Effects of ionizing radiation on expression of genes encoding cytoskeletal elements: Kinetics and dose effects

Woloschak, Gayle E.; Shearin-Jones, P.; Chang-Liu, Chin Mei

doi:10.1002/mc.2940030609

Cited by 38 publications

(25 citation statements)

References 19 publications

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“…43 On the other hand, a-tubulin, g-actin and interleukin 1 were similarly induced both by g-rays and neutrons. 44,45 In the present study, both neutron and photon irradiation activated CArGregulated gene expression (Figs 1 and 2). However, the higher cytotoxic efficacy of neutrons was not reflected in Activation of CArG promoters for gene therapy O Greco et al stronger promoter activation.…”

Section: Discussionsupporting

confidence: 58%

Gene therapy vectors containing CArG elements from the Egr1 gene are activated by neutron irradiation, cisplatin and doxorubicin

et al. 2005

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Section: Discussionsupporting

confidence: 58%

Gene therapy vectors containing CArG elements from the Egr1 gene are activated by neutron irradiation, cisplatin and doxorubicin

et al. 2005

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“…These regulons are rapidly and readily induced and control a series of genes, including those encoding for AOEs (14). This biological principle was also found to be relevant in the mammalian system (15)(16)(17)(18)(19)(20)(21)(22). Most studies of higher organisms examined the AOE response hours and days after irradiation and are, therefore, confounded by influences, such as inflammation, secondary to radiation per se.…”

mentioning

confidence: 94%

“…Most studies of higher organisms examined the AOE response hours and days after irradiation and are, therefore, confounded by influences, such as inflammation, secondary to radiation per se. No study on early events of AOE transcription has been reported to date, to our knowledge, although it is known that as soon as 30 min after ionizing irradiation SOD activity can be significantly elevated (18). When they approached this problem, de Toledo and coworkers (7) showed by in vitro studies that mRNA levels for Cu-Zn SOD and CAT in fibroblasts were not increased 1-6 hr after ionizing irradiation at low (3.6 Gy) or high (20 Gy) doses.…”

mentioning

confidence: 95%

Transcription and activity of antioxidant enzymes after ionizing irradiation in radiation-resistant and radiation-sensitive mice

Hardmeier

Hoeger

Fang-Kircher

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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The involvement of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase in radiobiological processes has been described at the enzyme activity level. We irradiated radiationresistant (RR) and radiation-sensitive (RS) mice and studied antioxidant enzymes at the transcriptional and activity level. In addition, aromatic hydroxylation and lipid peroxidation parameters were determined to study radiation resistance at the oxidation level. RS BALB͞c͞J Him mice and RR C3H He͞Him mice were whole-body-irradiated with x-rays at 2, 4, and 6 Gy and killed 5, 15, and 30 min after irradiation. mRNA was isolated from liver and hybridized with probes for antioxidant enzymes and ␤-actin as a housekeeping gene control. Antioxidant enzyme activities were determined by standard assays. Parameters for aromatic hydroxylation (o-tyrosine) and lipid peroxidation (malondialdehyde) were determined by HPLC methods. Antioxidant transcription was unchanged in contrast to antioxidant activities; SOD and CAT activities were elevated within 15 min in RR animals but not in RS mice, at all doses studied. Glutathione peroxidase activity was not different between RR and RS mice and was only moderately elevated after irradiation. No significant differences were found between RR and RS animals at the oxidation level, although a radiation dose-dependent increase of oxidation products was detected in both groups. We found that ionizing irradiation led to increased antioxidant activity only minutes after irradiation in the absence of increased transcription of these antioxidant enzymes. RR animals show higher antioxidant enzyme activities than do RS mice, but oxidation products are comparable in RS and RR mice. As unchanged transcription of antioxidant enzymes could not have been responsible for the increased antioxidant enzyme activities, preformed antioxidant enzymes should have been released by the irradiation process. This would be in agreement with previous studies of preformed, stored SOD. The finding of higher SOD and CAT activities in RR than in RS animals could point to a role for these antioxidant enzymes for the process of radiation sensitivity.

