar studies on oxygen reduction leading to formation of reactive oxygen radicals on asbestos surfaces. The supposition then is that these radicals will injure pulmonary cells and somehow are involved in fibrogenic and possibly carcinogenic (13) mechanisms.…”

Section: Introductionmentioning

confidence: 93%

Asbestos-induced lung disease.

Brody

1993

Environ Health Perspect

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This review attempts to deal with two major questions concerning asbestos-induced lung disease: How does inhaled asbestos cause cell proliferation and fibrosis? and Will there continue to be risk from exposure to asbestos in schools and public buildings? The first is a scientific question that has spawned many interesting new experiments over the past 10 years, and there appear to be two hypothetical schemes which could explain, at least in part, the fibroproliferative effects of asbestos fibers. One supports the view that toxic oxygen radicals generated on fiber surfaces and/or intracellularly are the central mediators of disease. The second hypothesis is not mutually exclusive of the first, but, in my opinion, may be integral to it, i.e., the cellular injury induced by oxygen radicals stimulates the elaboration ofmultiple varieties of growth factors and cytokines that mediate the pathogenesis of asbestosis. There is increasing evidence that molecules such as platelet-derived growth factor and transforming growth factor i, both synthesized and secreted by activated lung macrophages, are responsible, respectively, for the increased interstitial cell populations and extracellular matrix proteins that are the hallmarks of asbestos-induced fibrosis. The challenge today is to establish which combinations of the many factors released actually are playing a role in disease pathogenesis. The issue of continued risk currently is more a question of policy and perception than science because a sufficient database has not yet been established to allow full knowledge ofthe circumstances under which asbestos in buiMingsconstitutes an ongoing health hazard. The litigious nature of this question does not help its resolution. In as much as public policy statements and risk assessment are not within my purview, I have focused on the state-of-the-art ofasbestos as a complete carcinogen. It appears tobe generaily nongenotoxic, but all asbestos fiber types can induce chromosomal mutations and aneuploidy, perhaps through their ability to disrupt normal chromosome segregation.

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Section: Introductionmentioning

confidence: 93%

Asbestos-induced lung disease.

Brody

1993

Environ Health Perspect

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“…However, contradictory data suggested that nitric oxide is either protective or cytotoxic in acute and chronic phase of inflammatory response, modulation of cytostasis, cell growth and differentiation 29) . Extracellular mechanism of ROS generation is also important with respect to various free radicals formed by interaction of asbestos fibers in cell-free solutions of H 2 O 2 or physiological saline generate superoxide radicals by redox reactions on the fiber surface [31][32][33] .…”

Section: Generation and Release Of Reactive Oxygen Species (Ros) Frommentioning

confidence: 99%

In Vitro Studies on Biological Effects of Fibrous Minerals.

Ishihara

2001

INDUSTRIAL HEALTH

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Asbestos substitutes have been used recently in industrial various applications. Since certain asbestos substitutes have similar characteristics of asbestos, they require urgent in vitro and in vivo evaluation of these asbestos substitutes prior to occupational applications. Though in vitro studies do not offer precise assessment of toxicity of the fibers, it is possible to provide useful information as to the biological effects of asbestos and its substitutes. This review articles described the findings of in vitro experiments in investigation of biological effects of asbestos and man made mineral fibers (MMMF) and their correlation with in vivo assays; 1. Cytotoxicity, geometry and dimension of fibers. 2. In vitro biological effects of fibers on a mass basis and a numerical basis. 3. Mechanism of cytotoxicity, carcinogenecity and cell proliferation including in vitro cytokines production. The relationships between the in vitro and the in vivo biological effects of fibers do not always coincide. Therefore, safety of the fibers must be assessed in both in vivo and in vitro using an inert fiber as negative control. Additionally, evaluation of safety of these fibers in vitro must be conducted in comparable concentrations, sizes and numbers of fibers for used in in vivo experiments.

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“…Under these circumstances, asbestos-induced cell death is ameliorated. Extracellular mechanisms may also be important in the generation of AOS by asbestos as asbestos fibers in cell-free solutions of H202 or physiological saline generate superoxide (07 and hydroxyl (OH') radicals by redox reactions occurring on the fiber surface (16)(17)(18). Recently, the generation of AOS has been reported by rockwool and glass fibers (19).…”

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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Formation of oxy radicals by oxygen reduction arising from the surface activity of asbestos

Cited by 109 publications

References 11 publications

Asbestos-induced lung disease.

Asbestos-induced lung disease.

In Vitro Studies on Biological Effects of Fibrous Minerals.

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

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