title: Resveratrol (3,5,4'-trihydroxystilbene) protects pregnant mother and fetus from the immunotoxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin.
abstract: METHODS
  The "fetal basis of adult disease" hypothesis proposes that prenatal exposure to environmental stress can lead to increased susceptibility to clinical disorders later in life. In utero exposure of fetus to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to alterations in T-cell differentiation in the thymus and increased susceptibility to autoimmune disease later in life. TCDD triggers toxicity through activation of aryl hydrocarbon receptor and severely affects maternal and fetal immune system during pregnancy.
  
  
  RESULTS
  In this study, using a mouse model, we investigated if administration of resveratrol (RES; 3,5,4'-trihydroxystilbene) would inhibit immunotoxicity induced by TCDD during pregnancy in the mother and fetus. We observed that RES protected not only normal nonpregnant mice but also pregnant mothers and their fetuses from TCDD-induced thymic atrophy, apoptosis, and alterations in the expression of T-cell receptor and costimulatory molecules as well as T-cell differentiation. In addition, there was significantly reduced expression of CYP1A1 in thymi of both the mother and the fetus when RES was used in vivo post-TCDD exposure.
  
  
  CONCLUSIONS
  In conclusion, these studies demonstrate that consumption of RES, a natural plant product, during pregnancy, may afford protection to the mother and the fetus from the toxicity induced by environmental pollutants that mediate their effects through activation of aryl hydrocarbon receptor.
authors: Department of Pathology, Microbiology & Immunology, University of South Carolina School of Medicine, Columbia, SC 29208, USA.
authors: Narendra P
authors: NP
authors: Singh
authors: Ugra S
authors: US
authors: Singh
authors: Mitzi
authors: M
authors: Nagarkatti
authors: Prakash S
authors: PS
authors: Nagarkatti
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001284:Atrophy / Q000517:prevention & control; D002454:Cell Differentiation / Q000187:drug effects; D002478:Cells, Cultured; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics / Q000378:metabolism; D004785:Environmental Pollutants / Q000633:toxicity*; D005260:Female; D005333:Fetus / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects; D018811:Maternal Exposure / Q000009:adverse effects; D051379:Mice; D008810:Mice, Inbred C57BL; D000072317:Polychlorinated Dibenzodioxins / Q000633:toxicity*; D011247:Pregnancy; D020011:Protective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D018336:Receptors, Aryl Hydrocarbon / Q000037:antagonists & inhibitors; D000077185:Resveratrol; D013267:Stilbenes / Q000494:pharmacology / Q000627:therapeutic use*; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000378:metabolism; D013950:Thymus Gland / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology
chemical_list: D004785:Environmental Pollutants; D000072317:Polychlorinated Dibenzodioxins; D020011:Protective Agents; D018336:Receptors, Aryl Hydrocarbon; D013267:Stilbenes; D019363:Cytochrome P-450 CYP1A1; D000077185:Resveratrol