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Altered neurometabolite levels, including glutathione (GSH) and gamma-aminobutyric acid (GABA), have been proposed as potential contributors to the biology underlying ASD

Chronic alcohol consumption inhibits sulfation and glucuronidation while depleting hepatic glutathione stores

Further analysis confirmed that FOXO4-positive cells co-expressed Leydig cell markers, specifically StAR and CYP11A1, indicating that FOXO4 is indeed expressed in human Leydig cells [1]

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