Journal Article

Induction of heme oxygenase in mammalian cells by mineral fibers: distinctive effect of reactive oxygen species

Keiji Suzuki and Tom K. Hei

in Carcinogenesis

Volume 17, issue 4, pages 661-667
Published in print April 1996 | ISSN: 0143-3334
Published online April 1996 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/17.4.661
Induction of heme oxygenase in mammalian cells by mineral fibers:
                    distinctive effect of reactive oxygen species

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Exponentially growing human-hamster hybrid [AL] cells treated with a 40 μg/ml (8μ/cm2) dose of UICC standard reference chrysotile fibers induced heme oxygenase (HO) protein with a maximum expression level at 8 h post-treatment. While the constitutive HO expression was detectable in non-treated AL cells, the protein level was increased ∼4.5-fold in fiber-treated cells. The induction was dose-dependent at fiber concentration between 2.5 μg/ml (0.5 μg/cm2) and 40 μg/ml (8μg/cm2) with the induced HO concentrated mostly in the cytoplasm as shown by immunostaining. Several other types of mineral fibers examined including crocidolites, tremolites, and erionites also induced HO synthesis with varying degree of efficiency. In general, chrysotile and crocidolite were more efficient inducers of HO than tremolite and erionite when compared at fiber doses that resulted in∼50% survival (LD50) level. The effects of antioxidant enzymes on HO induction were examined by concurrent treatment of fiber-exposed cultures with SOD and catalase. Although addition ofsuperoxide dismutase (SOD) and catalase inhibited HO induction in a dose-dependent manner, they offered no protection on fiber-mediated clonogenic toxicity in the same population of treated cells. These results suggest that reactive oxygen species (ROS) produced by asbestos fibers play an essential role in the induction of HO and that different mineral fibers, when applied at equitoxic doses, often result in different oxidative stress status as determined by the induction of HO proteins.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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