Bcl-2 gene family expression in the brain of rat offspring after gestational and lactational dioxin exposure

Shwu Fen Chang, Yu Yo Sun, Liang Yo Yang, Ssu Yao Hu, Shih-Ying Tsai, Wen Sen Lee, Yi-Hsuan Lee

Research output: Contribution to journalArticle

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Abstract

Recent epidemiological studies have shown that dioxin, a persistent organic pollutant, is related to cognitive and behavioral abnormalities in the offspring of exposed cohort. In order to investigate the possible impact of dioxin in survival gene expression during brain development, we established an animal model of gestational and lactational dioxin-exposed rat offspring. The expressions of dioxin-responsive gene cytochrome P450 1A1 (CYP1A1), apoptotic gene Bax, and anti-apoptotic genes Bcl-2 and Bcl-xL were examined in rat liver and brains using Western blot analysis and RT-PCR. The results showed that treatment of pregnant rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (2 μg/kg body weight through oral delivery) at gestation day 15 resulted in an increase of Bcl-xL in offspring male liver and cerebral cortex, but a decrease in female offspring. In contrast, the expression of Bcl-x L in the cerebellum was decreased in male, but increased in female. Bcl-2, another antiapoptotic gene, was also downregulated in P0 female liver, cerebral cortex, but was not observed in male. In the 4-month-old offspring, however, the Bcl-2 protein levels in the liver and cerebellum of both male and female pups were higher in the TCDD group as compared with the control group. However, the Bcl-2 level in the cerebral cortex of TCDD-treated groups was higher than the control group only in female but not male offspring at 4 months old. The expression of Bax showed no significant changes upon TCDD exposure at P0 stage, but was significantly reduced in the 4-month-old male cortex. These results indicate that early exposure of dioxin could affect the development of certain brain regions with gender difference, in terms of its differential effect on expressions of Bcl-xL, Bcl-2, and Bax.

Original languageEnglish
Pages (from-to)471-480
Number of pages10
JournalAnnals of the New York Academy of Sciences
Volume1042
DOIs
Publication statusPublished - 2005

Fingerprint

bcl-2 Genes
Dioxins
Rats
Brain
Genes
Liver
Gene Expression
Cerebral Cortex
Cerebellum
Organic pollutants
Control Groups
Gene expression
Cytochrome P-450 Enzyme System
Animals
Offspring
Gene
Rat
Epidemiologic Studies
Down-Regulation
Animal Models

Keywords

  • Bax
  • Bcl-2
  • Bcl-x
  • Brain
  • Cerebellum
  • Cerebral cortex
  • Dioxin
  • Liver

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

Bcl-2 gene family expression in the brain of rat offspring after gestational and lactational dioxin exposure. / Chang, Shwu Fen; Sun, Yu Yo; Yang, Liang Yo; Hu, Ssu Yao; Tsai, Shih-Ying; Lee, Wen Sen; Lee, Yi-Hsuan.

In: Annals of the New York Academy of Sciences, Vol. 1042, 2005, p. 471-480.

Research output: Contribution to journalArticle

Chang, Shwu Fen ; Sun, Yu Yo ; Yang, Liang Yo ; Hu, Ssu Yao ; Tsai, Shih-Ying ; Lee, Wen Sen ; Lee, Yi-Hsuan. / Bcl-2 gene family expression in the brain of rat offspring after gestational and lactational dioxin exposure. In: Annals of the New York Academy of Sciences. 2005 ; Vol. 1042. pp. 471-480.
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abstract = "Recent epidemiological studies have shown that dioxin, a persistent organic pollutant, is related to cognitive and behavioral abnormalities in the offspring of exposed cohort. In order to investigate the possible impact of dioxin in survival gene expression during brain development, we established an animal model of gestational and lactational dioxin-exposed rat offspring. The expressions of dioxin-responsive gene cytochrome P450 1A1 (CYP1A1), apoptotic gene Bax, and anti-apoptotic genes Bcl-2 and Bcl-xL were examined in rat liver and brains using Western blot analysis and RT-PCR. The results showed that treatment of pregnant rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (2 μg/kg body weight through oral delivery) at gestation day 15 resulted in an increase of Bcl-xL in offspring male liver and cerebral cortex, but a decrease in female offspring. In contrast, the expression of Bcl-x L in the cerebellum was decreased in male, but increased in female. Bcl-2, another antiapoptotic gene, was also downregulated in P0 female liver, cerebral cortex, but was not observed in male. In the 4-month-old offspring, however, the Bcl-2 protein levels in the liver and cerebellum of both male and female pups were higher in the TCDD group as compared with the control group. However, the Bcl-2 level in the cerebral cortex of TCDD-treated groups was higher than the control group only in female but not male offspring at 4 months old. The expression of Bax showed no significant changes upon TCDD exposure at P0 stage, but was significantly reduced in the 4-month-old male cortex. These results indicate that early exposure of dioxin could affect the development of certain brain regions with gender difference, in terms of its differential effect on expressions of Bcl-xL, Bcl-2, and Bax.",
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AU - Lee, Wen Sen

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AB - Recent epidemiological studies have shown that dioxin, a persistent organic pollutant, is related to cognitive and behavioral abnormalities in the offspring of exposed cohort. In order to investigate the possible impact of dioxin in survival gene expression during brain development, we established an animal model of gestational and lactational dioxin-exposed rat offspring. The expressions of dioxin-responsive gene cytochrome P450 1A1 (CYP1A1), apoptotic gene Bax, and anti-apoptotic genes Bcl-2 and Bcl-xL were examined in rat liver and brains using Western blot analysis and RT-PCR. The results showed that treatment of pregnant rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (2 μg/kg body weight through oral delivery) at gestation day 15 resulted in an increase of Bcl-xL in offspring male liver and cerebral cortex, but a decrease in female offspring. In contrast, the expression of Bcl-x L in the cerebellum was decreased in male, but increased in female. Bcl-2, another antiapoptotic gene, was also downregulated in P0 female liver, cerebral cortex, but was not observed in male. In the 4-month-old offspring, however, the Bcl-2 protein levels in the liver and cerebellum of both male and female pups were higher in the TCDD group as compared with the control group. However, the Bcl-2 level in the cerebral cortex of TCDD-treated groups was higher than the control group only in female but not male offspring at 4 months old. The expression of Bax showed no significant changes upon TCDD exposure at P0 stage, but was significantly reduced in the 4-month-old male cortex. These results indicate that early exposure of dioxin could affect the development of certain brain regions with gender difference, in terms of its differential effect on expressions of Bcl-xL, Bcl-2, and Bax.

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KW - Dioxin

KW - Liver

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