PharmacoNutrition Reviewed

I don’t know whether many of you already read this article. As it is not (yet?) listed in the PubMed and has been published in a rather new journal (Current Aging Science) most probably not.
Anyway, I very much liked reading the review by Alberto Sanz and Rhoda Stefanatos (University of Tampere, Finland) which again deals with the pros and cons of the Mitochondrial Free Radical Theory of Aging (MFRTA).

“The Mitochondrial Free Radical Theory of Aging (MFRTA) proposes that mitochondrial free radicals, produced as by-products during normal metabolism, cause oxidative damage. According to MFRTA, the accumulation of this oxidative damage is the main driving force in the aging process. Although widely accepted, this theory remains unproven, because the evidence supporting it is largely correlative. For example, long-lived animals produce fewer free radicals and have lower oxidative damage levels in their tissues. However, this does not prove that free radical generation determines life span. In fact, the longest-living rodent -Heterocephalus glaber- produces high levels of free radicals and has significant oxidative damage levels in proteins, lipids and DNA.

In summary, available data concerning the role of free radicals in longevity control are contradictory, and do not prove MFRTA. In fact, the only way to test this theory is by specifically decreasing mitochondrial free radical production without altering other physiological parameters (e.g. insulin signalling). If MFRTA is true animals producing fewer mtROS must have the ability to live much longer than their experimental controls.”

The full text article is available here.

Source: Journal of Neurochemistry (2007), 100: 736-746
Article Type: Original Contribution
Authors: F. Herrera, V. Martin, G. Garcia-Santos, J. Rodriguez-Blanco, I. Antolin, C. Rodriguez

Image taken from:
http://www.virginia.edu/insideuva/2005/11/images/Jet_Lag_Graphic.jpg

Life depends on information. Melatonin, which occurs ubiquitiously in plants and animals, has been suggested as one of the first signals appearing on earth. In vertebrates, it is mainly synthesized in the pineal gland (but also other tissues) from the neurotransmitter serotonin. Melatonin, due to its chronobiotic activity, effectively attenuates jet lag symptoms, especially with eastbound flights. Moreover, melatonin has been shown to prevent neuronal cell death both in vitro and in vivo.
The article by Herrera et al. provides further inside in the mechanism of melatonin-mediated neuroprotection. The authors suggest for melatonin a novel, direct antioxidant effect targeted to the mitochondria, the key source of potentially deleterious reactive oxygen species (ROS) in cells. The protective effects of melatonin in murine hippocampal cells, however, where detected with a melatonin concentration of 1 mM (= 1000 µM), which is in contrast not only to the low micromolar concentrations that have been reported as physiological concentrations of melatonin but also to pharmacological levels, which range between 100 nM-10 µM (Kolar et al.). Bearing in mind these facts, it is somewhat difficult to estimate whether melatonin exerts the aforementioned mode of action in vivo, too.