A comparison of radiation-induced mitochondrial damage between neural progenitor stem cells and differentiated cells

Shimura, Tsutomu; Sasatani, Megumi; Kawai, Hidehiko; Kamiya, Kenji; Kobayashi, Junya; Komatsu, Kenshi; Kunugita, Naoki

doi:10.1080/15384101.2017.1284716

Cited by 32 publications

(23 citation statements)

References 30 publications

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“…Moreover, radiation promotes not only ROS generation but also OXPHOS. In general, radiation causes mitochondrial damage and ROS production [128]. Irradiated tumor cells might use metabolism through glycolysis rather than OXPHOS because of mitochondrial damage [129].…”

Section: Mtor-dependent Antioxidant Mechanism In Solidmentioning

confidence: 99%

mTOR-Mediated Antioxidant Activation in Solid Tumor Radioresistance

Woo

Lee

Jung

et al. 2019

Journal of Oncology

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Radiotherapy is widely used for the treatment of cancer patients, but tumor radioresistance presents serious therapy challenges. Tumor radioresistance is closely related to high levels of mTOR signaling in tumor tissues. Therefore, targeting the mTOR pathway might be a strategy to promote solid tumor sensitivity to ionizing radiation. Radioresistance is associated with enhanced antioxidant mechanisms in cancer cells. Therefore, examination of the relationship between mTOR signaling and antioxidant mechanism-linked radioresistance is required for effective radiotherapy. In particular, the effect of mTOR signaling on antioxidant glutathione induction by the Keap1-NRF2-xCT pathway is described in this review. This review is expected to assist in the identification of therapeutic adjuvants to increase the efficacy of radiotherapy.

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Section: Mtor-dependent Antioxidant Mechanism In Solidmentioning

confidence: 99%

mTOR-Mediated Antioxidant Activation in Solid Tumor Radioresistance

Woo

Lee

Jung

et al. 2019

Journal of Oncology

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“…2A and 2B, right panels). 21 Cells were continuously treated with the antioxidant N-acetylcysteine (NAC) at a final concentration of 1 mM during FR. Media was changed at 2-or 3-d intervals.…”

Section: Mitochondrial Oxphos Is Enhanced In Response To Long-term Frmentioning

confidence: 99%

“…Long-term FR-induced activation of mitochondrial OXPHOS is thought to be associated with the increased energy demands required for DNA DSBs repair. 7,21 We investigated focus formation of g-H2AX, the marker for DSBs, and Rad51, a marker for homologous recombination repair, to identify ongoing DNA repair in TIG-3 and MRC-5 cells. CR or FR treatment with 0.4Gy induced prolonged DSB repair as evidenced by g-H2AX and Rad51 foci formation at 24 hours after IR in irradiated cells (Fig.…”

Section: Cr or Long-term Fr Prolongs Dna Repairmentioning

confidence: 99%

“…24 Cell cycle analysis indicated that long-term FR had a negligible effect on IR-induced G2-arrest in TIG-3 and MRC-5 cells. 21…”

Section: Cr or Long-term Fr Prolongs Dna Repairmentioning

confidence: 99%

“…We recently determined that repeated exposure to fractionated radiation (FR) with low doses of X-rays for 31 d (long-term) induces mitochondrial damage in human fibroblasts. 20,21 Mitochondria are thought to be a major target for oxidative stress induced by long-term FR. 22 However, the mechanism of IR-induced mitochondrial damage remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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ATM-mediated mitochondrial damage response triggered by nuclear DNA damage in normal human lung fibroblasts

et al. 2017

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Ionizing radiation (IR) elevates mitochondrial oxidative phosphorylation (OXPHOS) in response to the energy requirement for DNA damage responses. Reactive oxygen species (ROS) released during mitochondrial OXPHOS may cause oxidative damage to mitochondria in irradiated cells. In this paper, we investigated the association between nuclear DNA damage and mitochondrial damage following IR in normal human lung fibroblasts. In contrast to low-doses of acute single radiation, continuous exposure of chronic radiation or long-term exposure of fractionated radiation (FR) induced persistent Rad51 and γ-H2AX foci at least 24 hours after IR in irradiated cells. Additionally, long-term FR increased mitochondrial ROS accompanied with enhanced mitochondrial membrane potential (ΔΨm) and mitochondrial complex IV (cytochrome c oxidase) activity. Mitochondrial ROS released from the respiratory chain complex I caused oxidative damage to mitochondria. Inhibition of ATM kinase or ATM loss eliminated nuclear DNA damage recognition and mitochondrial radiation responses. Consequently, nuclear DNA damage activates ATM which in turn increases ROS level and subsequently induces mitochondrial damage in irradiated cells. In conclusion, we demonstrated that ATM is essential in the mitochondrial radiation responses in irradiated cells. We further demonstrated that ATM is involved in signal transduction from nucleus to the mitochondria in response to IR.

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The role of DNA damage in neural stem cells ageing

Zhong,

Wang,

Yang

et al. 2024

Journal Cellular Physiology

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Neural stem cells (NSCs) are pluripotent stem cells with the potential to differentiate into a variety of nerve cells. NSCs are susceptible to both intracellular and extracellular insults, thus causing DNA damage. Extracellular insults include ultraviolet, ionizing radiation, base analogs, modifiers, alkyl agents and others, while intracellular factors include Reactive oxygen species (ROS) radicals produced by mitochondria, mismatches that occur during DNA replication, deamination of bases, loss of bases, and more. When encountered with DNA damage, cells typically employ three coping strategies: DNA repair, damage tolerance, and apoptosis. NSCs, like many other stem cells, have the ability to divide, differentiate, and repair DNA damage to prevent mutations from being passed down to the next generation. However, when DNA damage accumulates over time, it will lead to a series of alterations in the metabolism of cells, which will cause cellular ageing. The ageing and exhaustion of neural stem cell will have serious effects on the body, such as neurodegenerative diseases. The purpose of this review is to examine the processes by which DNA damage leads to NSCs ageing and the mechanisms of DNA repair in NSCs.

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A comparison of radiation-induced mitochondrial damage between neural progenitor stem cells and differentiated cells

Cited by 32 publications

References 30 publications

mTOR-Mediated Antioxidant Activation in Solid Tumor Radioresistance

mTOR-Mediated Antioxidant Activation in Solid Tumor Radioresistance

ATM-mediated mitochondrial damage response triggered by nuclear DNA damage in normal human lung fibroblasts

The role of DNA damage in neural stem cells ageing

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