Longterm Effects of Neonatal Treatment with Cortisol and/or Estrogen in the Female BALB/c Mouse

Ways, Susan C.; Bern, Howard A.

doi:10.3181/00379727-160-40396

“…Data from another laboratory showed similar alterations in estrous cycles of rats following neonatal exposure to genistein with prolonged periods in estrus [72]. This is similar to mice exposed perinatally to DES [10,73] further supporting the idea that developmental exposure to estrogens causes disruptions in estrous cyclicity.…”

Section: Altered Estrous Cyclicitysupporting

confidence: 56%

Disruption of the developing female reproductive system by phytoestrogens: Genistein as an example

Jefferson¹,

Padilla-Banks²,

Newbold³

2007

Molecular Nutrition Food Res

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Studies in our laboratory have shown that exposure to genistein causes deleterious effects on the developing female reproductive system. Mice treated neonatally on days 1-5 by subcutaneous injection of genistein (0.5-50 mg/kg) exhibited altered ovarian differentiation leading to multioocyte follicles (MOFs) at 2 months of age. Ovarian function and estrous cyclicity were also disrupted by neonatal exposure to genistein with increasing severity observed over time. Reduced fertility was observed in mice treated with genistein (0.5, 5, or 25 mg/kg) and infertility was observed at 50 mg/kg. Mammary gland and behavioral endpoints were also affected by neonatal genistein treatment. Further, transgenerational effects were observed; female offspring obtained from breeding genistein treated females (25 mg/kg) to control males had increased MOFs. Thus, neonatal treatment with genistein at environmentally relevant doses caused adverse consequences on female development which is manifested in adulthood. Whether adverse effects occur in human infants exposed to soy-based products such as soy infant formulas is unknown but the neonatal murine model may help address some of the current uncertainties since we have shown that many effects obtained from feeding genistin, the glycosolated form of genistein found in soy formula, are similar to those obtained from injecting genistein.

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“…A role for endogenous estrogen and the devel? nity (42,43), pronounced thymic atrophy (44,45), depressed activity of natural killer cells (46,47), and stimulation ofthe reticuloendothelial system (48,49). Administration of pharmacologic or suprapharmacologic lev?…”

Section: Diethylstilbestrol: a Modelmentioning

confidence: 99%

Prenatal Immunotoxicant Exposure and Postnatal Autoimmune Disease

Holladay¹

1999

Environmental Health Perspectives

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Reports in humans and rodents indicate that immune development may be altered following perinatal exposure to immunotoxic compounds, including chemotherapeutics, corticosteroids, polycyclic hydrocarbons, and polyhalogenated hydrocarbons. Effects from such exposure may be more dramatic or persistent than following exposure during adult life. For example, prenatal exposure to the insecticide chlordane or to the polycyclic aromatic hydrocarbon benzo[(italic)a(/italic)]pyrene produces what appears to be lifelong immunosuppression in mice. Whether prenatal immunotoxicant exposure may predispose the organism to postnatal autoimmune disease remains largely unknown. In this regard, the therapeutic immunosuppressant cyclosporin A (CsA) crosses the placenta poorly. However, lethally irradiated rodents exposed to CsA postsyngeneic bone marrow transplant (i.e., during re-establishment of the immune system) develop T-cell-mediated autoimmune disease, suggesting this drug may produce a fundamental disruption in development of self-tolerance by T cells. The environmental contaminant 2,3,7, 8-tetrachlorodibenzo-(italic)p(/italic)-dioxin (TCDD) crosses the placenta and produces fetal thymic effects (italic)in vivo(/italic) similar to effects of CsA in fetal thymic organ culture, including inhibited thymocyte maturation and reduced expression of thymic major histocompatability complex class II molecules. These observations led to the suggestion that gestational exposure to TCDD may interfere with normal development of self-tolerance. Possibly supporting this hypothesis, when mice predisposed to development of autoimmune disease were treated with TCDD during gestation, postnatal autoimmunity was exacerbated. Similar results have been reported for mice exposed to diethylstilbestrol during development. These reports suggest that prenatal exposure to certain immunotoxicants may play a role in postnatal expression of autoimmunity.

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“…Administration of pharmacologic or suprapharmacologic levels of steroidal and nonsteroidal estrogenic compounds further results in numerous alterations of immune function, particularly when administered perinatally during lymphoid organ organogenesis. Effects of such administration in rodents include myelotoxicity (40,41), suppression of cell-mediated immunity (42,43), pronounced thymic atrophy (44,45), depressed activity of natural killer cells (46,47), and stimulation of the reticuloendothelial system (48,49). Studies of women exposed in utero to DES, a synthetic nonsteroidal compound possessing estrogenic activity, suggest possible adverse affects on the postnatal human immune system.…”

Section: Diethyistilbestrol: a Model Estrogenmentioning

confidence: 99%

Prenatal immunotoxicant exposure and postnatal autoimmune disease.

Holladay

¹

1999

Environ Health Perspect

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Reports in humans and rodents indicate that immune development may be altered following perinatal exposure to immunotoxic compounds, including chemotherapeutics, corticosteroids, polycyclic hydrocarbons, and polyhalogenated hydrocarbons. Effects from such exposure may be more dramatic or persistent than following exposure during adult life. For example, prenatal exposure to the insecticide chlordane or to the polycyclic aromatic hydrocarbon benzo[(italic)a(/italic)]pyrene produces what appears to be lifelong immunosuppression in mice. Whether prenatal immunotoxicant exposure may predispose the organism to postnatal autoimmune disease remains largely unknown. In this regard, the therapeutic immunosuppressant cyclosporin A (CsA) crosses the placenta poorly. However, lethally irradiated rodents exposed to CsA postsyngeneic bone marrow transplant (i.e., during re-establishment of the immune system) develop T-cell-mediated autoimmune disease, suggesting this drug may produce a fundamental disruption in development of self-tolerance by T cells. The environmental contaminant 2,3,7, 8-tetrachlorodibenzo-(italic)p(/italic)-dioxin (TCDD) crosses the placenta and produces fetal thymic effects (italic)in vivo(/italic) similar to effects of CsA in fetal thymic organ culture, including inhibited thymocyte maturation and reduced expression of thymic major histocompatability complex class II molecules. These observations led to the suggestion that gestational exposure to TCDD may interfere with normal development of self-tolerance. Possibly supporting this hypothesis, when mice predisposed to development of autoimmune disease were treated with TCDD during gestation, postnatal autoimmunity was exacerbated. Similar results have been reported for mice exposed to diethylstilbestrol during development. These reports suggest that prenatal exposure to certain immunotoxicants may play a role in postnatal expression of autoimmunity.

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Longterm Effects of Neonatal Treatment with Cortisol and/or Estrogen in the Female BALB/c Mouse

Cited by 15 publications

References 6 publications

Disruption of the developing female reproductive system by phytoestrogens: Genistein as an example

Disruption of the developing female reproductive system by phytoestrogens: Genistein as an example

Prenatal Immunotoxicant Exposure and Postnatal Autoimmune Disease

Prenatal immunotoxicant exposure and postnatal autoimmune disease.

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