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“…Since we and others have found that ionizing radiation increases PKC activity (11)(12)(13) and PKC has been shown to regulate K+ channels in excitable cells (14), we sought to determine whether channel activity was dependent on PKC activation. After chronically exposing A549 cells to phorbol esters before radiation, PKC activity was measured and found to be downregulated to 10o of untreated controls.…”

mentioning

confidence: 99%

Potassium-channel activation in response to low doses of gamma-irradiation involves reactive oxygen intermediates in nonexcitatory cells.

Kuo

Saad

Koong

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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Active oxygen species are generated during pathophysiologic conditions such as inflammation and ionizing radiation exposure. We tested the hypothesis that an early cellular event in response to these species involves regulation of ion channels. We exposed cells to y-irradiation or treated them with hydrogen peroxide, xanthine/xanthine oxidase, or [3H]thymidine and then monitored channel activity by the technique of whole-cell voltage clamping. Recordings showed that both normal and tumor cells exhibit an increase in K+ currents after treatment with radiation, H202, and xanthine/xanthine oxidase but not with high specific activity[3H]thymidine, suggesting that the signal for K+ channel activation originates at the cell membrane. A single noncytotoxic dose of 10 cGy induced measurable levels of K+ currents, suggesting that the induction of currents regulates biochemical changes in response to stress. To test whether channel activity is sensitive to active oxygen species, we pretreated cells with N-acetyl-L-cysteine (NAC) to increase cellular pools of free radical scavengers before radiation. In NAC-pretreated cells, K+ channel activation by -irradiation was abolished. It has previously been shown that protein kinase C (PKC) is activated by ionizing radiation and can regulate K+ channels in some cells. However, the effect of radiation on induction of K+ channel activity was independent of PKC, -since cells chronically exposed to phorbol esters still produced K+ currents after radiation. These results suggest that an early cellular response to oxidative stress is the activation of K+ channels.The cell membrane acts to maintain the intracellular concentration of ions, permitting changes in ion levels to result in induction of early response genes (1). The ability of ion channels to act as modulators of conductance is due to their innate property of rapid conformational alterations to initiate or respond to signal transduction. Type I cells of the carotid body, which have active sodium, calcium, and potassium channels, show only reduced K+ channel activity when the pressure of 02 in the surrounding medium is decreased (2), indicating a direct response of a channel to an environmental stimulus. Another means of altering channel activity is through phosphorylation and dephosphorylation. Phosphorylation of channel proteins by different protein kinases such as protein kinase A and protein kinase C (PKC) can result in either increased or decreased K+ currents in excitatory cells (3-6).We have characterized the human lung adenocarcinoma cell line A549 with respect to its voltage-dependent channel activity. Before exposure to ionizing radiation, hydrogen peroxide, and xanthine/xanthine oxidase, these cells did not possess any voltage-dependent K+ currents. After exposure to ionizing radiation, A549 cells increased their voltagedependent K+ currents in a dose-dependent manner but did not display altered chloride currents. Furthermore, exposure of these cells to hydrogen peroxide also resulted in increased voltage-depe...

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Effects of ionizing radiation on expression of genes encoding cytoskeletal elements: Kinetics and dose effects

Cited by 38 publications

References 19 publications

Gene therapy vectors containing CArG elements from the Egr1 gene are activated by neutron irradiation, cisplatin and doxorubicin

Gene therapy vectors containing CArG elements from the Egr1 gene are activated by neutron irradiation, cisplatin and doxorubicin

Transcription and activity of antioxidant enzymes after ionizing irradiation in radiation-resistant and radiation-sensitive mice

Potassium-channel activation in response to low doses of gamma-irradiation involves reactive oxygen intermediates in nonexcitatory cells.

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