Strahlenbedingte Entwicklungsstörungen

Fritz-Niggli, H

doi:10.1007/978-3-642-80710-7_6

Cited by 4 publications

(6 citation statements)

References 106 publications

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“…Although malformation is seldom induced during these stages, these are the most sensitive stages with respect to embryonic lethality. Damaging effects result after single irradiation doses below 25 R and even as low as 5 R (Fritz-Niggli, 1972). 50% embryonic lethality is obtained after single irradiation doses of 100-150 R (Rugh and Wohlfromm, 1965).…”

Section: Discussionmentioning

confidence: 97%

Effects of acute X-irradiation on pre-implantation embryos and on the implantation reaction in the mouse

Aldeen

Konermann

1978

Radiat Environ Biophys

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Pregnant mice were treated on the 1st, 2nd, and 3rd day of pregnancy by a single dose of 300 R X-rays. Uterine dissections at day 6 p.c. topographically revealed decrease of the implantation sites from 9.67 per female in the controls to 8.00 in females irradiated on day 1, to 6.63 in females irradiated on day 2, and to 7.00 in females irradiated on day 3 p.c; Among a number of 22 implantations after irradiation on day 1, 19 after irradiation on day 2 and 11 after irradiation on day 3, however no living embryo could be detected on histological examination. The degree of damage as indicated by the total resorptions was highest (94,7%) after irradiation on day 2 p.c., and lowest (31,8%) after irradiation on day 1 p.c. Since the decidual cell reaction was either unaffected or only slightly reduced after irradiation on day 2 p.c. as indicated by cytomorphological criteria and the alkaline phosphatase reaction, not maternal effects but direct effects only of the irradiation on the embryo must account for embryonic deaths.

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Section: Discussionmentioning

confidence: 97%

Effects of acute X-irradiation on pre-implantation embryos and on the implantation reaction in the mouse

Aldeen

Konermann

1978

Radiat Environ Biophys

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“…5-17. Yamada, T., Yukawa, O., Asami, K., et al (1982) 1903-1907(Fritz-Niggli, 1959. Radiation-induced malformations in mammals (rabbits) were first described by v. Hippel and Pagenstecher (1907), and the report of v. Klot (1911) is among the first to document radiogenic termination of pregnancy in man.…”

Section: Referencesmentioning

confidence: 99%

“…In contrast to lethality as a single definite endpoint, further complications arise from both the broad variety of inducible malformations and from the degree of their expression. In the past, numerous experiments with rodents have been performed primarily to determine 'critical periods' for the induction of malformations, mainly based on 'morphological defects visible at birth' or skeletal defects observed in selectively stained fetuses (Russell, 1950(Russell, , 1954(Russell, , 1956Rugh, 1969;Fritz-Niggli, 1972;UNSCEAR, 1977). The phase dependency of malformations can be systematised roughly in so far as systemic defects and more organspecific defects are concerned.…”

Section: Malformations In Uteromentioning

confidence: 99%

Biological effects after prenatal irradiation (embryo and fetus)

Valentin¹

2003

Ann ICRP

123

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In its 1990 recommendations, the ICRP considered the radiation risks after exposure during prenatal development. This report is a critical review of new experimental animal data on biological effects and evaluations of human studies after prenatal radiation published since the 1990 recommendations.Thus, the report discusses the effects after radiation exposure during pre-implantation, organogenesis, and fetogenesis. The aetiology of long-term effects on brain development is discussed, as well as evidence from studies in man on the effects of in-utero radiation exposure on neurological and mental processes. Animal studies of carcinogenic risk from in-utero radiation and the epidemiology of childhood cancer are discussed, and the carcinogenic risk to man from in-utero radiation is assessed. Open questions and needs for future research are elaborated.The report reiterates that the mammalian embryo and fetus are highly radiosensitive. The nature and sensitivity of induced biological effects depend upon dose and developmental stage at irradiation. The various effects, as studied in experimental systems and in man, are discussed in detail. It is concluded that the findings in the report strengthen and supplement the 1990 recommendations of the ICRP.

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“…The extension of damage through several cell generations differs basicly from the redistributive tigroid reactions that follow a "primary irritation" of adult neurons and that have been cited above. The extreme radiosensitivity of the DNA in early neuroblasts (see [16,27]) provides evidence that origin and transfer of tigroid maturation damage is mediated by DNA defects. Biogenesis of ribosomal RNA results from transcription in the nucleolar organizer (chromocenter), where the r-DNA acts as matrix for the ribosomal RNA [31,39].…”

Section: Extended Tigroid Maturation Disturbancesmentioning

confidence: 99%

“…Radiation teratogenesis affects particularly the developing central nervous system with its prolonged and complicated genesis [16,21,[25][26][27]56]. Irradiation during early neurogenesis produces predominantly gross anatomical defects due to disturbances of organ induction and due to loss of blastema, the latter partly compensable by cell substitution and tissue reorganization [18,45,46].…”

Section: Introductionmentioning

confidence: 99%

The formation of tigroid substance during postnatal maturation of the brain of mice after pre- and perinatal X-irradiation

Konermann

Schwald

1980

Radiat Environ Biophys

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Using Nissl stained slices of postnatal brain, tigroid formation in neurons of the cortex, thalamus, cerebellum, hippocampus, gyrus dentatus and nucleus mot. trigemini was examined in X-irradiated mice. Following exposure on days 13, 16, 18.5 or 22 post conception with doses ranging from 0.5 Gy to 3.0 Gy tigroid formation was studied by means of a selective microphotometrical measurement technique. After irradiation, a fluctuating diminution in the tigroid density was observed in relation to the controls. It was dependent both on the dose and on the stage of development during exposure. In several brain regions fluctuating tigroid responses, being most pronounced during the "critical periods" of postnatal brain maturation, resulted in a longterm compensation of a deficit in the tigroid density after irradiation with 0.05 Gy. After the higher doses the density diminution was either not compensated or was progressive. The late tigroid responses decrease from irradiation on day 13 p.c. to irradiation day 22 p.c. Hence, this type of late maturation impairment was either extended through several cell generations or it was induced to a lesser degree in the early postmitotic neurons. Changes in the total RNA-content of the brain are concomitant with the range of the tigroid responses during the second and the beginning of the third week after birth. The tigroid reactions were interpreted as a chain of interdependent processes of retardation and stabilization. Accordingly, to obtain a better understanding of long-term maturation defects, a comprehensive evaluation of the whole chain of events will be required.

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Strahlenbedingte Entwicklungsstörungen

Cited by 4 publications

References 106 publications

Effects of acute X-irradiation on pre-implantation embryos and on the implantation reaction in the mouse

Effects of acute X-irradiation on pre-implantation embryos and on the implantation reaction in the mouse

Biological effects after prenatal irradiation (embryo and fetus)

The formation of tigroid substance during postnatal maturation of the brain of mice after pre- and perinatal X-irradiation

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