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Does taking glutathione cause headaches? 

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This suggest that osmotic depletion of glutathione is not due to cellular efflux of intact glutathione.
Overall, glutathione in both forms are well tolerated.
These findings could be explained by an increase of glutathione synthesis brought about by the stimulation of glutathione synthetase activity.
— Our results show that blood pressure–lowering drugs prevent a significant proportion of headaches.
Open accessJournal ArticleDOI
19 Apr 2006-JAMA
222 Citations
Epidemiological, pathophysiological, and clinical evidence link estrogen to migraine headaches.
Glutathione applied to cultured astrocytes elicited increased levels of intracellular inositol-1,4,5-trisphosphate, suggesting that glutathione receptors were coupled to phospholipase C. The localization of glutathione receptors on astrocytes and the activation of a second messenger system by glutathione suggest that glutathione may be a neuropeptide in the central nervous system.
Specific glutathione binding sites in the brain were largely localized to the white matter, suggesting the presence of glutathione receptors on neuroglial cells.
During the 270 min after the administration of glutathione in a dose of 0.15 mmol·kg−1 the concentrations of glutathione, cysteine, and glutamate in plasma did not increase significantly, suggesting that the systemic availability of glutathione is negligible in man. Because of hydrolysis of glutathione by intestinal and hepatic γ-glutamyltransferase, dietary glutathione is not a major determinant of circulating glutathione, and it is not possible to increase circulating glutathione to a clinically beneficial extent by the oral administration of a single dose of 3 g of glutathione.
These data suggest the following metabolic interaction in glutathione metabolism of brain cells: the ectoenzyme γ-glutamyl transpeptidase uses as substrate the glutathione released by astrocytes to generate the dipeptide CysGly that is subsequently used by neurons as precursor for glutathione synthesis.

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