Influence of Oxygen on the Repair of Direct Radiation Damage to DNA by Thiols in Model Systems

Becker, Dávid; Summerfield, Stephen; Gillich, S.; Sevilla, Michael D.

doi:10.1080/09553009414550631

Cited by 29 publications

(13 citation statements)

References 60 publications

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“…In the cell, and in the absence of O 2 , such damage can be reduced by reactions with SH groups. 36 However, the formation of ROO · , organic peroxides by reaction of free radicals with O 2 , is an irreversible process which is said to "fix" or make permanent the R · lesions. It has been demonstrated in living systems that for fixation to occur, O 2 must be present or administered within several 10 −3 s of exposure to ionising radiation.…”

Section: Resultsmentioning

confidence: 99%

Low energy electron stimulated desorption from DNA films dosed with oxygen

Mirsaleh-Kohan

Bass

Cloutier

et al. 2012

The Journal of Chemical Physics

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Desorption of anions stimulated by 1-18 eV electron impact on self-assembled monolayer (SAM) films of single DNA strands is measured as a function of film temperature (50-250 K). The SAMs, composed of 10 nucleotides, are dosed with O 2 . The OH − desorption yields increase markedly with exposure to O 2 at 50 K and are further enhanced upon heating. In contrast, the desorption yields of O − , attributable to dissociative electron attachment to trapped O 2 molecules decrease with heating. Irradiation of the DNA films prior to the deposition of O 2 shows that this surprising increase in OH − desorption, at elevated temperatures, arises from the reaction of O 2 with damaged DNA sites. These results thus appear to be a manifestation of the so-called "oxygen fixation" effect, well known in radiobiology.

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Section: Resultsmentioning

confidence: 99%

Low energy electron stimulated desorption from DNA films dosed with oxygen

Mirsaleh-Kohan

Bass

Cloutier

et al. 2012

The Journal of Chemical Physics

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“…It is important to determine the impact of short-term exposure to low glucose prior to therapy since it is likely that short term exposure to low glucose and low oxygen may also occur in solid tumors. The radiation resistance induced by short-term low oxygen exposure has been extensively studied in cells and purified DNA (34–36). However, the impact of either short- or long- term glucose deprivation on the response of human cancer cells to γ radiation induced oxidative stress has not been demonstrated.…”

Section: Introductionmentioning

confidence: 99%

Glucose deprivation increases nuclear DNA repair protein Ku and resistance to radiation induced oxidative stress in human cancer cells

Ayene

Ward

et al. 2009

Cell Biochemistry & Function

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Recent studies have indicated that nutrient deprivation particularly glucose may play a major role in tumor cell tolerance to a generally oxidative stress environment in solid tumors. Here, we studied the impact of glucose deprivation on the response of human colon (HT29)0020and prostate (DU145) cancer cells to γ radiation. A significant decrease in intracellular glucose level was observed in glucose deprived cells as measured by bioreductive assay. The survival of HT29 and DU145 were increased by 30 and 100% respectively when these cells were exposed to γ radiation in the absence of glucose compared to that in the presence of glucose. In glucose depleted medium, glutathione (GSH), a free radical scavenger, content remained the same, and showed no correlation with the radiation resistance induced by glucose deprivation. GRP78, a stress response survival protein, was not significantly increased in cells deprived of glucose for 4 hours compared to those cells in glucose. DNA repair protein Ku, which is known to play a major role in cellular resistance to radiation, was significantly increased in glucose deprived cancer cells that showed enhanced radiation resistance. These results have demonstrated, for the first time, that glucose deprivation mediated stress increased the expression of nuclear Ku and resistance to radiation induced oxidative stress in human cancer cells. The additional resistance caused by glucose deprivation in cancer cells has clinical significance since solid tumors are known to have low level of glucose due to diffusion limited blood supply and higher metabolic activity.

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“…Ionizing radiation can, however, have immediate and delayed side effects on normal tissues, including its effect as a potent carcinogen. The sensitivity of cells to ionizing radiation depends especially on the rate of differentiation and accompanying factors of the tissue, as well as on the efficiency of the intrinsic antioxidative defense [2].…”

Section: Introductionmentioning

confidence: 99%

Melatonin protects against ionizing radiation‐induced oxidative damage in corpus cavernosum and urinary bladder in rats

Şener¹,

Atasoy

Ersoy³

et al. 2004

Journal of Pineal Research

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The objective of this study was to examine the potential radioprotective properties of pharmacological doses of melatonin on corpus cavernosum and bladder tissues of whole-body irradiated (IR) rats. A total of 32 male Sprague-Dawley rats were exposed to irradiation performed with a LINAC which produced 6 MV photons at a focus 100 cm distant from the skin. Under ketamine anesthesia, each rat received a single whole-body dose of 800 cGy. Immediately before and after IR, rats were treated with either saline or melatonin (20 and 10 mg/kg, i.p.) and decapitated at 12 hr after exposure to irradiation. Another group of rats was followed for 72 hr after IR, where melatonin injections were repeated once daily. Tissue levels of malondialdehyde (MDA), an index of lipid peroxidation, and glutathione (GSH), a key antioxidant, were estimated in corpus cavernosum and urinary bladder. Tissues were also examined microscopically. The results demonstrate that both 12 and 72 hr following IR, tissue levels of MDA were elevated (P < 0.001), while GSH levels were reduced (P < 0.01) in both tissues. On the other hand, melatonin reversed these changes significantly (P < 0.05-0.01), concomitant with the improvement in histological appearances. Our results show that whole-body irradiation causes oxidative damage in the tissues of the genitourinary system. As melatonin administration reversed oxidative organ injury, as assessed by biochemical and histopathological findings, it is suggested that supplementing cancer patients with adjuvant therapy of melatonin may have some benefit for successful radiotherapy.

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Influence of Oxygen on the Repair of Direct Radiation Damage to DNA by Thiols in Model Systems

Cited by 29 publications

References 60 publications

Low energy electron stimulated desorption from DNA films dosed with oxygen

Low energy electron stimulated desorption from DNA films dosed with oxygen

Glucose deprivation increases nuclear DNA repair protein Ku and resistance to radiation induced oxidative stress in human cancer cells

Melatonin protects against ionizing radiation‐induced oxidative damage in corpus cavernosum and urinary bladder in rats

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