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Oxidative damage pathways in relation to normal tissue injury

Departments of ¹ Radiation Oncology, Neurosurgery and Cancer Biology, Brain Tumor Center of Excellence and ² Hypertension & Vascular Disease Center, General Surgery, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA

View larger version (35K): [in this window] [in a new window]   Figure 1. ROS/RNOS, the primary antioxidant enzymes and antioxidants. Abbreviations are indicated in the text. GPx, glutathione peroxidase; GR, glutathione reductase; GSH, glutathione; GSSG, glutathione disulphide; MPO, myeloperoxidase; NADPH oxidase, nicotinamide adenine dinucleotide phosphate oxidase; NOS, nitric oxide synthase; Prx, peroxiredoxin; RNOS, reactive nitrogen oxide species; SOD, superoxide dismutase; TR, thioredoxin reductase; Trx, thioredoxin; Trx-S-S-Trx, thioredoxin disulfide.

View larger version (12K): [in this window] [in a new window]   Figure 2. Radiation-induced generation of ROS is abolished by preincubation with the antioxidant NAC, the AT1RA losartan and the NADPH oxidase inhibitors DPI and apocynin. Rat brain microvascular endothelial cells were irradiated with 0–10 Gy -rays and ROS generation measured at 1 h post-irradiation using the oxidative-sensitive fluorescence probe H2DCFDA (A). In panels B and C, cells were pre-incubated with 5 mM NAC, 10 µM losartan, 10 µM DPI or apocynin for 30 min, respectively, prior to treatment with 10 Gy -rays. Mean±SE; n = 3; *p<0.05.

View larger version (27K): [in this window] [in a new window]   Figure 3. Putative pathways by which radiation-induced generation of ROS/RNOS can lead to chronic oxidative stress as well as activation of the intrinsic normal tissue RAS and generation of additional ROS resulting in the development and progression of radiation-induced late effects.