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 citas
Etiquetas de revisión
Solo mecanismosDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Ensayo clínico controlado (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas
- Resultado principal
- Solo mecanismos
- Consumo medido con
- No se indica
Quién lo pagó
- Financiación
- Financiación independiente
- Universidad u hospital
- Johns Hopkins University
- Gobierno
- National Institutes of Health
- Gobierno
- National Institute of Mental Health
- Gobierno
- National Institute of Neurological Disorders and Stroke
- Gobierno
- NIMH NIH HHS
- Gobierno
- NINDS NIH HHS
- Subvenciones
- 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)
Según 6 financiadores declarados.
Publicación
- Publicado
- 2017-01-01 · Mol Neuropsychiatry · vol. 3 · número 4 · págs. 214–222
- Editorial
- Karger Publishers
- Citado
- 79 citas · más que el 93% de estudios similares · 3.3× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 84 trabajos
- Acceso
- Acceso abierto (copia en repositorio)
- Áreas de investigación
- Genomics, phytochemicals, and oxidative stress · Sulfur Compounds in Biology · Tryptophan and brain disorders
- Palabras clave
- Sulforaphane, Glutathione, Oxidative stress, Schizophrenia (object-oriented programming), Medicine, Isothiocyanate, Human brain, Internal medicine, Pharmacology, Neuroscience, Psychology, Chemistry, Psychiatry, Biochemistry
11 autores
- Thomas W. Sedlak🇺🇸Johns Hopkins University; Johns Hopkins Medicine
- Leslie G. Nucifora🇺🇸Johns Hopkins University; Johns Hopkins Medicine
- Minori Koga🇺🇸Johns Hopkins University; Johns Hopkins Medicine
- Lindsay S. Shaffer🇺🇸Johns Hopkins University; Johns Hopkins Medicine
- Cecilia P. Higgs🇺🇸Johns Hopkins University; Johns Hopkins Medicine
- Teppei Tanaka🇺🇸Johns Hopkins University; Johns Hopkins Medicine
- Anna M. Wang🇺🇸Johns Hopkins University; Johns Hopkins Medicine
- Jennifer Marie Coughlin🇺🇸Johns Hopkins University; Johns Hopkins Medicine
- Peter B. Barker🇺🇸Johns Hopkins University; Johns Hopkins Medicine
- Jed W. Fahey🇺🇸Johns Hopkins University; Johns Hopkins Medicine
- Akira Sawa🇺🇸Johns Hopkins University; Johns Hopkins Medicine
Resumen
El texto original del estudio, en el idioma en que se publicó.
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.
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