Journal article
Nitric oxide-induced resistance to hydrogen peroxide stress is a glutamate cysteine ligase activity-dependent process
Free radical biology & medicine, Vol.38(10), pp.1361-1371
2005
DOI: 10.1016/j.freeradbiomed.2005.01.023
PMID: 15855054
Abstract
Nitric oxide (
NO) is a reactive nitrogen species known to be involved in cytotoxic processes. Cells respond to cytotoxic injury by stress response induction leading to the development of cellular resistance. This report describes an
NO-induced stress response in Chinese hamster fibroblasts (HA1), which leads to glutathione synthesis-dependent resistance to H
2O
2-mediated oxidative stress. The development of resistance to H
2O
2 was completely abolished by the inhibition of glutamate cysteine ligase (GCL) during the first 8 h of recovery after
NO exposure. Altered thiol metabolism was observed immediately after
NO exposure as demonstrated by up to 75% decrease in intracellular thiol pools (glutathione, γ-glutamylcysteine, and cysteine), which then reaccumulated during the
NO-mediated development of resistance. Immunoreactive protein and activity associated with GCL decreased immediately after exposure to
NO and then reaccumulated during the development of resistance to H
2O
2 challenge. Moreover, compared to N
2 controls the activity levels of GCL in
NO-exposed cells increased approximately twofold 24 h after H
2O
2 challenge. These results demonstrate that
NO exposure is capable of inducing an adaptive response to H
2O
2-mediated oxidative stress in mammalian cells, which involves alterations in thiol metabolism and is dependent upon glutathione synthesis and increased GCL activity.
Details
- Title: Subtitle
- Nitric oxide-induced resistance to hydrogen peroxide stress is a glutamate cysteine ligase activity-dependent process
- Creators
- Lisa A Ridnour - Division of Radiation and Cancer Biology, Department of Radiation Oncology, Washington University School of Medicine, 4511 Forest Park Boulevard, Room 411, St. Louis, MO 63108, USAJulia E Sim - Division of Radiation and Cancer Biology, Department of Radiation Oncology, Washington University School of Medicine, 4511 Forest Park Boulevard, Room 411, St. Louis, MO 63108, USAJinah Choi - School of Natural Science, University of California at Merced, P.O. Box 2039, Merced, CA 95344, USADale A Dickinson - Department of Environmental Health Sciences, School of Public Health, University of Alabama at Birmingham, 1665 University Boulevard, Ryals 31, Birmingham, AL 35294-0022, USAHenry J Forman - School of Natural Science, University of California at Merced, P.O. Box 2039, Merced, CA 95344, USAIman M Ahmad - Free Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, B180 Medical Labs, University of Iowa, Iowa City, IA 52242, USAMitchell C Coleman - Free Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, B180 Medical Labs, University of Iowa, Iowa City, IA 52242, USAClayton R Hunt - Division of Radiation and Cancer Biology, Department of Radiation Oncology, Washington University School of Medicine, 4511 Forest Park Boulevard, Room 411, St. Louis, MO 63108, USAPrahbat C Goswami - Division of Radiation and Cancer Biology, Department of Radiation Oncology, Washington University School of Medicine, 4511 Forest Park Boulevard, Room 411, St. Louis, MO 63108, USADouglas R Spitz - Division of Radiation and Cancer Biology, Department of Radiation Oncology, Washington University School of Medicine, 4511 Forest Park Boulevard, Room 411, St. Louis, MO 63108, USA
- Resource Type
- Journal article
- Publication Details
- Free radical biology & medicine, Vol.38(10), pp.1361-1371
- DOI
- 10.1016/j.freeradbiomed.2005.01.023
- PMID
- 15855054
- NLM abbreviation
- Free Radic Biol Med
- ISSN
- 0891-5849
- eISSN
- 1873-4596
- Publisher
- Elsevier Inc
- Language
- English
- Date published
- 2005
- Academic Unit
- Pathology; Orthopedics and Rehabilitation; Radiation Oncology
- Record Identifier
- 9984040020402771
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