Induction of mRNAs for glutathione synthesis-related proteins in mouse liver by low doses of γ-rays

Kojima, Shuji; Matsuki, Osamu; Nomura, Takaharu; Kubodera, Akiko; Honda, Yumiko; Honda, Susumu; Tanooka, Hiroshi; Wakasugi, Hiro; Yamaoka, Kunihiro

doi:10.1016/s0304-4165(98)00043-9

Cited by 72 publications

(37 citation statements)

References 27 publications

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“…In the same manner, we found that 0.25 Gy γ-ray irradiation induced the mRNAs for glutathione synthesis-related proteins in mouse liver [10] and brain [11], and γ-glutamylcysteine synthetase (γ-GCS) in mouse liver [12]. Furthermore, it was also found that 0.25 Gy γ-ray irradiation elevated glutathione in Raw 264.7 cells [13,14] and this cells acquired the radio-resistance [14,15].…”

Section: Introductionsupporting

confidence: 65%

Activation of Antioxidant System by Low Dose Radiation and Its Applicable Possibility for Treatment of Reactive Oxygen Species-Related Diseases

Yamaoka

2006

J. Clin. Biochem. Nutr.

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Summary We clarified that adequate oxygen stress induced by low dose irradiation activates not only chemical biological protective function, such as induction of the synthesis of superoxide dismutase, glutathione peroxidase, and heat shock protein 70, but also the biomembrane function, such as enhanced membrane fluidity and ATPase activity. It is possible that activation of these mechanisms alleviates in vivo oxidation injuries resulting in alleviation of pathologic condition, such as symptoms of hepatopathy and diabetes mellitus. Namely, adequate activation of the functions of the living body by low dose irradiation can contribute to suppressing aging and to preventing or reducing reactive oxygen species related diseases which are thought to involve peroxidation and have been regarded as the diseases for which radon spring water is an effective treatment. Clarification in detail of the mechanisms of these phenomena is required to understand the effects of low dose irradiation or radon inhalation on the functions of the living body, including adaptive response.

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Section: Introductionsupporting

confidence: 65%

Activation of Antioxidant System by Low Dose Radiation and Its Applicable Possibility for Treatment of Reactive Oxygen Species-Related Diseases

Yamaoka

2006

J. Clin. Biochem. Nutr.

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“…As an example, a whole-body X-ray dose of 200 mGy increased superoxide dismutase (SOD), glutathione peroxidase (GPx), and GPx mRNA in spleens of C57BL/6NJcl and BALB/c mice, which was not the case for a large dose of 4,000 mGy (Kataoka 2013). Another study suggested that the levels of reduced glutathione (GSH), glutathione reductase (GR), γ-glutamylcysteine synthetase (γ-GCS), and thioredoxin (TRX) increased in liver shortly after whole body irradiation with 500 mGy of gamma rays (Kojima et al 1998a). In addition, the levels of GSH, GR, γ-GCS, and TRX increased in the brain shortly after 500 mGy of gamma rays (Kojima et al 1998b).…”

Section: Benefits Of Low and Moderate Radiation Dosesmentioning

confidence: 99%

Radiation-hormesis phenotypes, the related mechanisms and implications for disease prevention and therapy

Scott

2014

J. Cell Commun. Signal.

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Humans are continuously exposed to ionizing radiation throughout life from natural sources that include cosmic, solar, and terrestrial. Much harsher natural radiation and chemical environments existed during our planet’s early years. Mammals survived the harsher environments via evolutionarily‐conserved gifts ̶ a continuously evolving system of stress‐induced natural protective measures (i.e., activated natural protection [ANP]). The current protective system is differentially activated by stochastic (i.e., variable) low‐radiation‐dose thresholds and when optimally activated in mammals includes antioxidants, DNA damage repair, p53‐related apoptosis of severely‐damaged cells, reactive‐oxygen‐species (ROS)/reactive‐nitrogen‐species (RNS)‐ and cytokine‐regulated auxiliary apoptosis that selectively removes aberrant cells (e.g., precancerous cells), suppression of disease promoting inflammation, and immunity against cancer cells. The intercellular‐signaling‐based protective system is regulated at least in part via epigenetic reprogramming of adaptive‐response genes. When the system is optimally activated, it protects against cancer and some other diseases, thereby leading to hormetic phenotypes (e.g., reduced disease incidence to below the baseline level; reduced pain from inflammation‐related problems). Here, some expressed radiation hormesis phenotypes and related mechanisms are discussed along with their implications for disease prevention and therapy.

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“…Our previous studies also have shown that low doses of ionizing radiation, a generator of ROS, effectively induce GSH in various tissues and in cultured cells. [15][16][17][18][19][20] Thus, a similar effect could be anticipated for NO.…”

Section: )mentioning

confidence: 82%

“…This elevation was accompanied by elevated activity of γ-glutamylcysteine synthetase (γ-GCS), which is the rate-limiting enzyme for de novo GSH synthesis. [15][16][17][18] It was subsequently confirmed that this phenomenon is a post-transcriptional event; the elevation of glutathione levels in these organs follows the induction of mRNAs coding for γ-GCS. 19,20) This phenomenon is considered to be an adaptive response of living cells against ROS.…”

Section: Introductionmentioning

confidence: 99%

Low-level Nitric Oxide Blunts Oxidant Injury via Up-regulating Glutathione Synthes.

Kurozumi

Kojima

2002

JOURNAL OF HEALTH SCIENCE

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The elevation of cellular glutathione (GSH) level induced by low concentrations of an nitric oxide (NO)-donor, sodium nitroprusside (SNP), and its effect on oxidant-induced cell injury were examined in RAW264.7 cells. The cellular GSH level increased 6 hr after exposure of the cells to SNP at low concentrations ranging from 0.1 to 0.5 mM, and the elevation followed the induction of mRNA coding for γ-glutamylcysteine synthetase, the ratelimiting enzyme of the de novo glutathione synthesis pathway. Pre-treatment of cells with low concentration of SNP (less than 0.25 mM) at 12 hr prior to exposure to menadione (MEND), an superoxide anion (O 2 -)-donor, significantly suppressed the cell injury induced by MEND alone. Simultaneous treatment with a higher concentration of SNP (1.0 mM or more) also blunted the MEND-induced cell injury. Low and high doses of NO both seem to show a preventive effect against oxidant injury: NO may protect against oxidant injury by up-regulating GSH synthesis at low concentrations, while at high concentrations it may directly react with radical oxygen species (ROS), thus acting as a free radical scavenger and blunting oxidant injury. These results suggest that modulation of the cellular glutathione metabolism through intracellular NO is a potential mechanism for enhancing the antioxidant defense of cells.

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Induction of mRNAs for glutathione synthesis-related proteins in mouse liver by low doses of γ-rays

Cited by 72 publications

References 27 publications

Activation of Antioxidant System by Low Dose Radiation and Its Applicable Possibility for Treatment of Reactive Oxygen Species-Related Diseases

Activation of Antioxidant System by Low Dose Radiation and Its Applicable Possibility for Treatment of Reactive Oxygen Species-Related Diseases

Radiation-hormesis phenotypes, the related mechanisms and implications for disease prevention and therapy

Low-level Nitric Oxide Blunts Oxidant Injury via Up-regulating Glutathione Synthes.

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