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Neurobehavioral effects of the exposure to mercury vapor and methylmercury during postnatal period on mice.
Lee, Jin-Yong; Yoshida, Minoru; Satoh, Masahiko; Watanabe, Chiho.
Afiliação
  • Lee JY; Laboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya, 464-8650 Japan.
  • Yoshida M; Department of Nursing, Tokyo Junshin University, 2-600 Takiyama-machi, Hachioji, Tokyo, 192-0011 Japan.
  • Satoh M; Laboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya, 464-8650 Japan.
  • Watanabe C; Interfaculty Initiative in Planetary Health, Nagasaki University, 1-12-4 Sakamoto, Nagasaki, 852-8523 Japan.
Toxicol Res ; 40(1): 111-124, 2024 Jan.
Article em En | MEDLINE | ID: mdl-38223668
ABSTRACT
In this study, we investigated the neurobehavioral alterations and modifications of gene expression in the brains of female mice exposed to low-level mercury vapor and/or methylmercury during postnatal development. The mice were exposed to low-level mercury vapor at a mean concentration of 0.094 mg/m3 and supplied with tap water containing 5 ppm methylmercury from postnatal day 11 to 12 weeks of age. Behavioral analyses were performed at 17 weeks of age. Total locomotor activity in the open field test and the retention trial performance in the passive avoidance test were significantly reduced in the combined exposure group compared with those in the control group. The differences in locomotor activity and performance in the retention trial at 17 weeks were no longer detected at 45 weeks. These results suggest that the effect of aging on the behavioral abnormalities resulting from postnatal exposure to mercury complexes are not significant. In the microarray analysis of brains in the combined exposure group, the gene expression levels of Ano2 and Sgk1 were decreased. Real-time RT-PCR analysis confirmed these changes caused by combined mercury exposure, showing significant downregulation of Ano2 and Sgk1 in the cerebrum. These genes play key roles in the brain as a calcium-activated chloride channel and as a kinase that responds to cellular stress, respectively. Our findings provide insight into the neurobehavioral changes caused by combined mercury exposure.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article