Induction of hepatic monooxygenases in female rats and offspring in correlation with TCDD tissue concentrations after single treatment during pregnancy

Korte, Maria; Stahlmann, Ralf; Neubert, Diether

doi:10.1016/0045-6535(90)90244-n

Cited by 10 publications

(2 citation statements)

References 12 publications

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“…We have directly compared the developmental toxicity of TCDD after chronic administration (Bell et al 2007b)with acute administration of a single dose on Gestational Day 15 (GD15) (Bell et al 2007a): surprisingly chronic administration yielded delay in balanopreputial separation (BPS) at all three dose groups, whereas only the highest dose group yielded a delay in BPS in the acute dose study ; this finding was unexpected, since the chronic dosing study was designed to give similar body burdens of TCDD to those seen in the acute dose study. This experimental system is complicated by the post-parturition delivery of TCDD via milk (Korte et al 1990;Moore et al 1976;Nau et al 1986). The majority of TCDD in offspring of dosed dams arises from lactational transfer of TCDD (Hurst et al 2000a;Li et al 1995), and there is evidence that chronic dosing protocols can result in higher TCDD delivery to the offspring (Korte et al 1992).…”

Section: Introductionmentioning

confidence: 99%

Relationships between Tissue Levels of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), mRNAs, and Toxicity in the Developing Male Wistar(Han) Rat

Bell¹,

Clode²,

Fan³

et al. 2007

Toxicological Sciences

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We compared the effects of a single acute dose, or chronic fetal exposure, to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the male reproductive system of the Wistar(Han) rat. Tissue samples were taken from dams on gestation day (GD)16 and GD21, and from offspring on postnatal days (PND)70 and 120. Steady-state concentration of TCDD was demonstrated in the chronic study: body burdens were comparable in both studies. Fetal TCDD concentrations were comparable after acute and chronic exposure, and demonstrate more potent toxicity after chronic versus acute dosing. In maternal liver, cytochrome P450 (CYP)1A1 and CYP1A2 RNA were induced. In fetus, there was induction of both CYP1A1 and CYP1A2 RNA at medium and high doses, but inadequate evidence for induction at low dose in either study. The low level induction of CYP1A1 RNA at low dose in fetus argues against AhR activation in fetus as a mechanism of toxicity of TCDD in causing delay in balanopreputial separation (BPS), and the greater induction of CYP1A1 RNA in PND70 offspring liver from chronically-dosed dams suggests that lactational transfer of TCDD is crucial to this toxicity. These data characterize the maternal and fetal disposition of TCDD, induction of CYP1A1 RNA as a measure of AhR activation, and suggest that lactational transfer of TCDD determines the difference in delay in BPS between the two studies.

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Section: Introductionmentioning

confidence: 99%

Relationships between Tissue Levels of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), mRNAs, and Toxicity in the Developing Male Wistar(Han) Rat

Bell¹,

Clode²,

Fan³

et al. 2007

Toxicological Sciences

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“…26 While nursing represents the predominant source of perinatal exposure to TCDD, transplacental exposure also occurs. 27,28 Perinatal TCDD exposure of rodents has been shown to alter a variety of immune functions. In rats, these include suppression of the following: T cell mitogen responsiveness, 21,29 skin graft rejection time, 21 graft versus host activity, 21 and DTH responsiveness.…”

Section: 378-tetrachlorodibenzo-p-dioxin (Tcdd)mentioning

confidence: 99%

The rat as a model in developmental immunotoxicology

Smialowicz

2002

Hum Exp Toxicol

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Evidence is presented to demonstrate that the rat is a sensitive rodent species for developmental immunotoxicity testing of chemicals. A battery of immune function assays was performed in adult rats, which were exposed perinatally (i.e., during gestational, lactational, and//or juvenile development) to three different classes of environmental chemicals. The chemicals employed were the following: the organotins di-n-octyltindichloride (DOTC) and tributyltin oxide (TBTO); the polyhalogenated aromatic hydrocarbon 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); and the organochlorine pesticides methoxychlor (MXC) and heptachlor (HEP). Suppression of immune function was observed in adult rats exposed to each of these chemicals during immune system development. The duration of immune function suppression in the rats so exposed ranged from three weeks (i.e., DOTC and MXC) to 19 months (i.e., TCDD) after the last exposure to the chemical.

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Resistance to Trichinella spiralis infection, induction of hepatic monooxygenases, and concentrations in thymus and liver in rats after perinatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin

Korte¹,

Stahlmann²,

Thiel³

et al. 1991

Chemosphere

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Induction of hepatic monooxygenases in female rats and offspring in correlation with TCDD tissue concentrations after single treatment during pregnancy

Cited by 10 publications

References 12 publications

Relationships between Tissue Levels of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), mRNAs, and Toxicity in the Developing Male Wistar(Han) Rat

Relationships between Tissue Levels of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), mRNAs, and Toxicity in the Developing Male Wistar(Han) Rat

The rat as a model in developmental immunotoxicology

Resistance to Trichinella spiralis infection, induction of hepatic monooxygenases, and concentrations in thymus and liver in rats after perinatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin

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