TY - JOUR
T1 - Involvement of oxidative stress in hydroquinone-induced cytotoxicity in catalase-deficient Escherichia coli mutants
AU - Horita, Masako
AU - Wang, Da Hong
AU - Tsutsui, Ken
AU - Sano, Kuniaki
AU - Masuoka, Noriyoshi
AU - Kira, Shohei
N1 - Funding Information:
We would like to express our gratitude to Dr P.C. Loewen for kindly supplying bacterial strain UM255 and to Y. Ueno and M. Kawasaki for their assistance. This work was supported by Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture of Japan (No. 14570299).
PY - 2005/10
Y1 - 2005/10
N2 - Hydroquinone is a benzene-derived metabolite. To clarify whether the reactive oxygen species (ROS) are involved in hydroquinone-induced cytotoxicity, we constructed transformants of Escherichia coli (E. coli) strains that express mammalian catalase gene derived from catalase mutant mice (Csb, Csc) and the wild-type (Csa) using a catalase-deficient E. coli UM255 as a recipient. Specific catalase activities of these tester strains were in order of Csa > Csc > Csb > UM255, and their susceptibility to hydrogen peroxide (H2O2) showed UM255 > Csb > Csc > Csa. We found that hydroquinone exposure reduced the survival of catalase-deficient E. coli mutants in a dose-dependent manner significantly, especially in the strains with lower catalase activities. Hydroquinone toxicity was also confirmed using zone of inhibition test, in which UM255 was the most susceptible, showing the largest zone of growth inhibition, followed by Csb, Csc and Csa. Furthermore, we found that hydroquinone-induced cell damage was inhibited by the pretreatment of catalase, ascorbic acid, dimethyl sulfoxide (DMSO), and ethylenediaminetetraacetic acid (EDTA), and augmented by superoxide dismutase (both CuZnSOD and MnSOD). The present results suggest that H2O2 is probably involved in hydroquinone-induced cytotoxicity in catalase-deficient E. coli mutants and catalase plays an important role in protection of the cells against hydroquinone toxicity.
AB - Hydroquinone is a benzene-derived metabolite. To clarify whether the reactive oxygen species (ROS) are involved in hydroquinone-induced cytotoxicity, we constructed transformants of Escherichia coli (E. coli) strains that express mammalian catalase gene derived from catalase mutant mice (Csb, Csc) and the wild-type (Csa) using a catalase-deficient E. coli UM255 as a recipient. Specific catalase activities of these tester strains were in order of Csa > Csc > Csb > UM255, and their susceptibility to hydrogen peroxide (H2O2) showed UM255 > Csb > Csc > Csa. We found that hydroquinone exposure reduced the survival of catalase-deficient E. coli mutants in a dose-dependent manner significantly, especially in the strains with lower catalase activities. Hydroquinone toxicity was also confirmed using zone of inhibition test, in which UM255 was the most susceptible, showing the largest zone of growth inhibition, followed by Csb, Csc and Csa. Furthermore, we found that hydroquinone-induced cell damage was inhibited by the pretreatment of catalase, ascorbic acid, dimethyl sulfoxide (DMSO), and ethylenediaminetetraacetic acid (EDTA), and augmented by superoxide dismutase (both CuZnSOD and MnSOD). The present results suggest that H2O2 is probably involved in hydroquinone-induced cytotoxicity in catalase-deficient E. coli mutants and catalase plays an important role in protection of the cells against hydroquinone toxicity.
KW - Catalase
KW - Catalase-deficient E. coli mutants
KW - Hydrogen peroxide
KW - Hydroquinone
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U2 - 10.1080/10715760500232008
DO - 10.1080/10715760500232008
M3 - Article
C2 - 16298729
AN - SCOPUS:25444452416
SN - 1071-5762
VL - 39
SP - 1035
EP - 1041
JO - Free Radical Research
JF - Free Radical Research
IS - 10
ER -