Fibre-induced lipid peroxidation leads to DNA adduct formation in <i>Salmonella typhimurium</i> TA104 and rat lung fibroblasts

Howden, Peter J.; Faux, Stephen P.

doi:10.1093/carcin/17.3.413

Cited by 44 publications

(21 citation statements)

References 23 publications

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“…23 Asbestos-associated iron causes DNA strand breaks, 2 increased DNA oxidation in the form of 8OH2dG, 2 as well as lipid peroxidation. 3 Ghio and Stonehuerner 33 have shown in vitro direct oxidation and subsequent activation of complement protein (C5) by crocidolite asbestos in a concentration-dependent manner. Here, we examined the potential oxidative activation of TGF-b 1 by both crocidolite and chrysotile asbestos.…”

Section: Discussionmentioning

confidence: 99%

“…These ROS are formed indirectly through macrophage and inflammatory cell stimulation and directly on the alveolar surfaces through Fenton reactions catalyzed by the iron content of the asbestos. 1 ROS have been demonstrated to contribute to asbestos-induced alveolar cell injury and carcinogenesis through generation of DNA strand breaks, 2 lipid peroxidation 3 and apoptosis. 1 These cytotoxic and fibrogenic effects can be decreased through the use of antioxidants 4 and through the treatment of asbestos with iron-chelating agents.…”

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confidence: 99%

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Asbestos-derived reactive oxygen species activate TGF-β1

Pociask

Sime

Brody

2004

Laboratory Investigation

133

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Transforming growth factor-beta 1 (TGF-b 1 ) is a potent peptide that inhibits epithelial and mesenchymal cell proliferation and stimulates the synthesis of extracellular matrix components. This cytokine is produced in a biologically latent complex bound to a latent-associated peptide (LAP), and it is the disassociation of this complex that regulates TGF-b activity. A number of mechanisms have been shown to activate TGF-b 1 . We show here that reactive oxygen species (ROS), generated by the iron in chrysotile or crocidolite asbestos, mediate the biological activity of TGF-b 1 . Recombinant human latent TGF-b 1 was activated in a cell free system in the presence of asbestos and ascorbic acid. Latent TGF-b 1 was overexpressed in both A549 and mink lung epithelial cell lines through an adenovirus vector containing the full-length construct for porcine TGF-b 1 . This latent TGF-b 1 was activated in a concentration-dependant fashion by introducing asbestos into the cell cultures. This activation was reduced significantly through the use of superoxide dismutase, catalase or deferoxamine. Amino-acid constituents of the LAP were oxidized as demonstrated by the appearance of carbonyls detected by Western analysis. The oxidized LAP could no longer form a complex with TGF-b 1 . Our data support the postulate that ROS derived from asbestos provide a mechanism for activating TGF-b 1 in the alveolar environment by oxidizing amino acids in LAP.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Asbestos-derived reactive oxygen species activate TGF-β1

Pociask

Sime

Brody

2004

Laboratory Investigation

133

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“…It has been recently demonstrated that the OH formed is able to produce 8-OHdG in DNA both in cell-free systems using plasmid or calf thymus DNA or after incubation of mammalian cells with the fibers. (50,61). However, in some experiments, the experimental conditions included the addition of H202 (61), which enhances the sensitivity of the assay.…”

Section: Chromosome Damagementioning

confidence: 99%

“…(50,61). However, in some experiments, the experimental conditions included the addition of H202 (61), which enhances the sensitivity of the assay. The nature of the incubation medium certainly plays an important role in the generation of ROS, as emphasized by Chao et al (54), who studied DNA damage in culture medium with different iron concentrations.…”

Section: Chromosome Damagementioning

confidence: 99%

Mechanisms of fiber-induced genotoxicity.

Jaurand

1997

Environ Health Perspect

117

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The mechanisms of particle-induced genotoxicity have been investigated mainly with asbestos fibers. The results are summarized and discussed in this paper. DNA damage can be produced by oxidoreduction processes generated by fibers. The extent of damage yield depends on experimental conditions: if iron is present, either on fibers or in the medium, damage is increased. However, iron reactivity does not explain all the results obtained in cell-free systems, as breakage of plasmid DNA was not directly associated with the amount of iron released by the fibers. The proximity of DNA to the site of generation of reactive oxygen species (ROS) is important because these species have an extremely short half-life. Damage to cellular DNA can be produced by oxidoreduction processes that originate from cells during phagocytosis. Secondary molecules that are more stable than ROS are probably involved in DNA damage. Oxidoreduction reactions originating from cells can induce mutations. Genotoxicity is also demonstrated by chromosomal damage associated with impaired mitosis, as evidenced by chromosome missegregation, spindle changes, alteration of cell cycle progression, formation of aneuploid and polyploid cells, and nuclear disruption. In some of these processes, the particle state and fiber dimensions are considered important parameters in the generation of genotoxic effects.

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“…It appears that LFP are generated in all biological systems. Besides several human and animal studies, they were also detected during plant ageing [14][15][16] and even in yeasts 17,18 and bacteria 19 . LFP were extractable to chloroform from various biological membranes.…”

Section: Characterization Of Fluorescent End-productsmentioning

confidence: 98%