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Da Monozyten, nachdem sie aus dem Knochenmark bergetreten sind, nur 24-48 h im Blut zirkulieren und nach Auswanderung nie zurck ins Blut rezirkulieren, ist ein nachweisbarer GSH-Mangel in Monozyten immer Hinweis auf Synthesemngel (Synthesemngel oder Mangel an SH-Gruppen spendenden Aminosuren) oder GSH-Verlust (Ausscheidung schadstoffkonjugierter GSH-Molekle ber die Niere)

These findings reveal the importance of mTOR in improving tendon structural integrity by promoting type I collagen production, offering a potential therapeutic target for IGF-1 in tendon repair applications