TitleDietary supplementation with (R)-alpha-lipoic acid reverses the age-related accumulation of iron and depletion of antioxidants in the rat cerebral cortex.
Publication TypeJournal Article
Year of Publication2005
AuthorsSuh JH, Moreau R, Heath S-HD, Hagen TM
JournalRedox Rep
Volume10
Issue1
Pagination52-60
Date Published2005
ISSN1743-2928
KeywordsAging, Animals, Antioxidants, Brain, Cerebral Cortex, Dietary Supplements, Iron, Male, Rats, Rats, Inbred F344, Thioctic Acid
Abstract

Accumulation of divalent metal ions (e.g. iron and copper) has been proposed to contribute to heightened oxidative stress evident in aging and neurodegenerative disorders. To understand the extent of iron accumulation and its effect on antioxidant status, we monitored iron content in the cerebral cortex of F344 rats by inductively coupled plasma atomic emission spectrometry (ICP-AES) and found that the cerebral iron levels in 24-28-month-old rats were increased by 80% (p<0.01) relative to 3-month-old rats. Iron accumulation correlated with a decline in glutathione (GSH) and the GSH/GSSG ratio, indicating that iron accumulation altered antioxidant capacity and thiol redox state in aged animals. Because (R)-alpha-Lipoic acid (LA) is a potent chelator of divalent metal ions in vitro and also regenerates other antioxidants, we monitored whether feeding LA (0.2% [w/w]; 2 weeks) could lower cortical iron and improve antioxidant status. Results show that cerebral iron levels in old LA-fed animals were lower when compared to controls and were similar to levels seen in young rats. Antioxidant status and thiol redox state also improved markedly in old LA-fed rats versus controls. These results thus show that LA supplementation may be a means to modulate the age-related accumulation of cortical iron content, thereby lowering oxidative stress associated with aging.

DOI10.1179/135100005X21624
Alternate JournalRedox Rep.
PubMed ID15829111
Grant ListES00210 / ES / NIEHS NIH HHS / United States
P01 AT002034 / AT / NCCIH NIH HHS / United States
R01 AG17141A / AG / NIA NIH HHS / United States