International journal of radiation biology and related studies in physics, chemistry, and medicine最新文献

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Effect of the inducers of cellular differentiation and of ionizing radiation on thymus lymphocytes: chromatin degradation and programmed cell death. 细胞分化诱导剂和电离辐射对胸腺淋巴细胞的影响:染色质降解和程序性细胞死亡。
I V Filippovich, N I Sorokina, V A Soldatenkov, T M Alfyerova, Z A Trebenok
{"title":"Effect of the inducers of cellular differentiation and of ionizing radiation on thymus lymphocytes: chromatin degradation and programmed cell death.","authors":"I V Filippovich,&nbsp;N I Sorokina,&nbsp;V A Soldatenkov,&nbsp;T M Alfyerova,&nbsp;Z A Trebenok","doi":"10.1080/09553008814550941","DOIUrl":"https://doi.org/10.1080/09553008814550941","url":null,"abstract":"<p><p>The cytotoxic response of thymocytes to chemical inducers of differentiation does not represent a non-specific toxic action of these drugs. The death of thymocytes treated with the inducers or with gamma-rays is associated with internucleosomal chromatin fragmentation. All treatments are more effective on the most radiosensitive sub-population of these cells. This subpopulation is characterized by the maximal level of spontaneous DNA lesions. Incubation of thymocytes with the inducers of differentiation raises the level of these lesions. It is suggested that the processes of thymocyte death after the inducer treatment or irradiation and of cellular differentiation have features in common, and the capacity of thymocytes to limit or reverse the potentially lethal effects of these treatments is determined by the level of pre-existing spontaneous DNA lesions.</p>","PeriodicalId":14254,"journal":{"name":"International journal of radiation biology and related studies in physics, chemistry, and medicine","volume":"53 4","pages":"617-28"},"PeriodicalIF":0.0,"publicationDate":"1988-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09553008814550941","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14386666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 18
A comparison of the radiation sensitivities of non-tumorigenic and tumorigenic human hybrid cell lines. 非致瘤性和致瘤性人类杂交细胞系辐射敏感性的比较。
M Colman, S Bhatt, M Candelaria, C Sun, J L Redpath
{"title":"A comparison of the radiation sensitivities of non-tumorigenic and tumorigenic human hybrid cell lines.","authors":"M Colman,&nbsp;S Bhatt,&nbsp;M Candelaria,&nbsp;C Sun,&nbsp;J L Redpath","doi":"10.1080/09553008814550931","DOIUrl":"https://doi.org/10.1080/09553008814550931","url":null,"abstract":"<p><p>The radiation sensitivities of two related non-tumorigenic and two related tumorigenic human hybrid cell lines (HeLa x skin fibroblast) have been studied. The data show that the transformation from the non-tumorigenic to the tumorigenic state, which is accompanied by the loss of skin fibroblast chromosomes 11 and 14, is not associated with any major changes in radiation sensitivity. The data do indicate, however, a trend toward a steeper and longer initial slope to the cell survival curve for the tumorigenic cell lines, along with a subsequent reduced ability to accumulate sublethal radiation injury at low doses. Both nontumorigenic and tumorigenic cell lines have the capability of repairing sublethal injury.</p>","PeriodicalId":14254,"journal":{"name":"International journal of radiation biology and related studies in physics, chemistry, and medicine","volume":"53 4","pages":"609-16"},"PeriodicalIF":0.0,"publicationDate":"1988-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09553008814550931","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14386665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Radiation-induced potentially lethal damage: DNA lesions susceptible to fixation. 辐射引起的潜在致命损伤:DNA损伤容易固定。
G Iliakis
{"title":"Radiation-induced potentially lethal damage: DNA lesions susceptible to fixation.","authors":"G Iliakis","doi":"10.1080/09553008814550901","DOIUrl":"https://doi.org/10.1080/09553008814550901","url":null,"abstract":"<p><p>The various postirradiation incubation conditions reported to uncover potentially lethal damage (PLD) induced by ionizing radiation are outlined and critically discussed. The process of damage fixation is the most characteristic determinant in distinguishing between PLD and other forms of damage (lethal or non-lethal). The results compiled indicate the induction of two forms of PLD (termed alpha- and beta-PLD). Evidence is presented that repair and fixation of alpha-PLD may underlie the