[CD59 mutation and DNA oxidative damage in A(L) cells induced by crocidolite fibers].
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
; 22(1): 43-6, 2004 Feb.
Article
en Zh
| MEDLINE
| ID: mdl-15033018
OBJECTIVE: To determine the effects of buthionine sulfoximine (BSO) and free radical scavenger, dimethyl sulfoxide (DMSO), on mutation frequency and the formation of 8-hydroxydeoxyganosine (8-OHdG) induced by crocidolite fibers in human-hamster hybrid (A(L)) cells. METHODS: The cytotoxicity and mutagenicity were determined by the formation of colonies. 8-OHdG was examined by immunoperoxidase staining. Non-protein sulfhydryl (NPSH) compound was assayed by modified Tietze's method. RESULTS: The level of NPSH in A(L) cell pretreated with 25 micro mol/L of BSO was decreased to 2 nmol/10(7) cells, only 5% of the control after 24 h. The mutation frequency of CD59 gene of A(L) cell in crocidolite alone treated group was 208 +/- 18 while that in BSO pretreated group (397 +/- 55) was about twice the former (P < 0.05). The mutation frequency of CD59 gene in the group treated with crocidolite and in the presence of DMSO (57 +/- 8) was 72.6% less than that in crocidolite alone treated group. Crocidolite fibers induced a dose-effect relationship in the formation of 8-OHdG in A(L) cells (y = 150 + 20x, r = 0.9621). The level of 8-OHdG in cells was 289 +/- 6 at the dose of 6 micro g/cm(2) crocidolite, which was about twice the control group (137 +/- 9). In the presence of DMSO, 8-OHdG level decreased to 170 +/- 3 at the same dose of crocidolite. CONCLUSION: Free radicals are the important inducer of mutagenesis and DNA damage in A(L) cells caused by crocidolite, which has dose-effect relationship.
Buscar en Google
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
ADN
/
Asbesto Crocidolita
/
Antígenos CD59
/
Desoxiguanosina
/
Mutación
Límite:
Animals
/
Humans
Idioma:
Zh
Revista:
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
Asunto de la revista:
MEDICINA OCUPACIONAL
Año:
2004
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
China