Effect of methionine dietary supplementation on mitochondrial oxygen radical generation and oxidative DNA damage in rat liver and heart

@article{Gmez2009EffectOM,
  title={Effect of methionine dietary supplementation on mitochondrial oxygen radical generation and oxidative DNA damage in rat liver and heart},
  author={Jos{\'e} Mar{\'i}a G{\'o}mez and Pilar Caro and In{\'e}s S{\'a}nchez and Alba Naud{\'i} and Mariona Jov{\'e} and Manuel Portero-Ot{\'i}n and M{\'o}nica L{\'o}pez-Torres and R. Pamplona and Gustavo Barja},
  journal={Journal of Bioenergetics and Biomembranes},
  year={2009},
  volume={41},
  pages={309-321}
}
Methionine restriction without energy restriction increases, like caloric restriction, maximum longevity in rodents. Previous studies have shown that methionine restriction strongly decreases mitochondrial reactive oxygen species (ROS) production and oxidative damage to mitochondrial DNA, lowers membrane unsaturation, and decreases five different markers of protein oxidation in rat heart and liver mitochondria. It is unknown whether methionine supplementation in the diet can induce opposite… 
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TLDR
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The mitochondrial free radical theory of aging.
  • G. Barja
  • Biology
    Progress in molecular biology and translational science
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Short-term dietary methionine supplementation affects one-carbon metabolism and DNA methylation in the mouse gut and leads to altered microbiome profiles, barrier function, gene expression and histomorphology
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Mitochondrial ROS and mtDNA fragments inside nuclear DNA as a main effector of ageing: the "cell aging regulation system”
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References

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TLDR
It is suggested that the decrease in mitROS generation and oxidative damage to mtDNA that occurs during dietary restriction is due to restriction of a single aminoacid: methionine, and for the first time that restriction of dietary amino acids different from methionines decreases mitochondrial protein oxidative modification and AIF, and increases SIRT1, in rat liver.
Effect of Lipid Restriction on Mitochondrial Free Radical Production and Oxidative DNA Damage
TLDR
The results deny a role for lipids and reinforce the possible role of dietary proteins as being responsible for the decrease in mitochondrial ROS production and DNA damage in caloric restriction.
Methionine restriction decreases mitochondrial oxygen radical generation and leak as well as oxidative damage to mitochondrial DNA and proteins
TLDR
For the first time, it is found that methionine restriction profoundly decreases mitROS production, decreases oxidative damage to mtDNA, lowers membrane unsaturation, and decreases all five markers of protein oxidation measured in rat heart and liver mitochondria.
Protein Restriction Without Strong Caloric Restriction Decreases Mitochondrial Oxygen Radical Production and Oxidative DNA Damage in Rat Liver
TLDR
Part of the decrease in aging rate induced by caloric restriction can be due to the decreased intake of proteins acting through decreases in mitochondrial ROS production and oxidative DNA damage, and these tissue oxidative stress-linked parameters can be lowered by restricting only the intake of dietary protein.
Forty percent and eighty percent methionine restriction decrease mitochondrial ROS generation and oxidative stress in rat liver
TLDR
40% isocaloric MetR is enough to decrease ROS production and oxidative stress in rat liver, which suggests that the lowered intake of methionine is responsible for the decrease in oxidative stress observed in DR.
Carbohydrate restriction does not change mitochondrial free radical generation and oxidative DNA damage
TLDR
The results of the present study indicate that the lowered ingestion of dietary proteins is responsible for the decrease in mitochondrial ROS production and oxidative damage in mtDNA that occurs during caloric restriction.
Long-term consumption of a methionine-supplemented diet increases iron and lipid peroxide levels in rat liver.
TLDR
Results indicate that long-term consumption of excess L-methionine by rats may affect primarily iron metabolism rather than the antioxidant defense system and, consequently, induce an accumulation of iron.
Methionine restriction decreases endogenous oxidative molecular damage and increases mitochondrial biogenesis and uncoupling protein 4 in rat brain.
TLDR
It is hypothesized that MetR can be responsible, at least in part, for the decrease in endogenous oxidative damage in CR, and beneficial MetR-induced changes likely derived from metabolic reprogramming at the cellular and tissue level can play a key role in the protection against aging-associated neurodegenerative disorders.
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