- Tytuł:
- Selenite restores Pax6 expression in neuronal cells of chronically arsenic-exposed Golden Syrian hamsters
- Autorzy:
-
Aguirre-Vázquez, Alain
Sampayo-Reyes, Adriana
González-Escalante, Laura
Hernández, Alba
Marcos, Ricard
Castorena-Torres, Fabiola
Lozano-Garza, Gerardo
Taméz-Guerra, Reyes
Bermúdez de León, Mario - Powiązania:
- https://bibliotekanauki.pl/articles/1038549.pdf
- Data publikacji:
- 2017
- Wydawca:
- Polskie Towarzystwo Biochemiczne
- Tematy:
-
arsenic
selenite
α-tocopherol
neuronal cells
hamster - Opis:
- Arsenic is a worldwide environmental pollutant that generates public health concerns. Various types of cancers and other diseases, including neurological disorders, have been associated with human consumption of arsenic in drinking water. At the molecular level, arsenic and its metabolites have the capacity to provoke genome instability, causing altered expression of genes. One such target of arsenic is the Pax6 gene that encodes a transcription factor in neuronal cells. The aim of this study was to evaluate the effect of two antioxidants, α-tocopheryl succinate (α-TOS) and sodium selenite, on Pax6 gene expression levels in the forebrain and cerebellum of Golden Syrian hamsters chronically exposed to arsenic in drinking water. Animals were divided into six groups. Using quantitative real-time reverse transcriptase (RT)-PCR analysis, we confirmed that arsenic downregulates Pax6 expression in nervous tissues by 53 ± 21% and 32 ± 7% in the forebrain and cerebellum, respectively. In the presence of arsenic, treatment with α-TOS did not modify Pax6 expression in nervous tissues; however, sodium selenite completely restored Pax6 expression in the arsenic-exposed hamster forebrain, but not the cerebellum. Although our results suggest the use of selenite to restore the expression of a neuronal gene in arsenic-exposed animals, its use and efficacy in the human population require further studies.
- Źródło:
-
Acta Biochimica Polonica; 2017, 64, 4; 635-639
0001-527X - Pojawia się w:
- Acta Biochimica Polonica
- Dostawca treści:
- Biblioteka Nauki
Artykuł