Exposure to bisphenol A during embryonic/fetal life and infancy increases oxidative injury and causes underdevelopment of the brain and testis in mice.
Life Sci
; 74(24): 2931-40, 2004 Apr 30.
Article
em En
| MEDLINE
| ID: mdl-15051418
ABSTRACT
We investigated the modifications in endogenous antioxidant capacity and oxidative damage in the brain, liver, kidney and testis in mice exposed to bisphenol A (BPA), an environmental endocrine disrupter. Mice were exposed to BPA throughout embryonic/fetal life and during lactation by feeding their pregnant/lactating mothers BPA at 5 or 10 microg per milliliter of drinking water. At the age of four weeks, male mice were sacrificed. Exposure to BPA increased the activity of catalase and glutathione peroxidase in the liver and kidney, respectively. It also increased thiobarbituric acid-reactive substances in the brain, kidney and testis, and decreased the wet weight of the brain, kidney and testis. Our results suggest that exposure to BPA throughout embryonic/fetal life and during infancy induces tissue oxidative stress and peroxidation, ultimately leading to underdevelopment of the brain, kidney and testis.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fenóis
/
Efeitos Tardios da Exposição Pré-Natal
/
Testículo
/
Encéfalo
/
Estresse Oxidativo
/
Exposição Materna
/
Estrogênios não Esteroides
Tipo de estudo:
Etiology_studies
Limite:
Animals
/
Pregnancy
Idioma:
En
Ano de publicação:
2004
Tipo de documento:
Article