The influence of dietary vitamin E, fat, and methionine on blood cholesterol profile, homocysteine levels, and oxidizability of low density lipoprotein in the gerbil

Hidiroglou, Nick; Gilani, G. Sarwar; Long, Lori; Zhao, Xin; Madère, René; Cockell, Kevin A.; Belonge, Bart; Ratnayake, W. M. N.; Peace, Robert W.

doi:10.1016/j.jnutbio.2004.04.009

Cited by 40 publications

(18 citation statements)

References 58 publications

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“…Although Brude et al [19] found a negative association between tHcy and ␤ -carotene intake in male smokers, no correlation was detected with either serum ␤ -carotene or serum vitamin E. Moreover, in the study by Mansoor et al [22] , the negative relationship of tHcy with serum ␤ -carotene as depicted by univariate linear regression analysis could not be confirmed in the evaluation by multivariate models. Furthermore, supplementing vitamin E among hemodialysis patients and triathletes [23,25] as well as in an animal study among gerbils [24] did not result in any change in tHcy.…”

Section: Discussionmentioning

confidence: 80%

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Effect of Antioxidant Vitamins on the Plasma Homocysteine Level in a Free-Living Elderly Population

Breilmann

Pons-Kühnemann²,

Brunner³

et al. 2010

Ann Nutr Metab

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Background: The factors influencing total plasma homocysteine levels (tHcy) are of special interest in the attempt to reduce cardiovascular risk. Aim: This investigation aimed to assess the independent effects of antioxidant vitamins on tHcy in elderly people. Methods: Our cross-sectional analysis included data of 184 subjects (≧60 years) from the longitudinal study in an aging population in Giessen (GISELA), Germany. We examined the effects of plasma levels, intake and supplementation of vitamin C, vitamin E, and β-carotene on tHcy. Results: The mean tHcy was within the normal range in this population. Serum folate, the estimated glomerular filtration rate (eGFR), and plasma vitamin C showed a negative association with tHcy in simple regression analysis. In a subsequent multiple regression analysis, eGFR, serum folate, and plasma vitamin C were the relevant independent predictors of tHcy. Intake and supplementation of vitamin C, as well as plasma levels, intake and supplementation of vitamin E, and β-carotene were not associated with tHcy. Conclusion: Vitamin C may be an independent predictor of tHcy in free-living elderly people and, therefore, should be considered in attempts to reduce tHcy.

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Section: Discussionmentioning

confidence: 80%

“…Four studies showed a negative correlation between tHcy and plasma levels or the intake of ␤ -carotene and vitamin C [19][20][21][22] , while several other trials failed to show an association between tHcy and plasma or serum levels or the intake of antioxidant vitamins [23][24][25][26] .…”

mentioning

confidence: 99%

Effect of Antioxidant Vitamins on the Plasma Homocysteine Level in a Free-Living Elderly Population

Breilmann

Pons-Kühnemann²,

Brunner³

et al. 2010

Ann Nutr Metab

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“…Second, it has been found that the protein methionine content is inversely related to maximum life span in mammals (16), which makes sense since methionine is among the protein amino acids most susceptible to oxidation by ROS (17). Third, methionine dietary supplementation damages many vital organs (like cardiovascular system and liver) and increases oxidative stress (31,32), and similar negative effects have been found in rats fed high protein diets (31,33). Fourth, knocking out methionine sulfoxide reductase-A (an enzyme that reduces methionine sulfoxide back to methionine through a thioredoxindependent reaction) lowers maximum longevity and increases protein carbonyls in mice (17), whereas overexpression of this enzyme in Drosophila increases its life span and delays aging (18).…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that addition of oxidized glutathione to mitochondrial complex I increases its rate of superoxide radical generation (37), and the same seems to occur after addition of homocysteine to rat heart mitochondria (38), suggesting that MitROS production can be regulated by thiol agents. Toxic effects of dietary methionine have been related to its conversion to and increase in homocysteine levels (31,39). Homocysteine has a free thiol group that can react with protein thiols, leading to protein mixed disulfides.…”

Section: Discussionmentioning

confidence: 99%

Methionine restriction decreases mitochondrial oxygen radical generation and leak as well as oxidative damage to mitochondrial DNA and proteins

et al. 2006

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Previous studies have consistently shown that caloric restriction (CR) decreases mitochondrial reactive oxygen species (ROS) (mitROS) generation and oxidative damage to mtDNA and mitochondrial proteins, and increases maximum longevity, although the mechanisms responsible for this are unknown. We recently found that protein restriction (PR) also produces these changes independent of energy restriction. Various facts link methionine to aging, and methionine restriction (MetR) without energy restriction increases, like CR, maximum longevity. We have thus hypothesized that MetR is responsible for the decrease in mitROS generation and oxidative stress in PR and CR. In this investigation we subjected male rats to exactly the same dietary protocol of MetR that is known to increase their longevity. We have found, for the first time, that MetR 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. The concentration of complexes I and IV also decreases in MetR. The decrease in mitROS generation occurs in complexes I and III in liver and in complex I in heart mitochondria, and is due to an increase in efficiency of the respiratory chain in avoiding electron leak to oxygen. These changes are strikingly similar to those observed in CR and PR, suggesting that the decrease in methionine ingestion is responsible for the decrease in mitochondrial ROS production and oxidative stress, and possibly part of the decrease in aging rate, occurring during caloric restriction.

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“…This toxicity far exceeds that produced by any other amino acid, 61 leading to damage in some vital organs and increases in tissue oxidative stress 62,63 with similar negative effects to those observed in rats fed diets with a high protein content. Chronic and excessive methionine supplementation increases plasma hydroperoxides and low-density lipoprotein cholesterol, 64 induces vascular 65 and kidney damage with tubular hypertrophy, 66 raises iron accumulation and lipid peroxidation, and leads to liver dysfunction, 67 besides other alterations in other organs. In addition, methionine supplementation strongly increases methionine and its two more nearly derived methionine cycle metabolites, S-adenosylmethyonine (SAM) and S-adenosylhomocysteine (SAH), in rat liver and kidney.…”

Section: Effect On Longevitymentioning

confidence: 99%

The Mitochondrial Free Radical Theory of Aging

Barja

2014

Progress in Molecular Biology and Translational Science

163

126

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The influence of dietary vitamin E, fat, and methionine on blood cholesterol profile, homocysteine levels, and oxidizability of low density lipoprotein in the gerbil

Cited by 40 publications

References 58 publications

Effect of Antioxidant Vitamins on the Plasma Homocysteine Level in a Free-Living Elderly Population

Effect of Antioxidant Vitamins on the Plasma Homocysteine Level in a Free-Living Elderly Population

Methionine restriction decreases mitochondrial oxygen radical generation and leak as well as oxidative damage to mitochondrial DNA and proteins

The Mitochondrial Free Radical Theory of Aging

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