Abstract

Paraquat is an herbicide widely used in agriculture, that proved to have toxic effect on many animal models. Moreover, it is considered a potential etiologic factor of Parkinson's disease. Ascidians are invertebrate chordates, whose larval central nervous system shares basic structural homologies with the vertebrate one. Ascidian larvae exposed to paraquat developed specific alterations of the CNS, that were characterized by histological and immunohistochemical analysis. Tyrosine hydroxylase ( TH) expression was examined by “in situ” hybridization. A decrease of dopamine content in anterior CNS of treated larvae was observed. In combined treatments with paraquat and l-ascorbic acid, a common anti-oxidant, the severity of the malformations was significantly reduced, confirming that the oxidative stress is involved in the toxicity mechanism of paraquat on ascidians. For its sensitivity to paraquat and its simple chordate body plan, ascidian larva is a promising animal model to further investigate the molecular mechanism of paraquat neurotoxicity.

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