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• W1566852951 abstract "Arsenic (As) is a notoriously poisonous metalloid with known hazardous effects to human health. The project described in this thesis was aimed at elucidating the probable mechanism of As-induced neurotoxicity in vivo and in vitro. The animal studies in this thesis were designed to answer questions about the effect of As on the peripheral nervous system after sub-acute and chronic intoxication of laboratory rats. Protein composition analysis showed compositional changes in sciatic nerves proteins. Protein expression of neurofilament heavy (NF-H) and neurofilament medium (NF-M) remained unchanged. Neurofilament protein light (NF-L) expression was reduced, while μ- and m-calpain protein expression was increased, both in a dose/time pattern. Furthermore, NF-H protein was hypophosphorylated; while NF-L and microtubule-associated protein tau (MAP-tau) proteins were phosphorylated. In the in vitro studies, effects of As species were tested in various cell culture models and the manner of their hyperphosphorylation was further studied for a better understanding of the disruption of neuroskeletal integrity by As. In vitro studies showed that the compositional changes were not caused by the changes on RNA expression levels, rather a post-translational activity. Cells treated with arsenite showed cleavage of p35 to p25 by calpain, which is mediated by an increase of Ca2+ in the cells. Over expression of calpain results in hyperphosphorylation of NF-L and activated calpain is also responsible for NF-L degradation." @default.
• W1566852951 created "2016-06-24" @default.
• W1566852951 creator A5006267668 @default.
• W1566852951 date "2008-02-14" @default.
• W1566852951 modified "2023-09-23" @default.
• W1566852951 title "Studies into the mechanism of arsenic-induced neurotoxicity" @default.
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• W1566852951 hasPublicationYear "2008" @default.
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