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CYP2R1 expression was not seen in FL83B mouse hepatocytes) and 1--hydroxylase (CYP27B1), along with the increased expression of 24-hydroxylase (CYP24A1), was observed in GSH-deficient hepatocytes

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Due to the exhaustion of cellular and extracellular GSH caused by numerous GSH-consuming pathways the severe inflammation and oxidative stress triggered by the viral infection steals GSH from crucial functions like NO-dependent vasodilatation, disallowing the patient of being protected from an inflammation that can become fatal