Methionine and homocysteine modulate the rate of ROS generation of isolated mitochondria in vitro

Dietary methionine restriction and supplementation in mammals have beneficial (antiaging) and detrimental effects respectively, which have been related to chronic modifications in the rate of mitochondrial ROS generation. However it is not known if methionine or its metabolites can have, in addition...

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Bibliographic Details
Published in:Journal of bioenergetics and biomembranes 2011-08, Vol.43 (4), p.377-386
Main Authors: Gomez, Jose, Sanchez-Roman, Ines, Gomez, Alexia, Sanchez, Carlota, Suarez, Henar, Lopez-Torres, Monica, Barja, Gustavo
Format: Article
Language:English
Subjects:
Animal Anatomy
Animal Biochemistry
Animals
Biochemistry
Bioorganic Chemistry
Chemistry
Chemistry and Materials Science
Dietary restrictions
Histology
Homocysteine
Homocysteine - metabolism
Homocysteine - pharmacology
Hydrogen Peroxide - metabolism
Kidneys
Male
Metabolites
Methionine - metabolism
Methionine - pharmacology
Mice
Mitochondria
Mitochondria - drug effects
Mitochondria - metabolism
Mitochondria, Liver - drug effects
Mitochondria, Liver - metabolism
Morphology
Organic Chemistry
Rats
Rats, Wistar
Reactive Oxygen Species - metabolism
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Summary:Dietary methionine restriction and supplementation in mammals have beneficial (antiaging) and detrimental effects respectively, which have been related to chronic modifications in the rate of mitochondrial ROS generation. However it is not known if methionine or its metabolites can have, in addition, direct effects on the rate of mitochondrial ROS production. This is studied here for the methionine cycle metabolites S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), homocysteine and methionine itself in isolated rat liver, kidney, heart, and brain mitochondria. The results show that methionine increases ROS production in liver and kidney mitochondria, homocysteine increases it in kidney and decreases it in the other three organs, and SAM and SAH have no effects. The variations in ROS production are localized at complexes I or III. These changes add to previously described chronic effects of methionine restriction and supplementation in vivo.
ISSN:0145-479X
1573-6881
DOI:10.1007/s10863-011-9368-1