medwireNews: Results from an Australian study do not support the hypothesis that oxidative stress plays a primary role in the pathophysiology of bipolar disorder (BD).
An in vivo magnetic resonance spectroscopy (1H-MRS) study of 53 BD patients, aged an average of 22.8 years, and 51 age- and gender-matched mentally healthy controls demonstrated no significant between-group differences regarding glutathione levels in the anterior cingulate cortex, at 1.40 and 1.31 mM, respectively.
The researchers also found no significant correlations between glutathione levels and either Young Mania Rating Scale or Hamilton Depression Rating Scale scores in patients with BD.
Furthermore, there was no significant association between glutathione levels and age at disease onset or duration of illness in BD patients.
Lead author, Jim Lagopoulos (The University of Sydney), and colleagues explain that a number of previous studies showed that replenishment of glutathione diminishes oxidative cellular damage and reduces symptoms of depression in BD.
"Whilst the mechanism by which GSH [glutathione] exerts any clinical effect is unknown it has been proposed that it involves the bolstering of antioxidant defences by increasing the bioavailability of GSH, which in turn reverses clinical symptoms of depression," they comment.
However, the team the team adds that such a proposal is reliant on the implicit assumption that GSH levels are reduced in BD patients prior to GSH supplementation - an assumption not supported by the results of the current study.
"Collectively these results suggest that oxidative stress is not a core feature of young BD patients and as such any discernable therapeutic effects from GSH precursors (such as NAC [n-acetyl cysteine]) are likely to work via mechanisms other than a stoichiometric increase in the bioavailability of GSH," Lagopoulos et al conclude in the Journal of Psychiatric Research.
They add: "Further investigations using 1H-MRS in older patients with BD who have prolonged illness durations are warranted."
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