variation in radiosensitivity observed through the cycle. Beta-PLD appears to be sensitive only to postirradiation treatment in anisotonic sale solutions. Results obtained at the DNA and chromosome level, under conditions allowing repair or causing fixation of PLD, are reviewed and combined together to devise a qualitative model that outlines a possible sequence of events from damage fixation at the DNA level, to damage fixation at the chromosome level and, ultimately, to cell death. It is suggested that damage uncovered at the cellular level as potentially lethal, comprises DNA dsb (single, pairs or groups) and that fixation is mediated by forces transmitted to the double helix through alteration (local or general) in chromatin conformation. Changes in chromatin conformation are caused either as a result of the cell's progression through the cycle or in response to a postirradiation treatment. The fixation process leads to the induction of chromosome aberrations. The validity of the concept of PLD in in vivo systems is shown, and the possible importance of PLD repair in radiation therapy is reviewed. The concept of PLD is compared to the concept of sublethal damage, and the possibility that similar molecular lesions underlie both types of damage is discussed.</p>","PeriodicalId":14254,"journal":{"name":"International journal of radiation biology and related studies in physics, chemistry, and medicine","volume":"53 4","pages":"541-84"},"PeriodicalIF":0.0,"publicationDate":"1988-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09553008814550901","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14407848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 144
Studies of ionizing radiation as a promoter of neoplastic transformation in vitro. 电离辐射在体外促进肿瘤转化的研究。
J B Little, H Vetrovs
{"title":"Studies of ionizing radiation as a promoter of neoplastic transformation in vitro.","authors":"J B Little,&nbsp;H Vetrovs","doi":"10.1080/09553008814550981","DOIUrl":"https://doi.org/10.1080/09553008814550981","url":null,"abstract":"<p><p>The induction of malignant transformation was examined in a standard promotion protocol in which BALB/3T3 cells were incubated continuously with tritiated water (3HOH) following acute treatment with various doses of either X-rays or benzo(a)pyrene (BP). In no case was there any evidence that protracted exposure to ionizing radiation from 3HOH enhanced the yield of transformants induced by the primary carcinogen over that predicted if the effects of the two agents were additive.</p>","PeriodicalId":14254,"journal":{"name":"International journal of radiation biology and related studies in physics, chemistry, and medicine","volume":"53 4","pages":"661-6"},"PeriodicalIF":0.0,"publicationDate":"1988-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09553008814550981","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14386669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Transformation and mutagenic potential of porphyrin photodynamic therapy in mammalian cells. 卟啉光动力疗法在哺乳动物细胞中的转化及致突变潜力。
C J Gomer, N Rucker, A L Murphree
{"title":"Transformation and mutagenic potential of porphyrin photodynamic therapy in mammalian cells.","authors":"C J Gomer,&nbsp;N Rucker,&nbsp;A L Murphree","doi":"10.1080/09553008814550971","DOIUrl":"https://doi.org/10.1080/09553008814550971","url":null,"abstract":"<p><p>The transformation and mutagenic potential of porphyrin photodynamic therapy has been examined in mammalian cells. The mutagenic frequency in Chinese hamster cells at the Na+/K+ ATPase locus was measured by resistance to ouabain following treatment with either photodynamic therapy (PDT) or UV irradiation. The C3H 10T 1/2 mouse embryo cell system was used to document the transformation frequency following PDT, UV irradiation, gamma irradiation or exposure to 3-methylcholanthrene (MCA). Treatments with UV irradiation were effective in producing mutants resistant to ouabain, and treatments with UV irradiation, gamma irradiation and MCA generated transformants at frequencies comparable to those which are reported in the literature. However, PDT treatment conditions (which produced a full range of cytotoxicity) did not induce any mutagenic or transformation activity above background levels.</p>","PeriodicalId":14254,"journal":{"name":"International journal of radiation biology and related studies in physics, chemistry, and medicine","volume":"53 4","pages":"651-9"},"PeriodicalIF":0.0,"publicationDate":"1988-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09553008814550971","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14099279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 38
