Experimenteller Beitrag zur Pr�fung teratogener Wirkungen von Arzneimitteln an der Laboratoriumsratte

Brock, N; Kreybig, Th. von

doi:10.1007/bf00247005

Cited by 28 publications

(3 citation statements)

References 15 publications

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“…Gottchewski [7, 81 was able to induce pre-and postimplantation embryolethality and congenital malformations in rabbit embryos, the mothers having been treated with actinomycin D or cychlophosphamide (CPA) during the preimplantation period. Similar results were obtained by Brock and Von Kreybig [9] in the rats, after treatment with CPA on day 3 post coitum (PC). Hurley and Shrader [ 101 observed developmental retardation and morphological anomalies in rat preimplantation embryos, the mothers having been fed a zinc-deficient diet.…”

Section: Introductionsupporting

confidence: 87%

Developmental toxicity during the preimplantation period: Embryotoxicity and clastogenic effects of chlorambucil in the rat

Giavini

Bonanomi

Ornaghi

1984

Teratog Carcinog Mutagen

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To evaluate the toxicological effects of chemicals on preimplantation mammalian embryos, pregnant rats were treated with chlorambucil (0, 3, 6, and 12 mg/kg IP) on day 1, 2, or 3 of gestation (positive vaginal smear = day 0). Blastocysts were collected on day 4 and evaluated for gross morphology, cell number, and mitotic index. Some females treated on day 3 post coitum were sacrificed on day 20 and fetuses were evaluated for teratogenic effects. On day 4 of gestation a dose-related reduction of cell number/embryo was recorded; this effect was most manifest with treatment on day 3 post coitum. The mitotic index was significantly higher in all treated groups. A dose-related increase in "micronucleus-like bodies" has been observed in treated embryos. A comparison with the micronucleus test in the bone marrow revealed a major sensitivity of the embryonic material. No malformations have been observed in fetuses at term, but their weights were significantly reduced and a dose-related increase of postimplantation loss was recorded in treated females.

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Section: Introductionsupporting

confidence: 87%

Developmental toxicity during the preimplantation period: Embryotoxicity and clastogenic effects of chlorambucil in the rat

Giavini

Bonanomi

Ornaghi

1984

Teratog Carcinog Mutagen

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“…O n the other hand, a substance that in itself could act as a teratogen under certain circumstances can protect embryos against another teratogen. Fratta et al (1964), for instance, demonstrated a protective effect of chlorpromazine on teratogenesis obtained by nicotinamid deficiency, whereas, for instance, Brock & Kreybig ( 1964), showed a teratogenic effect of chlorpromazine on rats. Immobilization of the pregnant female increases the teratogenic effect of salicylate (Goldman et al 1963(Goldman et al , 1964 but this potentiation is prevented by chlorpromazine.…”

Section: Principles In Drug Teratogenesismentioning

confidence: 97%

Malformations Due to Toxic Influences

Källén

1968

Acta Ophthalmologica

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“…Treatment of rats during the pregastrulation stage with mutagens or other compounds has been shown to result in embryonic mortality or IUGR or in developmental abnormalities (Brock and von Kreybig, 1964;Spielmann et al, 1977;Giavini et al, 1984Giavini et al, , 1990Yokoi et al, 2007). Embryonic death and IUGR are thus common consequences of exposure to xenobiotic agents at the pregastrulation stage in rats and mice.…”

Section: Embryonic Mortality and Intrauterine Growth Retardation (Iugr)mentioning

confidence: 99%

Embryonic mortality and intrauterine growth retardation (IUGR) associated with placental alterations in pregnant rats treated with methyl methanesulfonate (MMS) at the peri-implantation stage

et al. 2008

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-Embryonic mortality and intrauterine growth retardation (IUGR) are induced by exposure of rodents to xenobiotic agents during the pregastrulation period of development. We examined the time course of the effects of methyl methanesulfonate (MMS), an alkylating agent, on conceptus development in order to clarify the relative roles of the embryo and the placenta in their induction. Pregnant rats were treated orally with a single dose of MMS (200 mg/kg) in the morning of gestation day (GD) 6 (peri-implantation stage). Embryonic mortality was increased on GD12 and thereafter by MMS treatment, with newly dead embryos showing placental hypoplasia at GD12. Embryo or fetal weight was also smaller for MMS-treated dams than for control dams from GD14 to GD20. The labyrinth zone and junctional zone (JZ) of the placenta were thinner in MMS-treated rats from GD12 to GD17 and from GD12 to GD20 (except for GD17), respectively. Furthermore, MMS-treated dams showed a smaller number of glycogen cells in the JZ on GD14. In contrast, the placental glycogen concentration was higher and the expression of glucose transporter 1 in the JZ remained at GD20. These results indicate that exposure of pregnant rats to MMS at the peri-implantation stage of embryogenesis affects placental development and growth. The placental impairment induced by MMS was likely responsible for the embryonic death observed 6 days after exposure of dams to this agent as well as for the IUGR of surviving embryos or fetuses throughout the gestation period.

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Experimenteller Beitrag zur Pr�fung teratogener Wirkungen von Arzneimitteln an der Laboratoriumsratte

Cited by 28 publications

References 15 publications

Developmental toxicity during the preimplantation period: Embryotoxicity and clastogenic effects of chlorambucil in the rat

Developmental toxicity during the preimplantation period: Embryotoxicity and clastogenic effects of chlorambucil in the rat

Malformations Due to Toxic Influences

Embryonic mortality and intrauterine growth retardation (IUGR) associated with placental alterations in pregnant rats treated with methyl methanesulfonate (MMS) at the peri-implantation stage

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