Dynamics of oxidative stress and urinary excretion of melatonin and its metabolites during acute ischemic stroke.

Abstract

Oxidative stress is a leading cause of neuronal damage in ischemic stroke. Melatonin may play a role in the antioxidant response. Melatonin and its metabolites may be involved in the modulation of oxidative stress in human acute stroke. No data are available in humans to establish this relationship. In this context, on the first and the fifth days post-stroke, we assessed serum total antioxidant capacity (TAC) and urine levels of melatonin, 6-sulfatoxymelatonin (aMT6S), and N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK), the last compound being produced in the brain after reaction of melatonin with reactive oxygen species. Compared to controls' values, TAC and levels of melatonin and aMT6S were reduced, without difference between the first and the fifth days post-stroke, whereas AFMK levels remained in the normal range at both time points. Melatonin catabolism might be speeded up in acute ischemic stroke in order to increase the antioxidant response.

• Authors: Thomas Ritzenthaler, Isabelle Lhommeau, Samuel Douillard, Tea Hee Cho, Jocelyne Brun, Thierry Patrice, Norbert Nighoghossian, Bruno Claustrat
• Journal: Neuroscience letters (Neurosci Lett) Vol. 544 Pg. 1-4 (Jun 07 2013) ISSN: 1872-7972 [Electronic] Ireland
• PMID: 23562888 (Publication Type: Journal Article)
• Copyright: Copyright © 2013. Published by Elsevier Ireland Ltd.

Chemical References

• Reactive Oxygen Species
• Melatonin

Topics

• Aged
• Comorbidity
• Female
• France (epidemiology)
• Humans
• Ischemia (epidemiology, urine)
• Male
• Melatonin (urine)
• Metabolism
• Middle Aged
• Oxidative Stress
• Prevalence
• Reactive Oxygen Species (urine)
• Risk Factors
• Stroke (epidemiology, urine)