Effect of dose rate on cell killing and DNA strand break repair in CHO cells exposed to internal beta-rays from incorporated [3H]thymidine. 剂量率对暴露于[3H]胸腺嘧啶内部β射线的CHO细胞的细胞杀伤和DNA链断裂修复的影响。
E Dikomey
{"title":"Effect of dose rate on cell killing and DNA strand break repair in CHO cells exposed to internal beta-rays from incorporated [3H]thymidine.","authors":"E Dikomey","doi":"10.1080/09553008814550991","DOIUrl":"https://doi.org/10.1080/09553008814550991","url":null,"abstract":"<p><p>Survival as well as repair of DNA strand breaks were studied in CHO cells after exposure to internal beta-rays from incorporated [3H]thymidine at 4 degrees C (equivalent to an exposure at 'infinitely high' dose rate) and at 37 degrees C (low dose rate). DNA strand breaks were determined by the alkaline unwinding technique. In cells exposed at 4 degrees C cell killing was five times higher (Do = 250 decays per cell) than in cells exposed at 37 degrees C (Do = 1280 decays per cell). Strand breaks induced by 3H decay at 37 degrees C were repaired with the same kinetics as those generated at 4 degrees C. Therefore the different degrees of cell killing at 4 degrees C and 37 degrees C cannot be attributed to a difference in the repair kinetics for DNA strand breaks.</p>","PeriodicalId":14254,"journal":{"name":"International journal of radiation biology and related studies in physics, chemistry, and medicine","volume":"53 4","pages":"667-78"},"PeriodicalIF":0.0,"publicationDate":"1988-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09553008814550991","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14386670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
The response of the International Commission on Radiological Protection to calls for a reduction in the dose limits for radiation workers and members of the public. 国际放射防护委员会对要求降低辐射工作人员和公众的剂量限制的反应。
P Green
{"title":"The response of the International Commission on Radiological Protection to calls for a reduction in the dose limits for radiation workers and members of the public.","authors":"P Green","doi":"10.1080/09553008814551001","DOIUrl":"https://doi.org/10.1080/09553008814551001","url":null,"abstract":"","PeriodicalId":14254,"journal":{"name":"International journal of radiation biology and related studies in physics, chemistry, and medicine","volume":"53 4","pages":"679-82"},"PeriodicalIF":0.0,"publicationDate":"1988-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09553008814551001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14386671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Factors influencing the uptake of iron and plutonium into cells. 影响铁和钚进入细胞的因素。
F Planas-Bohne, J Duffield
{"title":"Factors influencing the uptake of iron and plutonium into cells.","authors":"F Planas-Bohne,&nbsp;J Duffield","doi":"10.1080/09553008814552611","DOIUrl":"https://doi.org/10.1080/09553008814552611","url":null,"abstract":"<p><p>Uptake of 59Fe as well as 125I-labelled Fe-transferrin into HeLa cells points to the existence of a limited number of specific binding sites. This is in contrast to hepatocytes and hepatoma cells (Hep G2) where metal uptake from transferrin is very low, not saturable and cannot be prevented by an excess of the protein. Iron uptake into these cells is much higher from the citrate complex. The same is true for plutonium uptake into rat hepatocytes, while the uptake of this metal into Hep G2 cells is very small regardless of the ligand. In contrast to iron, plutonium presented as citrate is taken up into HeLa cells much better than plutonium presented as transferrin. The uptake of both metals from the citrate complex requires a high activation energy and can be prevented only by inhibition of oxidative phosphorylation. Other processes such as endocytosis, intactness of microtubuli, assembly of microfilaments or pH of the lysosomes do not seem to be of importance. Metal uptake from the citrate complex can be prevented only by the presence of other chelating agents and/or by transferrin. It can be assumed, therefore, that the metals react directly with constituents of the cell membrane, a process in which chelating agents can successfully compete if they form strong enough complexes with the metals.</p>","PeriodicalId":14254,"journal":{"name":"International journal of radiation biology and related studies in physics, chemistry, and medicine","volume":"53 3","pages":"489-500"},"PeriodicalIF":0.0,"publicationDate":"1988-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09553008814552611","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14407212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 17
