As the primary intracellular antioxidant, glutathione (GSH) is involved in free radical reactions in vivo involving paramagnetic iron II/III as catalysts or cofactors, suggesting that findings low tissue GSH by MRS could reflect T2 signal loss due to differences in iron content, rather than a genuine antioxidant deficit. This study estimated brain iron content using QSM to assess whether GSH deficits previously reported in patients with chronic fatigue syndrome (CFS) were genuine or simply a T2 signal loss. No iron content differences were found between patients and controls, supporting a genuine GSH deficit in CFS.
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