2005
DOI: 10.1016/j.neuro.2004.07.012
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Thimerosal Neurotoxicity is Associated with Glutathione Depletion: Protection with Glutathione Precursors

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Cited by 129 publications
(87 citation statements)
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“…Our data derived from in vivo experiments in rats, supports results of earlier in vitro studies (Lamirand et al, 2008). Other in vitro studies indicated that the exposure of neuronal cells to Met-Hg (Kim et al, 2005) or neuroblastoma cells to TM (James et al, 2005) results in a depletion of GSH which is both an antioxidant and a cofactor of deiodinases (Goswani and Rosenberg, 1988;Bhat et al, 1989;Croteau et al, 1998;Goemann et al, 2010). Thus, cerebellar D2 activity might be impaired due to a lack of the reducing cofactor.…”
Section: Disruption Of Brain Th Homeostasis By Environmental Toxicantssupporting
confidence: 88%
“…Our data derived from in vivo experiments in rats, supports results of earlier in vitro studies (Lamirand et al, 2008). Other in vitro studies indicated that the exposure of neuronal cells to Met-Hg (Kim et al, 2005) or neuroblastoma cells to TM (James et al, 2005) results in a depletion of GSH which is both an antioxidant and a cofactor of deiodinases (Goswani and Rosenberg, 1988;Bhat et al, 1989;Croteau et al, 1998;Goemann et al, 2010). Thus, cerebellar D2 activity might be impaired due to a lack of the reducing cofactor.…”
Section: Disruption Of Brain Th Homeostasis By Environmental Toxicantssupporting
confidence: 88%
“…54,55 In addition, alternative practitioners have been discussing the theory that anti-oxidant pathways are insufficient in patients with autism. This relationship has been noted in the past, and evidence of a predisposition of insufficient glutathione or anti-oxidant reserves in autistic patients has been described by James et al 56,57 Chez 58 previously reported a similar insufficiency in antioxidant protection in patients diagnosed with variants of Landau-Kleffner and concurrent autistic features. Insufficient anti-oxidant protection may not be the initial cause, but rather an endpoint of chronic ongoing inflammation.…”
Section: Human Evidence Of Ongoing Atypical Inflammatory Responsesupporting
confidence: 52%
“…Contiene 49,6% de Hg por peso. En soluciones salinas, se disocia en cloruro de etilHg y ácido tiosalicílico ( 69 ); una vez disociado, el etilHg tiene una altísima afinidad por los radicales sulfhidrilos (SH) que se encuentran en algunas enzimas antioxidantes, como el glutatión o las metalotioneínas (proteínas producidas por el hígado), enzimas que tienen un límite de unión al metal pesado (saturación), dejando libre al etilHg excedente ( [70][71][72] ). Esto permite aseverar que, una exposición elevada a timerosal, sobrepasaría los límites de saturación por parte de los antioxidantes naturales.…”
Section: Resultsunclassified