Sulforaphane Augments Glutathione and Influences Brain Metabolites in Human Subjects: A Clinical Pilot Study
Sedlak TW, Nucifora LG, Koga M, Shaffer LS, Higgs C, Tanaka T, Wang AM, Coughlin JM, Barker PB, Fahey JW, Sawa A
Molecular neuropsychiatry · 71 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- Controlled clinical trial (classified by our AI screen)
- Studied in
- People
- Main outcome
- Mechanisms only
- Intake measured by
- Not stated
Who paid for it
- Funding
- Independent funding
- University or hospital
- Johns Hopkins University
- Government
- National Institutes of Health
- Government
- National Institute of Mental Health
- Government
- National Institute of Neurological Disorders and Stroke
- Government
- NIMH NIH HHS
- Government
- NINDS NIH HHS
- Grants
- National Institute of Mental Health (R01 MH092443); National Institute of Mental Health (R01MH105660); National Institute of Mental Health (P50MH094268); National Institute of Neurological Disorders and Stroke (K08 NS057824)
Based on 6 listed funder(s).
Publication
- Published
- 2017-01-01 · Mol Neuropsychiatry · vol. 3 · issue 4 · pp. 214–222
- Publisher
- Karger Publishers
- Cited
- 79 citations · more than 93% of similar papers · 3.3× the field average
- Impact
- Top 10% most cited in its field
- References
- 84 works
- Access
- Open access (repository copy)
- Research areas
- Genomics, phytochemicals, and oxidative stress · Sulfur Compounds in Biology · Tryptophan and brain disorders
- Keywords
- Sulforaphane, Glutathione, Oxidative stress, Schizophrenia (object-oriented programming), Medicine, Isothiocyanate, Human brain, Internal medicine, Pharmacology, Neuroscience, Psychology, Chemistry, Psychiatry, Biochemistry
11 authors
From US
- Thomas W. SedlakJohns Hopkins University; Johns Hopkins Medicine
- Leslie G. NuciforaJohns Hopkins University; Johns Hopkins Medicine
- Minori KogaJohns Hopkins University; Johns Hopkins Medicine
- Lindsay S. ShafferJohns Hopkins University; Johns Hopkins Medicine
- Cecilia P. HiggsJohns Hopkins University; Johns Hopkins Medicine
- Teppei TanakaJohns Hopkins University; Johns Hopkins Medicine
Abstract
Schizophrenia and other neuropsychiatric disorders await mechanism-associated interventions. Excess oxidative stress is increasingly appreciated to participate in the pathophysiology of brain disorders, and decreases in the major antioxidant, glutathione (GSH), have been reported in multiple studies. Technical cautions regarding the estimation of oxidative stress-related changes in the brain via imaging techniques have led investigators to explore peripheral GSH as a possible pathological signature of oxidative stress-associated brain changes. In a preclinical model of GSH deficiency, we found a correlation between whole brain and peripheral GSH levels. We found that the naturally occurring isothiocyanate sulforaphane increased blood GSH levels in healthy human subjects following 7 days of daily oral administration. In parallel, we explored the potential influence of sulforaphane on brain GSH levels in the anterior cingulate cortex, hippocampus, and thalamus via 7-T magnetic resonance spectroscopy. A significant positive correlation between blood and thalamic GSH post- and pre-sulforaphane treatment ratios was observed, in addition to a consistent increase in brain GSH levels in response to treatment. This clinical pilot study suggests the value of exploring relationships between peripheral GSH and clinical/neuropsychological measures, as well as the influences sulforaphane has on functional measures that are altered in neuropsychiatric disorders.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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