Role of radioadaptation on radiation-induced thymic lymphoma in mice

Bhattacharjee, D.

doi:10.1016/s0027-5107(96)00125-x

Cited by 52 publications

(26 citation statements)

References 12 publications

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“…Radioadaptive resistance is a feature of many other species, including E. coli, algae, higher plant cells, and insect cells (94). In mice, wholebody preirradiation with LDIR reduced the incidence of thymic lymphoma from 46% to 16% with a challenging high dose of radiation, indicating the radioadaptive response (13). Similarly, in rabbits, Liu et al reported LDIR-induced radioprotection (98).…”

Section: Adaptive Response To Oxidative Stressmentioning

confidence: 99%

MnSOD in Oxidative Stress Response-Potential RegulationviaMitochondrial Protein Influx

Candas

2014

Antioxidants & Redox Signaling

276

178

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Significance: The mitochondrial antioxidant manganese superoxide dismutase (MnSOD) is encoded by genomic DNA and its dismutase function is fully activated in the mitochondria to detoxify free radical O 2 -generated by mitochondrial respiration. Accumulating evidence shows an extensive communication between the mitochondria and cytoplasm under oxidative stress. Not only is the MnSOD gene upregulated by oxidative stress, but MnSOD activity can be enhanced via the mitochondrial protein influx (MPI). Recent Advances: A cluster of MPI containing cytoplasmic/nuclear proteins, such as cyclins, cyclin-dependent kinases, and p53 interact with and alter MnSOD activity. These proteins modulate MnSOD superoxide scavenging activity via post-translational modifications in the mitochondria. In addition to well-established pathways in gene expression, recent findings suggest that MnSOD enzymatic activity can also be enhanced by phosphorylation of specific motifs in mitochondria. This review attempts to discuss the pre-and post-translational regulation of MnSOD, and how these modifications alter MnSOD activity, which induces a cell adaptive response to oxidative stress. Critical Issues: MnSOD is biologically significant to aerobic cells. Its role in protecting the cells against the deleterious effects of reactive oxygen species is evident. However, the exact network of MnSOD-associated cellular adaptive reaction to oxidative stress and its post-translational modifications, especially its enzymatic enhancement via phosphorylation, is not yet fully understood. Future Directions: The broad discussion of the multiple aspects of MnSOD regulation, including gene expression, protein modifications, and enzymatic activity, will shed light onto the unknown mechanisms that govern the prosurvival networks involved in cellular and mitochondrial adaptive response to genotoxic environment. Antioxid. Redox Signal. 20, 1599Signal. 20, -1617

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Section: Adaptive Response To Oxidative Stressmentioning

confidence: 99%

MnSOD in Oxidative Stress Response-Potential RegulationviaMitochondrial Protein Influx

Candas

2014

Antioxidants & Redox Signaling

276

178

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“…The most significant phenomena of LDIR-induced radioprotection include the reduction of the lethal and mutagenic effects caused by subsequent exposure to higher doses (105,154,173,193,204,227), resistance to subsequent radiation-induced genomic instability (96, 105,121,142), and activation of stress-sensitive transcription factors and gene regulators (68,69,202,228). Bhattacharjee and Ito (22) reported that whole-body pre-irradiation of Swiss mice with five repeated exposures to small doses of 1 cGy per day reduces the incidence of thymic lymphoma from 46% to 16% following 2 Gy IR (21). Additionally, IR-induced nontargeted effects from astronaut space exploration were mimicked by cranially irradiated Sprague Dawley rats; the results showed that levels of key proteins involved in mitochondrial fatty acid metabolism were reduced, and proteins involved in various cellular defense mechanisms, including antioxidants, were elevated in both irradiated and nonirradiated tissues (2,81).…”

Section: Features Of Ldir-induced Adaptive Responsementioning

confidence: 99%

Cell Cycle Regulators Guide Mitochondrial Activity in Radiation-Induced Adaptive Response

