［1］Buico A, Cassino C, Ravera M, et al. Oxidative stress and total antioxidant capacity in human plasma［J］. Redox Rep, 2009,14(3):125-131.
［2］Perluigi M, Giorgi A, Blarzino C, et al. Proteomics analysis of protein expression and specific protein oxidation in human papillomavirus transformed keratinocytes upon UVB irradiation［J］. J Cell Mol Med, 2008, ［Epub ahead of print］.
［3］Murphy MP. How mitochondria produce reactive oxygen species［J］. Biochem J, 2009,17(1):1-13.
［4］Sedeek M, Hébert RL, Kennedy CR,et al. Molecular mechanisms of hypertension: role of Nox family NADPH oxidases［J］. Curr Opin Nephrol Hypertens, 2009, 18(2):122-127.
［5］Kurosawa T, Nakamura H, Yamaura E, et al. Cytotoxicity induced by inhibition of thioredoxin reductases via multiple signaling pathways: role of cytosolic phospholipase A(2)alpha-dependent and-independent release of arachidonic acid［J］. J Cell Physiol, 2009, 219(3):606-616.
［6］Awda BJ, Mackenzie-Bell M, Buhr MM. Reactive oxygen species and boar sperm function［J］. Biol Reprod, 2009,81(3):553-561.
［7］Valko M, Rhodes CJ, Moncol J, et al. Free radicals, metals and antioxidants in oxidative stress-induced cancer［J］. Chem Biol Interact, 2006, 160(1):1-40.
［8］Valko M, Leibfritz D, Moncol J, et al. Free radicals and antioxidants in normal physiological functions and human disease［J］. Int J Biochem Cell Biol, 2007, 39(1):44-84.
［9］Park EM, Ramnath N, Yang GY, et al. High superoxide dismutase and low glutathione peroxidase activities in red blood cells predict susceptibility of lung cancer patients to radiation pneumonitis［J］. Free Radic Biol Med, 2007, 42(2):280-287.
［10］Karihtala P, Soini Y. Reactive oxygen species and antioxidant mechanisms in human tissues and their relation to malignancies［J］. APMIS, 2007, 115(2):81-103.
［11］Halliwell B. Oxidative stress and cancer: have we moved forward?［J］. Biochem J, 2007, 401(1):1-11.
［12］D'Autréaux B, Toledano MB. ROS as signaling molecules: mechanisms that generate specificity in ROS homeostasis［J］. Nat Rev Mol Cell Biol, 2007, 8(10):813-824.
［13］Ryter SW, Kim HP, Hoetzel A, et al. Mechanisms of cell death in oxidative stress［J］. Antioxid Redox Signal, 2007,9(1): 49-89.
［14］Kostyuk VA, Potapovich AI. Mechanisms of the suppression of free radical overproduction by antioxidants［J］. Front Biosci (Elite Ed), 2009, 1:179-88.
［15］Nicco C, Laurent A, Chereau C, et al. Differential modulation of normal and tumor cell proliferation by reactive oxygen species［J］. Biomed Pharmacother, 2005, 59(4):169-174.
［16］Mizutani H, Tada-Oikawa S, Hiraku Y, et al. Mechanism of apoptosis induced by doxorubicin through the generation of hydrogen peroxide［J］. Life Sci, 2005, 76(13):1439-1453.
 ［17］Kinnula VL, Crapo JD. Superoxide dismutases in malignant cells and human tumors［J］. Free Radic Biol Med, 2004, 36(6):718-744.
［18］Rhee SG. Cell signaling. H2O2, a necessary evil for cell signaling［J］. Science, 2006, 312(5782):1882-1883.
［19］Karawajew L, Rhein P, Czerwony G, et al. Stress-induced activation of the p53 tumor suppressor in leukemia cells and normal lymphocytes requires mitochondrial activity and reactive oxygen species［J］. Blood, 2005, 105(12):4767-4775.
［20］Kipp A, Banning A, Brigelius-Flohe R. Activation of the glutathione peroxidase 2 (GPx2) promoter by beta-catenin［J］. Biol Chem, 2007, 388(10):1027-1033.
［21］Snijders PJ, Steenbergen RD, Heideman DA, et al. HPV-mediated cervical carcinogenesis: concepts and clinical implications［J］. J Pathol, 2006, 208(2):152-164.
［22］Valdespino VM, Valdespino VE. Cervical cancer screening: state of the art［J］. Curr Opin Obstet Gynecol, 2006, 18(1):35-40.
［23］Kapeu AS, Luostarinen T, Jellum E, et al. Is smoking an independent risk factor for invasive cervical cancer? A nested case-control study within Nordic biobanks［J］. Am J Epidemiol, 2009,169(4):480-488.
［24］Vistad I, Kristensen GB, Fossa SD, et al. Intestinal malabsorption in long-term survivors of cervical cancer treated with radiotherapy［J］. Int J Radiat Oncol Biol Phys, 2009, 73(4):1141-1147.
［25］Kim YT, Kim JW, Choi JS, et al. Relation between deranged antioxidant system and cervical neoplasia［J］. Int J Gynecol Cancer, 2004, 14(5):889-895.
［26］Skrazydlewska E, Kozuszko B, Sulkowska M, et al. Antioxidant potential in esophageal, stomach and colorectal cancers［J］.Hepatogastroenterology, 2003, 50(49):126-131.
［27］Le Moan N, Tacnet F, Toledano MB. Protein-thiol oxidation, from single proteins to proteome-wide analyses［J］. Methods Mol Biol, 2008, 476:181-198.
［28］Beevi SS, Rasheed MH, Geetha A. Evidence of oxidative and nitrosative stress in patients with cervical squamous cell carcinoma［J］. Clin Chim Acta, 2007, 375(1-2):119-123.
［29］Chiou JF, Hu ML. Elevated lipid peroxidation and disturbed antioxidant enzyme activities in plasma and erythrocytes of patients with uterine cervicitis and myoma［J］. Clin Biochem, 1999, 32(3):189-192.
［30］Lee GJ, Chung HW, Lee KH, et al. Antioxidant vitamins and lipid peroxidation in patients with cervical intraepithelial neoplasia［J］. J Korean Med Sci, 2005, 20(2):267-272.
［31］Hofseth LJ, Hussain SP, Wogan GN, et al. Nitric oxide in cancer and chemoprevention［J］. Free Radic Biol Med, 2003, 34(8):955-968.
［32］Chen HH, Su WC, Chou CY, et al. Increased expression of nitric oxide synthase and cyclooxygenase-2 is associated with poor survival in cervical cancer treated with radiotherapy［J］. Int J Radiat Oncol Biol Phys, 2005, 63(4):1093-1100.
［33］Ding B, Chi SG, Kim SH, et al. Role of p53 in antioxidant defense of HPV-positive cervical carcinoma cells following H2O2 exposure［J］. J Cell Sci, 2007, 120(Pt 13):2284-2294.
［34］Srinivas P, Gopinath G, Banerji A, et al. Plumbagin induces reactive oxygen species, which mediate apoptosis in human cervical cancer cells［J］. Mol Carcinog, 2004, 40(4):201-211