This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Johnson, N. A.
Right arrow Articles by Fletcher, H. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Johnson, N. A.
Right arrow Articles by Fletcher, H. M.

 Previous Article  |  Next Article 

Journal of Bacteriology, November 2004, p. 7697-7703, Vol. 186, No. 22
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.22.7697-7703.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

8-Oxo-7,8-Dihydroguanine Is Removed by a Nucleotide Excision Repair-Like Mechanism in Porphyromonas gingivalis W83

N. A. Johnson,* R. McKenzie, L. McLean, L. C. Sowers, and H. M. Fletcher

Department of Biochemistry and Microbiology, School of Medicine, Loma Linda University, Loma Linda, California

Received 10 June 2004/ Accepted 17 August 2004

A consequence of oxidative stress is DNA damage. The survival of Porphyromonas gingivalis in the inflammatory microenvironment of the periodontal pocket requires an ability to overcome oxidative stress caused by reactive oxygen species (ROS). 8-Oxo-7,8-dihydroguanine (8-oxoG) is typical of oxidative damage induced by ROS. There is no information on the presence of 8-oxoG in P. gingivalis under oxidative stress conditions or on a putative mechanism for its repair. High-pressure liquid chromatography with electrochemical detection analysis of chromosomal DNA revealed higher levels of 8-oxoG in P. gingivalis FLL92, a nonpigmented isogenic mutant, than in the wild-type strain. 8-OxoG repair activity was also increased in cell extracts from P. gingivalis FLL92 compared to those from the parent strain. Enzymatic removal of 8-oxoG was catalyzed by a nucleotide excision repair (NER)-like mechanism rather than the base excision repair (BER) observed in Escherichia coli. In addition, in comparison with other anaerobic periodontal pathogens, the removal of 8-oxoG was unique to P. gingivalis. Taken together, the increased 8-oxoG levels in P. gingivalis FLL92 could further support a role for the hemin layer as a unique mechanism in oxidative stress resistance in this organism. In addition, this is the first observation of an NER-like mechanism as the major mechanism for removal of 8-oxoG in P. gingivalis.


* Corresponding author. Mailing address: Department of Biochemistry and Microbiology, School of Medicine, Loma Linda University, Loma Linda, CA 92350. Phone: (909) 558-1000, ext. 44472. Fax: (909) 558-4035. E-mail: NJOHNSON03b{at}SOM.LLU.EDU.


Journal of Bacteriology, November 2004, p. 7697-7703, Vol. 186, No. 22
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.22.7697-7703.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Henry, L. G., Sandberg, L., Zhang, K., Fletcher, H. M. (2008). DNA Repair of 8-Oxo-7,8-Dihydroguanine Lesions in Porphyromonas gingivalis. J. Bacteriol. 190: 7985-7993 [Abstract] [Full Text]