Alexandrou

2014

Antioxidants & Redox Signaling

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Significance: There are accruing concerns on potential genotoxic agents present in the environment including low-dose ionizing radiation (LDIR) that naturally exists on earth's surface and atmosphere and is frequently used in medical diagnosis and nuclear industry. Although its long-term health risk is being evaluated and remains controversial, LDIR is shown to induce temporary but significant adaptive responses in mammalian cells and animals. The mechanisms guiding the mitochondrial function in LDIR-induced adaptive response represent a unique communication between DNA damage and cellular metabolism. Elucidation of the LDIRregulated mitochondrial activity may reveal new mechanisms adjusting cellular function to cope with hazardous environmental stress. Recent Advances: Key cell cycle regulators, including Cyclin D1/CDK4 and Cyclin B1/ cyclin-dependent kinase 1 (CDK1) complexes, are actively involved in the regulation of mitochondrial functions via phosphorylation of their mitochondrial targets. Accumulating new evidence supports a concept that the Cyclin B1/CDK1 complex acts as a mediator in the cross talk between radiation-induced DNA damage and mitochondrial functions to coordinate cellular responses to low-level genotoxic stresses. Critical Issues: The LDIR-mediated mitochondrial activity via Cyclin B1/CDK1 regulation is an irreplaceable network that is able to harmonize vital cellular functions with adjusted mitochondrial metabolism to enhance cellular homeostasis. Future Directions: Further investigation of the coordinative mechanism that regulates mitochondrial activities in sublethal stress conditions, including LDIR, will reveal new insights of how cells cope with genotoxic injury and will be vital for future targeted therapeutic interventions that reduce environmental injury and cancer risk.

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“…In India, Bhattarcharjee (34) found that when he preirradiated Swiss mice for 5 days with 7-rays at the rate of 1 cGy/day, thymic lymphoma was induced in 16% (8/50) of the animals. A high 2-Gy dose induced lymphomas in 46% (23/50) of the mice, whereas if the animals were preirradiated before exposure to the 2-Gy dose, only 16% of them developed the cancers; i.e., the preirradiation seemed to cancel the induction of thymic lymphoma by the high dose (Table 10).…”

Section: Worldwide Experments With Other End Pointsmentioning

confidence: 99%

The Adaptive Response in Radiobiology: Evolving Insights and Implications

Wolff¹

1998

Environmental Health Perspectives

105

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The first of the regularly reproducible experiments to show that very low doses of ionizing radiation, like very low doses of chemical agents, could induce mechanisms whereby cells become better fit to cope with subsequent exposures to high doses were carried out on the induction of chromosome aberrations in cultures of human lymphocytes. If cells that had been exposed to a very low dose (1 cGy) of X rays were subsequently exposed to a relatively high dose (1 Gy), approximately half as many chromosome breaks were induced. Subsequent experiments showed that this adaptive response to low doses requires a certain minimal dose before it becomes active; occurs only within a relatively small window of dose; is dose-rate dependent; and depends on the genetic constitution of the people or animals exposed, with some being unresponsive. It was further shown that the response to the low-dose preexposure was not instantaneous but took approximately 4 to 6 hr to become fully active, and could be prevented if during this period protein synthesis was inhibited, i.e., a necessary protein (enzyme) was being induced. In fact, subsequent experiments with two-dimensional gel electrophoresis showed new proteins in cells irradiated with 1 to 2 cGy. The adaptation induced by low doses of radiation was therefore attributed to the induction of a novel efficient chromosome break repair mechanism that if active at the time of challenge with high doses would lead to less residual damage. This hypothesis was strengthened by a series of experiments in which it was found that inhibitors of poly(ADP-ribose)polymerase, an enzyme implicated in DNA strand break rejoining, could prevent the adaptive response. Although the phenomenon is well established in cellular systems, it is still problematical as to whether or not it will have any utility in establishing risks of ionizing radiation to humans. Newer experiments have now been carried out on the mechanisms underlying the effect and whether or not the effect can manifest itself as a decrease in the number of induced cancers and radiation-induced mortality. Experiments with restriction enzymes now indicate that doublestrand breaks in DNA can be triggering events in adaptation. In addition, preliminary experiments on the survival of whole-body irradiated mice have shown that multiple exposures to low adapting doses can have profound effects on survival, and other experiments have shown that adaptation can affect the induction of thymic lymphoma in irradiated mice. It therefore appears that the initial experiments behind the adaptive response have led to a vigorous worldwide effort to understand the basic mechanisms behind it. This effort is stimulated both by a desire to understand the basic cell biology behind the response and a desire to see if indeed this phenomenon affects the estimation of risks of low-level radiation exposure.Environ Health Perspect 106(Suppl 1):277-283 (1998). http.//ehpnetl.niehs.nih.gov/1998/Suppl-1/277-283wolff/abstract.html

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Role of radioadaptation on radiation-induced thymic lymphoma in mice

Cited by 52 publications

References 12 publications

MnSOD in Oxidative Stress Response-Potential RegulationviaMitochondrial Protein Influx

MnSOD in Oxidative Stress Response-Potential RegulationviaMitochondrial Protein Influx

Cell Cycle Regulators Guide Mitochondrial Activity in Radiation-Induced Adaptive Response

The Adaptive Response in Radiobiology: Evolving Insights and Implications

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