V Ponette, N Giocanti, H Tourbez, J Balosso, C Hennequin, V Favaudon
{"title":"脉冲暴露于电离辐射引起细胞放射敏感性的快速变化。","authors":"V Ponette, N Giocanti, H Tourbez, J Balosso, C Hennequin, V Favaudon","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>A linear electron accelerator, operated in a recurrent chopped mode, was used for time-resolved investigation of split-dose radiation recovery in 3 mammalian cell lines in vitro. The time intervals separating the sequential radiation exposures in this study ranged from fractions of a second to a few minutes. The primary pulse brought about rapid, synchronous oscillations of cellular radiosensitivity giving rise to a tetraphasic, W-shaped time-dependent profile whose first phase was accomplished by a large decrease of cell survival. Only the last phase correlated with sub-lethal damage repair determined by gamma-ray irradiation. The same profile was observed for the 3 cell lines investigated. However, the kinetics of the whole process varied extensively from one cell line to another. The first phase lasted 1 s only for Chinese hamster V79 fibroblasts, 6 s for human squamous carcinoma SQ20B cells, and as much as 25 s for human colon adenocarcinoma LoVo cells. The relative amplitude of this first phase grew with both the first and second radiation doses in the range explored. It is hypothesized that rapid oscillation of the cytotoxic potential of radiation may result from various mechanisms such as molecular recognition of radio-induced lesions, changes in chromatin structure, or differential activation of phospholipid-dependent transduction pathways.</p>","PeriodicalId":10555,"journal":{"name":"Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie","volume":"319 6","pages":"505-9"},"PeriodicalIF":0.0000,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Pulse exposure to ionizing radiation elicits rapid changes in cellular radiosensitivity.\",\"authors\":\"V Ponette, N Giocanti, H Tourbez, J Balosso, C Hennequin, V Favaudon\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>A linear electron accelerator, operated in a recurrent chopped mode, was used for time-resolved investigation of split-dose radiation recovery in 3 mammalian cell lines in vitro. The time intervals separating the sequential radiation exposures in this study ranged from fractions of a second to a few minutes. The primary pulse brought about rapid, synchronous oscillations of cellular radiosensitivity giving rise to a tetraphasic, W-shaped time-dependent profile whose first phase was accomplished by a large decrease of cell survival. Only the last phase correlated with sub-lethal damage repair determined by gamma-ray irradiation. The same profile was observed for the 3 cell lines investigated. However, the kinetics of the whole process varied extensively from one cell line to another. The first phase lasted 1 s only for Chinese hamster V79 fibroblasts, 6 s for human squamous carcinoma SQ20B cells, and as much as 25 s for human colon adenocarcinoma LoVo cells. The relative amplitude of this first phase grew with both the first and second radiation doses in the range explored. It is hypothesized that rapid oscillation of the cytotoxic potential of radiation may result from various mechanisms such as molecular recognition of radio-induced lesions, changes in chromatin structure, or differential activation of phospholipid-dependent transduction pathways.</p>\",\"PeriodicalId\":10555,\"journal\":{\"name\":\"Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie\",\"volume\":\"319 6\",\"pages\":\"505-9\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1996-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Pulse exposure to ionizing radiation elicits rapid changes in cellular radiosensitivity.
A linear electron accelerator, operated in a recurrent chopped mode, was used for time-resolved investigation of split-dose radiation recovery in 3 mammalian cell lines in vitro. The time intervals separating the sequential radiation exposures in this study ranged from fractions of a second to a few minutes. The primary pulse brought about rapid, synchronous oscillations of cellular radiosensitivity giving rise to a tetraphasic, W-shaped time-dependent profile whose first phase was accomplished by a large decrease of cell survival. Only the last phase correlated with sub-lethal damage repair determined by gamma-ray irradiation. The same profile was observed for the 3 cell lines investigated. However, the kinetics of the whole process varied extensively from one cell line to another. The first phase lasted 1 s only for Chinese hamster V79 fibroblasts, 6 s for human squamous carcinoma SQ20B cells, and as much as 25 s for human colon adenocarcinoma LoVo cells. The relative amplitude of this first phase grew with both the first and second radiation doses in the range explored. It is hypothesized that rapid oscillation of the cytotoxic potential of radiation may result from various mechanisms such as molecular recognition of radio-induced lesions, changes in chromatin structure, or differential activation of phospholipid-dependent transduction pathways.