DNA damage and repair in human lymphocytes and gastric mucosa cells exposed to chromium and curcumin

Citation
J. Blasiak et al., DNA damage and repair in human lymphocytes and gastric mucosa cells exposed to chromium and curcumin, TER CAR MUT, 19(1), 1999, pp. 19-31
Citations number
46
Categorie Soggetti
Pharmacology & Toxicology
Journal title
TERATOGENESIS CARCINOGENESIS AND MUTAGENESIS
ISSN journal
02703211 → ACNP
Volume
19
Issue
1
Year of publication
1999
Pages
19 - 31
Database
ISI
SICI code
0270-3211(1999)19:1<19:DDARIH>2.0.ZU;2-K
Abstract
Human population can be considered as a subject of combined exposure to che micals. Hexavalent chromium is a well-known mutagen and carcinogen. Curcumi n, a popular spice and pigment, is reported to have antineoplastic properti es. The single cell gel electrophoresis (Comet assay) is a sensitive techni que that allows detecting double- and single-strand DNA breaks caused by a broad spectrum of mutagens. In the present work the ability of curcumin to reduce DNA damage induced by chromium in human lymphocytes and gastric muco sa (GM) cells was investigated by using the comet assay. Chromium at 500 mu M evoked DNA damage measured as significant (P < 0.001), about a two-fold increase in comet tail moment of both lymphocytes and GM cells. Curcumin at 10, 25, and 50 mu M also damaged DNA of both types of cells in a dose-depe ndent manner: the increase in the tail moment reached about twenty times of the control value (P < 0.001). The combined action of chromium at 500 mu M and curcumin at 50 mu M resulted in the significant (P < 0.001) increase i n the comet tail moment of both types of cells. In each case, treated cells were able to recover within 60 min. Our study clearly demonstrates that cu rcumin does not inhibit DNA damaging action of hexavalent chromium in human lymphocytes and GM cells. Moreover, curcumin itself can damage DNA of thes e cells and the total effect of chromium and curcumin is additive. Further studies are needed to establish the role of interaction of curcumin with DN A in carcinogenesis. (C) 1999 Wiley-Liss, Inc.