Effect of environmental particulates on cultured human and bovine endothelium. Cellular injury via an oxidant-dependent pathway

Journal Article · Sat Jul 01 00:00:00 EDT 1989 · Laboratory Investigation; (USA)

OSTI ID:5598511

Garcia, J G; Dodson, R F; Callahan, K S ^[1]

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1. Univ. of Texas Health Center, Tyler

The effects of respirable environmental fibers on cultures of human umbilical vein and bovine pulmonary artery endothelial cell monolayers were studied. Interaction among endothelial cell monolayers and amosite and chrysotile asbestos, attapulgite, fiberglass, or latex beads resulted in rapid phagocytosis of the particulates. A gradient of time-dependent and concentration-dependent endothelial cell injury (measured by specific 51Cr release) was observed with amosite and attapulgite being markedly toxic. Chrysotile and fiberglass were much less toxic, and latex beads were not significantly injurious at any time or dose examined. Responses of bovine pulmonary artery and human endothelial vein endothelial cells to fiber phagocytosis and fiber-induced injury were similar. In human umbilical cell monolayers, fiber-mediated stimulation of the arachidonate metabolite prostacyclin paralleled endothelial cell injury; i.e. amosite and attapulgite were stimulatory, whereas fiberglass (0-500 micrograms/ml) and latex beads (10(9) beads/ml) did not significantly increase prostacyclin generation. Although chrysotile was only weakly cytotoxic, significant stimulation of prostacyclin was observed at the highest dose tested (500 micrograms/ml). To investigate whether toxic oxygen species may be involved in fiber-induced cytotoxicity, oxidant scavengers or inhibitors were used in injury studies. Both superoxide dismutase (a scavenger of O2-) and catalase (an inhibitor of H2O2) produced significant protection against fiber-mediated endothelial cell injury. In addition, chelation by deferoxamine of elemental Fe present in the fiber preparations was also protective, suggesting Fe, via the modified Haber-Weiss reaction, may promote hydroxyl radical formation and contribute to endothelial cell injury induced by these particulates.

• OSTI ID: 5598511
• Journal Information: Laboratory Investigation; (USA), Vol. 61:1; ISSN 0023-6837
• Country of Publication: United States
• Language: English

Related Subjects

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
59 BASIC BIOLOGICAL SCIENCES
ASBESTOS
TOXICITY
ENDOTHELIUM
PATHOLOGICAL CHANGES
FIBERGLASS
PARTICULATES
BIOLOGICAL PATHWAYS
CATALASE
CATTLE
CELL CULTURES
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BETA DECAY RADIOISOTOPES
BLOOD VESSELS
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CARDIOVASCULAR SYSTEM
CHROMIUM ISOTOPES
DOMESTIC ANIMALS
ELECTRON CAPTURE RADIOISOTOPES
ELEMENTS
ENZYMES
EVEN-ODD NUCLEI
INTERMEDIATE MASS NUCLEI
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MAMMALS
METALS
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NONMETALS
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OXIDOREDUCTASES
PARTICLES
PEROXIDASES
PRIMATES
RADIOISOTOPES
RUMINANTS
TISSUES
TRANSITION ELEMENTS
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