Progressive development of radiation damage in mouse kidneys and the consequences for reirradiation tolerance. 小鼠肾脏辐射损伤的进行性发展及其对再照射耐受的影响。
F A Stewart, J V Lebesque, A A Hart
{"title":"Progressive development of radiation damage in mouse kidneys and the consequences for reirradiation tolerance.","authors":"F A Stewart,&nbsp;J V Lebesque,&nbsp;A A Hart","doi":"10.1080/09553008814552541","DOIUrl":"https://doi.org/10.1080/09553008814552541","url":null,"abstract":"<p><p>The aim of this study was to investigate the influence of protracted overall treatment times on the development and repair of renal irradiation injury in mice. Functional kidney damage was measured, from the proportion of 51CrEDTA remaining in the plasma at 30 min after injection of the tracer. Damage was assessed at monthly intervals for up to 14 months after two equal doses of X-rays given in 1 day, 1 month or 6 months. There was no difference between the time of onset or rate of development of damage after two fractions in 1 day or 1 month, but there was a time lag of 7-15 weeks (depending on dose) before the development of damage after 2F given in 6 months. After this time lag the rate of progression of damage was the same for 2F/6 months as for 2F in the shorter intervals. There was therefore no indication of any increase in total tolerated dose for the kidney when the treatment time was protracted, although the time scales for onset of this damage differed. Tolerance of mouse kidneys to reirradiation at 6 months after single doses of 6-12 Gy was also assessed. All of the previously irradiated animals developed a more severe renal impairment after reirradiation than did the age-matched control mice. The most severe damage occurred in mice which received the highest initial radiation doses, but doses of only 6 Gy were sufficient to markedly reduce the tolerance to reirradiation. It was concluded from these studies that no additional dose-sparing (tissue recovery) took place in the kidneys during a 6-month interval. This was true even when the initial radiation dose alone was insufficient to cause measurable renal dysfunction.</p>","PeriodicalId":14254,"journal":{"name":"International journal of radiation biology and related studies in physics, chemistry, and medicine","volume":"53 3","pages":"405-15"},"PeriodicalIF":0.0,"publicationDate":"1988-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09553008814552541","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14385885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 50
Biochemical binding and distribution of protactinium-233 in the rat. 大鼠体内镤-233的生化结合与分布。
U Schuppler, F Planas-Bohne, D M Taylor
{"title":"Biochemical binding and distribution of protactinium-233 in the rat.","authors":"U Schuppler,&nbsp;F Planas-Bohne,&nbsp;D M Taylor","doi":"10.1080/09553008814552581","DOIUrl":"https://doi.org/10.1080/09553008814552581","url":null,"abstract":"<p><p>Following intravenous injection into male Sprague-Dawley rats 233Pa, like other elements, deposits predominantly in the skeleton (ca. 70-80 per cent), but unlike Pu and Am the liver deposition of 233Pa is low, about 2-3 per cent between 1 and 7 days. About 99 per cent of the injected 233Pa is lost from the plasma compartment in 3 days, a clearance comparable to that of Pu but much slower than that of Np, Am or Cm. On entering the liver cell cytosol 233Pa is bound rapidly to an unidentified protein of molecular mass 200 kDa and to a protein of 80 kDa, which is probably transferrin. Within a few hours the metal migrates to bind to a protein of greater than 400 kDa which has been tentatively identified as ferritin. Some 233Pa remains bound to small ligands until virtually all the intracellular 233Pa has been deposited in the lysosomes, or to a lesser extent in some other, as yet, unidentified organelles.</p>","PeriodicalId":14254,"journal":{"name":"International journal of radiation biology and related studies in physics, chemistry, and medicine","volume":"53 3","pages":"457-66"},"PeriodicalIF":0.0,"publicationDate":"1988-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09553008814552581","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14387124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 7
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