Hi Tarmyg,
Its for the reason OBS said.
The articles below are full text through PubMed
https://www.sciencedirect.com/scienc...464?via%3Dihub
"...Glutathione (GSH) is a tripeptide of glutamate, cysteine and glycine that contains an unusual γ-peptide bond between glutamate and cysteine (Fig. 1). Such a bond prevents GSH from being hydrolyzed by most peptidases. GSH is less easily oxidized than its precursors, cysteine and γ-glutamylcysteine."
https://onlinelibrary.wiley.com/doi/...1002/tox.22017
"These data suggested the tissues with low GSH concentration are highly vulnerable to MCLR toxicity and GSH was critical for the detoxification in MCLR-induced hepatotoxicity in vivo."
GSH = Glutathione and MCLR = microcystin-leucine-arginine ... (MCLR)-induced hepatotoxicity
https://www.nutritionjrnl.com/articl...123-X/fulltext
Highlights


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    The consumption of alcoholic beverages injures the liver through concurrent tissue oxidation and suppression of reduced glutathione synthesis, activity, and recycling.
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    The acute consumption of any ethanol will increase the level of hepatic oxidative stress.
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    Ethanol potentiates the hepatic oxidative stress–steatosis–hepatitis–fibrosis–cirrhosis–carc inoma transformative continuum.
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    Even an acute single episode of ethanol consumption initiates metabolic pathways that achieve ultimate expression as hepatic fibrosis and cirrhosis.
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    In the absence of abstinence, increasing hepatic antioxidant capacity may reduce the severity of ethanol-associated hepatic injury and its consequences.