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La supplémentation en acide ascorbique prévient les effets néfastes de l’exposition prénatale et postnatale au plomb sur la cellule de Purkinje et les protéines associées dans le cervelet de rats en développement.

Nous avons étudié les effets de la co-administration de plomb (Pb) et d'acide ascorbique sur le développement cérébelleux chez le rat. Avant l'accouplement, les rats ont été répartis au hasard en groupes de contrôle, Pb et Pb plus acide ascorbique (PA). On a administré du Pb à des rates gravides dans de l'eau potable (acétate à 0,3% de Pb) et de l'acide ascorbique (100 mg / kg) par intubation orale jusqu'à la fin de l'expérience. La progéniture a été sacrifiée au 21e jour après la naissance, l'âge auquel la morphologie du cortex cérébelleux chez les ratons en développement est similaire à celle du cerveau adulte. Dans le cervelet, l'exposition au Pb réduisait considérablement les cellules de Purkinje et l'acide ascorbique empêchait leur réduction. Parallèlement au changement des cellules de Purkinje, une exposition à long terme au Pb a considérablement réduit l'expression du marqueur synaptique (synaptophysine), de l'enzyme de synthèse de l'acide gamma-aminobutyrique (GABA) (acide glutamique décarboxylase 67) et de la protéine de base de la myéline axonale pendant l'ascorbine. le co-traitement acide atténue la réduction médiée par le Pb de ces protéines dans le cervelet des ratons. Cependant, les récepteurs glutamatergiques de N-méthyl-D-aspartate de type 1 (NMDAR1), la protéine de densité post-synaptique 95 (PSD95) et les antioxydants superoxyde dismutases (SOD) ont été modifiés; L'exposition au Pb augmentait l'expression de NMDAR1, PSD95 et SOD, tandis que la co-administration d'acide ascorbique atténuait l'induction induite par le Pb. Bien que d'autres études soient nécessaires sur la neurotoxicité de l'exposition au Pb, les résultats présentés ici suggèrent que l'exposition au développement au Pb a perturbé le développement normal des cellules de Purkinje en augmentant le stress glutamatergique et oxydant dans le cervelet. De plus, le co-traitement à l'acide ascorbique est bénéfique pour atténuer le mauvais développement des cellules de Purkinje induit par l'exposition au Pb induit par l'exposition au Pb dans le cervelet en développement.


Source: https://www.ncbi.nlm.nih.gov/pubmed/30488169


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