, Volume 27, Issue 2, pp 119–130

Atioxidative protection by melatonin

Multiplicity of mechanisms from radical detoxification to radical avoidance

DOI: 10.1385/ENDO:27:2:119

Cite this article as:
Hardeland, R. Endocr (2005) 27: 119. doi:10.1385/ENDO:27:2:119


Melatonin has been shown to protect against oxidative stress in various, highly divergent experimental systems. There are many reasons for its remarkable protective potential. Signaling effects comprise the upregulation of antioxidant enzymes, such as superoxide dismutases, peroxidases, and enzymes of glutathione supply, downregulation of prooxidant enzymes, such as nitric oxide synthases and lipoxygenases, and presumably also the control of quinone reductase 2. Other mechanisms are based on direct interactions with several reactive oxygen and nitrogen species. Among these reactions, the capacity of easily undergoing single-electron transfer reactions is of particular importance. Electron donation by melatonin is not only an aspect of direct radical scavenging, but additionally represents the basis for formation of the protective metabolites AMK (N1-acetyl-N2-formyl-5methoxykynuramine) and AMK (N1-acetyl-5methoxykynuramine). Recent investigations on mitochondrial metabolism indicate that melatonin as well as AMK are capable of supporting the electron flux through the respiratory chain, of preventing the breakdown of the mitochondrial membrane potential, and of decreasing electron leakage, thereby reducing the formation of superoxide anions. Radical avoidance is a new line of investigation, which exceeds mitochondrial actions and also comprises antiexcitatory effects and contributions to the maintenance of internal circadian phase relationships.

Key Words

Antioxidants free radicals kynuramines melatonin mitochondria 

Copyright information

© Humana Press Inc. 2005

Authors and Affiliations

  1. 1.Institute of Zoology, Anthropology and Developmental BiologyUniversity of GöttingenGöttingenGermany

Personalised recommendations