作者: Joanna A. Ruszkiewicz , Gabriel Teixeira de Macedo , Antonio Miranda-Vizuete , João B. Teixeira da Rocha , Aaron B. Bowman
DOI: 10.1016/J.NEURO.2018.08.007
关键词:
摘要: Abstract Methylmercury (MeHg) is an environmental pollutant linked to many neurological defects, especially in developing individuals. The thioredoxin (TRX) system a key redox regulator affected by MeHg toxicity, however the mechanisms and consequences of MeHg-induced dysfunction are not completely understood. This study evaluated role TRX C. elegans susceptibility during development. Worms lacking or overexpressing proteins from family were exposed for 1 h at different developmental stage: L1, L4 adult. without cytoplasmic exhibited age-specific when compared wild-type (wt). corresponded partially decreased total glutathione (GSH) levels enhanced degeneration dopaminergic neurons. In contrast, overexpression TRX-1/TRXR-1 did provide substantial protection against MeHg. Moreover, transgenic worms protein expression reductase (TRXR-1). Both mitochondrial TRX-2/TRXR-2, as well other thioredoxin-like proteins: TRX-3, TRX-4, TRX-5 show significant resistance Based on current findings, emerges important age-sensitive protectant toxicity elegans.