Folic Acid Effects on S-Adenosylmethionine, S-Adenosylhomocysteine, and DNA Methylation in Patients with Intermediate Hyperhomocysteinemia

Pizzolo, Francesca; Blom, Henk J.; Choi, Seul Ki; Girelli, Domenico; Guarini, Patrizia; Martinelli, Nicola; Stanzial, Anna Maria; Corrocher, Roberto; Olivieri, Oliviero; Friso, Simonetta

doi:10.1080/07315724.2011.10719939

Cited by 45 publications

(51 citation statements)

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“…However, an in vivo analysis of genomic monocyte DNA methylation in a subgroup of women from this same population, as determined by methyldeoxycytidine enrichment after radiolabeled infusions of [ 13 C 5 ]methionine, indicated that folate-dependent intracellular one-carbon metabolism was suppressed after 7 weeks of folate restriction (115 -20 lg DFE/day), but this effect was independent of the MTHFR genotype (131). Among a small group of hyperhomocysteinemic men with normal renal function and homozygous for the MTHFR C677T polymorphism, supplementation with 5 mg FA/day for 8 weeks also did not induce any genomic methylation changes in peripheral blood mononuclear cells (125).…”

Section: Mthfr Polymorphisms and Dna Methylationmentioning

confidence: 86%

Folate and DNA Methylation

Hoyt

Crowell

et al. 2012

Antioxidants & Redox Signaling

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Section: Mthfr Polymorphisms and Dna Methylationmentioning

confidence: 86%

Folate and DNA Methylation

Hoyt

Crowell

et al. 2012

Antioxidants & Redox Signaling

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“…Folate had decreased hepatic SAH content but did not affect SAM content which resulted in higher SAM/SAH ratio. Reduced serum homocysteine and SAM had been previo u s l y o b s e r v e d i n h i g h -f a t d i e t -i n d u c e d hyperhomocysteinaemic ApoE −/− mice supplemented with folate and vitamin B 12 [47], while another study reported decreased plasma homocysteine but increased plasma SAM as well as SAM/SAH ratio in patients with hyperhomocysteinaemia [33]. Collectively, it can be said that folate increases methylation ratio, either by increasing SAM or decreasing SAH.…”

Section: Discussionmentioning

confidence: 99%

Palm tocotrienol-rich fraction inhibits methionine-induced cystathionine β-synthase in rat liver

et al. 2015

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Oxidative stress plays an important role in cardiovascular diseases. The study investigated the effects of dietary palm tocotrienol-rich fraction on homocysteine metabolism in rats fed a high-methionine diet. Forty-two male Wistar rats were randomly assigned to six groups. Five groups were fed with high-methionine diet (1%) for 10 weeks. Groups 2 to 5 were also given dietary folate (8 mg/kg) and three doses of palm tocotrienol-rich fraction (30, 60 and 150 mg/kg) from week 6 to week 10. The last group was only given basal rat chow. High-methionine diet increased plasma homocysteine after 10 weeks, which was prevented by the supplementations of folate and high-dose palm tocotrienol-rich fraction. Hepatic S-adenosyl methionine (SAM) content was unaffected in all groups but S-adenosyl homocysteine (SAH) content was reduced in the folate group. Folate supplementation increased the SAM/SAH ratio, while in the palm tocotrienol-rich fraction groups, the ratio was lower compared with the folate. Augmented activity of hepatic cystathionine β-synthase and lipid peroxidation content by high-methionine diet was inhibited by palm tocotrienol-rich fraction supplementations (moderate and high doses), but not by folate. The supplemented groups had lower hepatic lipid peroxidation than the high-methionine diet. In conclusion, palm tocotrienol-rich fraction reduced high-methionine-induced hyperhomocysteinaemia possibly by reducing hepatic oxidative stress in high-methionine-fed rats. It may also exert a direct inhibitory effect on hepatic cystathionine β-synthase.

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“…The reduction in homocysteinemia and the increased availability of methyl compounds provided by vitamin supplementation, such as folic acid, may not be sufficient to affect genomic DNA methylation (107). Aberrant global DNA methylation is only an index of the potential for epigenetic dysregulation.…”

Section: Fig 5 Homocysteine Reactions Relevant To Epigenetic Marksmentioning

confidence: 99%

The Role of Redox Signaling in Epigenetics and Cardiovascular Disease

Kim

Ryan²,

Archer³

2013

Antioxidants & Redox Signaling

107

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Significance: The term epigenetics refers to the changes in the phenotype and gene expression that occur without alterations in the DNA sequence. There is a rapidly growing body of evidence that epigenetic modifications are involved in the pathological mechanisms of many cardiovascular diseases (CVDs), which intersect with many of the pathways involved in oxidative stress. Recent Advances: Most studies relating epigenetics and human pathologies have focused on cancer. There has been a limited study of epigenetic mechanisms in CVDs. Although CVDs have multiple established genetic and environmental risk factors, these explain only a portion of the total CVD risk. The epigenetic perspective is beginning to shed new light on how the environment influences gene expression and disease susceptibility in CVDs. Known epigenetic changes contributing to CVD include hypomethylation in proliferating vascular smooth muscle cells in atherosclerosis, changes in estrogen receptor-a (ER-a) and ER-b methylation in vascular disease, decreased superoxide dismutase 2 expression in pulmonary hypertension (PH), as well as trimethylation of histones H3K4 and H3K9 in congestive heart failure. Critical Issues: In this review, we discuss the epigenetic modifications in CVDs, including atherosclerosis, congestive heart failure, hypertension, and PH, with a focus on altered redox signaling. Future Directions: As advances in both the methodology and technology accelerate the study of epigenetic modifications, the critical role they play in CVD is beginning to emerge. A fundamental question in the field of epigenetics is to understand the biochemical mechanisms underlying reactive oxygen species-dependent regulation of epigenetic modification.

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Folic Acid Effects on S-Adenosylmethionine, S-Adenosylhomocysteine, and DNA Methylation in Patients with Intermediate Hyperhomocysteinemia

Cited by 45 publications

References 45 publications

Folate and DNA Methylation

Folate and DNA Methylation

Palm tocotrienol-rich fraction inhibits methionine-induced cystathionine β-synthase in rat liver

The Role of Redox Signaling in Epigenetics and Cardiovascular Disease

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