Forty percent and eighty percent methionine restriction decrease mitochondrial ROS generation and oxidative stress in rat liver

Abstract

Dietary restriction (DR) lowers mitochondrial reactive oxygen species (ROS) generation and oxidative damage and increases maximum longevity in rodents. Protein restriction (PR) or methionine restriction (MetR), but not lipid or carbohydrate restriction, also cause those kinds of changes. However, previous experiments of MetR were performed only at 80% MetR, and substituting dietary methionine with glutamate in the diet. In order to clarify if MetR can be responsible for the lowered ROS production and oxidative stress induced by standard (40%) DR, Wistar rats were subjected to 40% or 80% MetR without changing other dietary components. It was found that both 40% and 80% MetR decrease mitochondrial ROS generation and percent free radical leak in rat liver mitochondria, similarly to what has been previously observed in 40% PR and 40% DR. The concentration of complexes I and III, apoptosis inducing factor, oxidative damage to mitochondrial DNA, five different markers of protein oxidation, glycoxidation or lipoxidation and fatty acid unsaturation were also lowered. The results show that 40% isocaloric MetR is enough to decrease ROS production and oxidative stress in rat liver. This suggests that the lowered intake of methionine is responsible for the decrease in oxidative stress observed in DR.

Low hydrogen peroxide production in mitochondria of the long‐lived Arctica islandica: underlying mechanisms for slow aging

“…A trend for a lower CII content was also found in long-lived strains of drosophila (Neretti et al, 2009). More strikingly, a 40% or 80% methionine restriction in rats both increased longevity and decreased CII content to a greater extent than the decreases found for any other complexes of the ETS (Caro et al, 2008). Although few in number, these studies clearly suggest that it may be worth investigating CII content in relation to longevity in future studies.…”

“…CI content is also reduced in rat mitochondria after diet restriction treatments (Ayala et al, 2007;Caro et al, 2008). Complex I is known to be a major contributor to ROS production.…”

Antioxidant supplementation can reduce the survival costs of excess amino acid intake in honeybees

“…Diets high in protein or amino acids could push cells into oxidative stress by increasing ROS production from the mitochondria, impairing antioxidant defences against ROS or reducing the repair of oxidised molecules (López-Torres and . In support of this idea, in rats, reduced intake of both protein and amino acids reduces oxidative damage (Ayala et al, 2007;Caro et al, 2008;Sanz et al, 2004Sanz et al, , 2006). This appears to be because dietary manipulation lowers ROS production during electron transport in the mitochondria, both by reducing the concentration of mitochondrial respiratory complexes that generate ROS and also by changing the degree of electronic reduction of these complexes (the greater the level of reduction, the more ROS are produced) (Sanz et al, 2006).…”

Mitochondrial function and redox control in the aging eye: Role of MsrA and other repair systems in cataract and macular degenerations

“…It has been demonstrated in a number of models that caloric restriction decreases mitochondrial free radical generation thus decreasing macromolecule and mitochondrial damage (Barja, 2004). Interestingly restriction of methionine intake (40% and 80% restriction) has also been shown to decrease mitochondrial ROS generation and percent free radical leak in rat liver mitochondria (Caro et al, 2008). The same group also reported that protein restriction alone could decrease mitochondrial ROS production and mtDNA damage in rat liver (Sanz et al, 2004).…”