Oxidative stress in oral diseases

被引:78
作者
Kesarwala, A. H. [1 ]
Krishna, M. C. [2 ]
Mitchell, J. B. [2 ]
机构
[1] NCI, Canc Res Ctr, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA
[2] NCI, Ctr Canc Res, Radiat Biol Branch, NIH, Bldg 10 CRC,Room B3-B69,10 Ctr Dr, Bethesda, MD 20892 USA
基金
美国国家卫生研究院;
关键词
oxidative species; reactive oxygen species; reactive nitrogen species; cancer; radiation; SQUAMOUS-CELL CARCINOMA; DNA-DAMAGE; SUPEROXIDE-DISMUTASE; LIPID-PEROXIDATION; FREE-RADICALS; NECK-CANCER; MITOCHONDRIAL SUPEROXIDE; NASOPHARYNGEAL CARCINOMA; GENE-EXPRESSION; ARECA NUT;
D O I
10.1111/odi.12300
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Oxidative species, including reactive oxygen species (ROS), are components of normal cellular metabolism and are required for intracellular processes as varied as proliferation, signal transduction, and apoptosis. In the situation of chronic oxidative stress, however, ROS contribute to various pathophysiologies and are involved in multiple stages of carcinogenesis. In head and neck cancers specifically, many common risk factors contribute to carcinogenesis via ROS-based mechanisms, including tobacco, areca quid, alcohol, and viruses. Given their widespread influence on the process of carcinogenesis, ROS and their related pathways are attractive targets for intervention. The effects of radiation therapy, a central component of treatment for nearly all head and neck cancers, can also be altered via interfering with oxidative pathways. These pathways are also relevant to the development of many benign oral diseases. In this review, we outline how ROS contribute to pathophysiology with a focus toward head and neck cancers and benign oral diseases, describing potential targets and pathways for intervention that exploit the role of oxidative species in these pathologic processes.
引用
收藏
页码:9 / 18
页数:10
相关论文
共 109 条
[1]  
Ambrosone CB, 2005, CANCER RES, V65, P1105
[2]   THE CAUSES AND PREVENTION OF CANCER [J].
AMES, BN ;
GOLD, LS ;
WILLETT, WC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (12) :5258-5265
[3]   Mitochondria, oxidants, and aging [J].
Balaban, RS ;
Nemoto, S ;
Finkel, T .
CELL, 2005, 120 (04) :483-495
[4]   Hyperbaric oxygen therapy for late radiation tissue injury [J].
Bennett, Michael H. ;
Feldmeier, John ;
Hampson, Neil ;
Smee, Robert ;
Milross, Christopher .
COCHRANE DATABASE OF SYSTEMATIC REVIEWS, 2012, (05)
[5]   PRIMARY BRAIN-TUMORS IN FISCHER-344 RATS CHRONICALLY EXPOSED TO ACRYLONITRILE IN THEIR DRINKING-WATER [J].
BIGNER, DD ;
BIGNER, SH ;
BURGER, PC ;
SHELBURNE, JD ;
FRIEDMAN, HS .
FOOD AND CHEMICAL TOXICOLOGY, 1986, 24 (02) :129-137
[6]   Nucleo-cytoplasmic shuttling of high risk human Papillomavirus E2 proteins induces apoptosis [J].
Blachon, S ;
Bellanger, S ;
Demeret, C ;
Thierry, G .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (43) :36088-36098
[7]   Transient Alteration of Cellular Redox Buffering before Irradiation Triggers Apoptosis in Head and Neck Carcinoma Stem and Non-Stem Cells [J].
Boivin, Anthony ;
Hanot, Maite ;
Malesys, Celine ;
Maalouf, Mira ;
Rousson, Robert ;
Rodriguez-Lafrasse, Claire ;
Ardail, Dominique .
PLOS ONE, 2011, 6 (01)
[8]   CELLULAR PRODUCTION OF HYDROGEN-PEROXIDE [J].
BOVERIS, A ;
CHANCE, B ;
OSHINO, N .
BIOCHEMICAL JOURNAL, 1972, 128 (03) :617-&
[9]   Biochemistry and molecular cell biology of diabetic complications [J].
Brownlee, M .
NATURE, 2001, 414 (6865) :813-820
[10]   Nitric oxide, lipid peroxidation and antioxidant defence system in patients with active or inactive Behcet's disease [J].
Buldanlioglu, S ;
Turkmen, S ;
Ayabakan, HB ;
Yenice, N ;
Vardar, M ;
Dogan, S ;
Mercan, E .
BRITISH JOURNAL OF DERMATOLOGY, 2005, 153 (03) :526-530