The effect of X-rays on enzymes

Dale, W. M.

doi:10.1042/bj0341367

Cited by 150 publications

(27 citation statements)

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“…Radiation-resistant and radiation-sensitive bacteria are equally susceptible to DSBs (though not base damage) induced by ionizing radiation (123,206,302) but differ in the amount of protein damage, which is significantly more pronounced in radiation-sensitive bacteria (122). This observation has given rise to a new outlook on radiation toxicity, whereby protein oxidation is considered the main cause of radiation-induced cell death and the capacity to prevent and tolerate protein damage is a major determinant of radiation and desiccation resistance (115,(120)(121)(122)(123)164). D. radiodurans is endowed with strong oxidative stress prevention and tolerance mechanisms, which protect proteins from oxidative damage and sanitize the cells from toxic oxidized products.…”

Section: Prevention and Tolerance Of Dna And Protein Damage In D Radmentioning

confidence: 98%

Oxidative Stress Resistance inDeinococcus radiodurans

Slade

Radman

2011

Microbiol Mol Biol Rev

660

639

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SUMMARY Deinococcus radiodurans is a robust bacterium best known for its capacity to repair massive DNA damage efficiently and accurately. It is extremely resistant to many DNA-damaging agents, including ionizing radiation and UV radiation (100 to 295 nm), desiccation, and mitomycin C, which induce oxidative damage not only to DNA but also to all cellular macromolecules via the production of reactive oxygen species. The extreme resilience of D. radiodurans to oxidative stress is imparted synergistically by an efficient protection of proteins against oxidative stress and an efficient DNA repair mechanism, enhanced by functional redundancies in both systems. D. radiodurans assets for the prevention of and recovery from oxidative stress are extensively reviewed here. Radiation- and desiccation-resistant bacteria such as D. radiodurans have substantially lower protein oxidation levels than do sensitive bacteria but have similar yields of DNA double-strand breaks. These findings challenge the concept of DNA as the primary target of radiation toxicity while advancing protein damage, and the protection of proteins against oxidative damage, as a new paradigm of radiation toxicity and survival. The protection of DNA repair and other proteins against oxidative damage is imparted by enzymatic and nonenzymatic antioxidant defense systems dominated by divalent manganese complexes. Given that oxidative stress caused by the accumulation of reactive oxygen species is associated with aging and cancer, a comprehensive outlook on D. radiodurans strategies of combating oxidative stress may open new avenues for antiaging and anticancer treatments. The study of the antioxidation protection in D. radiodurans is therefore of considerable potential interest for medicine and public health.

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Section: Prevention and Tolerance Of Dna And Protein Damage In D Radmentioning

confidence: 98%

Oxidative Stress Resistance inDeinococcus radiodurans

Slade

Radman

2011

Microbiol Mol Biol Rev

660

639

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“…As early as the 1940s, there were reports that the inactivation of biological entities may be brought about equally by ionizations produced within the entity, or by the ionization of the surrounding medium (Dale, 1940(Dale, , 1942(Dale, , 1943Lea et al, 1944). Kotval and Gray (1947) had shown that a-particles which pass close to the chromatid thread, as well as those which pass through it, have a significant probability of producing chromatid and isochromatid breaks or chromatid exchanges.…”

Section: The Bystander Effectmentioning

confidence: 99%

Genomic instability and bystander effects induced by high-LET radiation

2003

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An understanding of the radiobiological effects of highlinear energy transfer (LET) radiation is essential for radiation protection and human risk assessment. Ever since the discovery of X-rays was made by Ro¨ntgen more than a century ago, it has always been accepted that the deleterious effects of ionizing radiation, such as mutation and carcinogenesis, are due mainly to direct damage to DNA. With the availability of a precision single-particle microbeam, it is possible to demonstrate, unequivocally, the presence of a bystander effect with many biological end points. These studies provide clear evidence that irradiated cells can induce a bystander mutagenic response in neighboring cells not directly traversed by a-particles, and that cell-cell communication processes play a critical role in mediating the bystander phenomenon. Following exposure to high-LET radiation, immortalized human bronchial (BEP2D) and breast (MCF-10F) cells have been shown to undergo malignant transformation through a series of successive steps, before becoming tumorigenic in nude mice. There is a progressive increase in genomic instability, determined either by gene amplification or allelic imbalance, with the highest incidence observed among established tumor cell lines, relative to transformed, nontumorigenic and control cell lines.

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“…Dale (17) in his experiments on the effect of x-rays on purified enzymes in aqueous solution observed that the percentage inhibition by a given x-ray dose was increased by an increase in the dilution of the preparation. The "dilution effect" as established earlier by Risse (18) and Fricke (19) on simpler compounds is a manifestation of the indirect action of ionizing radiations on solutes in aqueous solution through the production, in the solvent, of "activated molecules" (free radicals, H~O2, etc.).…”

Section: Resultsmentioning

confidence: 99%

The Effect of X-Radiation on the Glutathione Metabolism of Intact Erythrocytes in Vitro

Klebanoff

1958

The Journal of General Physiology

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The x-irradiation of intact washed erythrocytes results in an inhibition of the glyoxalase activity of the cells chiefly as a result of a decrease in the reduced glutathione level. The percentage inhibition is markedly increased by an increase in the dilution of the cells in physiological saline suggesting that the effect of radiation is indirect, v/a the production in the aqueous medium of free radicals, H,O2, etc. This is supported by the decrease in the inhibition produced by lowering the oxygen tension or by the addition of catalase. The inhibition of glyoxalase activity is also decreased by the addition of methylglyoxal, plasma, adenosine, inosine, glucose, and a number of other sugars to the erythrocyte suspension prior to radiation. Furthermore, some reactivation of the glyoxalase system results from the addition of plasma, glucose, adenosine, and inosine following radiation. These results are discussed in relation to the role of SH compounds, particularly glutathione, in the toxicity of ionizing radiations.The possible relationship of cellular sulfhydryl groups to the development of radiation injury has received wide attention in recent years, chiefly as a result of the investigations of Barron and coworkers (1-3). These investigators observed that a number of purified enzyme systems requiring intact sulfhydryl groups for optimum activity were inactivated by ionizing radiations with an ionic yield generally greater than that observed in the inactivation of enzymes not containing essential sulfhydryl groups (1, 2). Similarly, low molecular weight sulfhydryl compounds appeared to be oxidized with an exceptionally high ionic yield of over 3 (3). These observations, in conjunction with the established importance of sulfhydryl groups in many biological processes (see reference 4), suggested to Barron that the fundamental lesion produced by ionizing radiations in vivo may be the oxidation of SH 1 groups essential to the normal metabolism of the cell.

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The effect of X-rays on enzymes

Cited by 150 publications

References 1 publication

Oxidative Stress Resistance inDeinococcus radiodurans

Oxidative Stress Resistance inDeinococcus radiodurans

Genomic instability and bystander effects induced by high-LET radiation

The Effect of X-Radiation on the Glutathione Metabolism of Intact Erythrocytes in Vitro

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