Spermine prevent iron accumulation and depress lipofuscin accumulation in cultured myocardial cells.
The present work demonstrates that spermine prevents aging in cultured myocytes exposed to oxidative stress. It is found that physiological levels of spermine reduce lipofuscin accumulation with 20%, and that the antioxidative effect compares with vitamin E. By autometallography we also demonstrate that spermine prevent accumulation of free iron in the myocytes, probably by acting as a chelating agent. The effect compares to that of deferoxamine. These data provide additional insight into the antioxidative mechanism of spermine, and suggest that spermine may prevent diseases related to the Fenton reaction, as well as retard aging reactions.
Marzabadi
M R
MR
Webb-Waring Institute for Biomedical Research, University of Colorado Health Science Center, Denver, USA.
Lłvaas
E
E
D000818:Animals; D000831:Animals, Newborn; D000975:Antioxidants / Q000494:pharmacology*; D002478:Cells, Cultured; D003676:Deferoxamine / Q000494:pharmacology; D007501:Iron / Q000378:metabolism*; D007502:Iron Chelating Agents; D008062:Lipofuscin / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D013096:Spermine / Q000494:pharmacology*; D014810:Vitamin E / Q000494:pharmacology
D000975:Antioxidants; D007502:Iron Chelating Agents; D008062:Lipofuscin; D014810:Vitamin E; D013096:Spermine; D007501:Iron; D003676:Deferoxamine