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• W2328697757 abstract "Glutathione (GSH) is a critical intracellular antioxidant that is active in free radical scavenging and as a reducing equivalent in biological reactions. Recent studies have suggested that GSH can affect cellular function at the level of gene transcription as well, in particular by affecting NF-κB activation. Additionally, increased or decreased GSH levels in vitro have been tied to increased or decreased hepatocyte proliferation, respectively. Here, we investigated the effect of GSH on the liver's response to TNF-α injection and 2/3 partial hepatectomy (PH), using mice deficient for the modifier subunit of glutamate-cysteine ligase (GCLM), the rate-limiting enzyme in de novo GSH synthesis. We demonstrate that Gclm-/- mice have a delay in IκBα degradation after TNF-α injection, resulting in delayed NF-κB nuclear translocation. These mice display profound deficiencies in GSH levels both before and during regeneration, and after PH, Gclm-/- mice have an overall delay in cell cycle progression, with slower DNA synthesis, mitosis, and expression of cell cycle proteins. Moreover, there is a delay in expression of downstream targets of NF-κB in the regenerating liver in Gclm-/- mice. These data suggest that GSH may play a role in hepatic NF-κB activation in vivo, which is necessary for accurate timing of liver regeneration." @default.
• W2328697757 created "2016-06-24" @default.
• W2328697757 creator A5023040317 @default.
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• W2328697757 date "2012-01-01" @default.
• W2328697757 modified "2023-09-26" @default.
• W2328697757 title "Sustained Glutathione Deficiency Interferes with the Liver Response to TNF-α and Liver Regeneration after Partial Hepatectomy in Mice" @default.
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• W2328697757 doi "https://doi.org/10.4172/2325-9612.1000105" @default.
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