Effects of Heavy Ions on Rabbit Tissues: Loss of Electroretinogram and DNA Repair in Retinal Photoreceptor Cells

Keng, Peter C.; Lett, J. T.

doi:10.1080/09553008114550781

Cited by 16 publications

(3 citation statements)

References 11 publications

(14 reference statements)

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“…In the late 1970s, it was shown that DNA strand breaks (total strand breaks including single/double strand breaks) induced by high‐LET heavy ions are rejoined less efficiently than those by X‐rays, leaving higher rate of nonrejoined DNA breaks with high‐LET irradiations. This phenomenon is LET dependent and became maximal at 150–200 keV/μm LET range 68–70. In the early to mid 1990s, rejoining of DNA DSBs by heavy ions were measured first by neutral filter elution and then by pulsed field gel electrophoresis and static field gel electrophoresis (SFGE) 30, 35, 71–75.…”

Section: Repair Of Dsbs Induced By High‐let Heavy Ionsmentioning

confidence: 99%

Repair of DNA damage induced by accelerated heavy ions—A mini review

Okayasu

2011

Intl Journal of Cancer

113

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Increasing use of heavy ions for cancer therapy and concerns from exposure to heavy charged particles in space necessitate the study of the basic biological mechanisms associated with exposure to heavy ions. As the most critical damage induced by ionizing radiation is DNA double strand break (DSB), this review focuses on DSBs induced by heavy ions and their repair processes. Compared with X‐ or gamma‐rays, high‐linear energy transfer (LET) heavy ion radiation induces more complex DNA damage, categorized into DSBs and non‐DSB oxidative clustered DNA lesions (OCDL). This complexity makes the DNA repair process more difficult, partially due to retarded enzymatic activities, leading to increased chromosome aberrations and cell death. In general, the repair process following heavy ion exposure is LET‐dependent, but with nonhomologous end joining defective cells, this trend is less emphasized. The variation in cell survival levels throughout the cell cycle is less prominent in cells exposed to high‐LET heavy ions when compared with low LET, but this mechanism has not been well understood until recently. Involvement of several DSB repair proteins is suggested to underlie this interesting phenomenon. Recent improvements in radiation‐induced foci studies combined with high‐LET heavy ion exposure could provide a useful opportunity for more in depth study of DSB repair processes. Accelerated heavy ions have become valuable tools to investigate the molecular mechanisms underlying repair of DNA DSBs, the most crucial form of DNA damage induced by radiation and various chemotherapeutic agents.

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Section: Repair Of Dsbs Induced By High‐let Heavy Ionsmentioning

confidence: 99%

Repair of DNA damage induced by accelerated heavy ions—A mini review

Okayasu

2011

Intl Journal of Cancer

113

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“…Keng and Lett (Keng and Lett 1981) have also studied the effects on retinal photoreceptor cells of a variety of radiation qualities, including 6oCo y-rays, and heavy ions (LET of 90 and 35 keV km-'). Their result showed that a critical dose of 45 f 3 Gy was required to initiate a sudden loss in the b-wave of the ERG, independent of the type of radiation.…”

Section: Discussionmentioning

confidence: 99%

“…The experiments on rabbit retinas cited here have shown conclusively that destruction of proliferating cells are not involved in the loss of ERG, since this loss is independent of radiation quality. Furthermore, the abrupt threshold of dose required to produce the critical damage suggests that the disruption of a membrane and/or interference with a biochemical process is involved (Keng and Lett 1981). The interpretation is thus made that damage to the photoreceptor cells is responsible for the loss in ERG (Noell 1980).…”

Section: Discussionmentioning

confidence: 99%

Dose rate to the inner ear during Mossbauer experiments

Kliauga

Khanna

1983

Phys. Med. Biol.

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The most widely used technique for studying vibrations of the inner ear utilises the Mössbauer effect; this requires placement of a radioactive source on the basilar membrane. This source, although small in size and less than 37 MBq (1 mCi) in strength, is placed in close proximity to sensitive receptor cells. Using a series solution for the radiation field of a rectangular source the absorbed dose rate delivered to receptor cells at various depths and at points off-axis from the centre of the source is calculated. It is concluded that the dose delivered during the course of a Mössbauer experiment may well be sufficient to damage receptor cells and cause a loss of response.

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Cellular and tissue responses to heavy ions: Basic considerations

Lett

Cox

Bergtold

1986

Radiat Environ Biophys

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Responses of the S/S variant of the L5178Y murine leukemic lymphoblast, the photoreceptor cell of the rabbit retina and the lenticular epithelium of the rabbit to heavy ions (20Ne, 28Si, 40Ar and 56Fe) are described and discussed primarily from the standpoint of the need for a comprehensive theory of cellular radiosensitivity from which a general theory of tissue radiosensitivity can be constructed. The radiation responses of the very radiosensitive, repair-deficient S/S variant during the G1- and early S phases of the cell cycle were found to be unlike those of normally radioresistant cells in culture: the relative biological effectiveness (RBE) did not increase with the linear energy transfer (LET infinity) of the incident radiation. Such behavior could be anticipated for a cell which is lacking the repair system that operates in other (normal) cells when they are exposed to ionizing radiations in the G1 phase of the cell cycle. The S/S variant does exhibit a peak of radioresistance to X-photons mid-G1 + 8 h into the cell cycle, however, and as the LET infinity was increased, the repair capacity responsible for that radioresistance was reduced progressively. Sensory cells (photoreceptors) in the retina of the New Zealand white (NZW) rabbit are very radioresistant to ionizing radiations, and several years elapsed after localized exposure (e.g., 5-10 Gy) to heavy ions (20Ne, 40Ar) before photoreceptor cells were lost from the retina. During the first few weeks after such irradiations, damage to DNA in the photoreceptor cells was repaired to a point where it could not be demonstrated by reorienting gradient sedimentation under alkaline conditions, a technique that can detect DNA damage produced by less than 0.1 Gy of X-photons. Restitution of DNA structure was not permanent, however, and months or years later, but before loss of photoreceptor cells from the retina could be detected, progressive deterioration of the DNA structure began. Age dependencies of late sequelae from densely ionizing radiations are matters of concern both for the therapeutic uses of radiation and the risk/benefit considerations of environmental exposure, especially in outer space. A pilot experiment with a single acute exposure to 20Ne ions has illustrated the need for careful examination of the role of animal age at the time of irradiation in subsequent tissue responses.(ABSTRACT TRUNCATED AT 400 WORDS)

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Effects of Heavy Ions on Rabbit Tissues: Loss of Electroretinogram and DNA Repair in Retinal Photoreceptor Cells

Cited by 16 publications

References 11 publications

Repair of DNA damage induced by accelerated heavy ions—A mini review

Repair of DNA damage induced by accelerated heavy ions—A mini review

Dose rate to the inner ear during Mossbauer experiments

Cellular and tissue responses to heavy ions: Basic considerations

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