S-Adenosylmethionine Mediates Glutathione Efficacy by Increasing Glutathione S-Transferase Activity: Implications for S-Adenosyl Methionine as A Neuroprotective Dietary Supplement

Tchantchou, Flaubert; Graves, Michael V.; Falcone, Deane L.; Shea, Thomas B.

doi:10.3233/jad-2008-14306

Cited by 63 publications

(46 citation statements)

References 33 publications

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“…Indeed, SAM supplementation restored normal GSH/GSSG ratio potentiating GST and SOD activity, decreasing lipid peroxidation (LPO) acting like an antioxidant. These results are in agreement with papers analyzing GSH levels and GST activity on ApoE deficient mice [101].…”

Section: Involvement Of Sam In Oxidative Stress and Neurodegenerationsupporting

confidence: 82%

“…The positive effect of SAM supplementation may be in part ascribed also to the increase in GST activity, the enzyme that plays a pivotal role in quenching oxidative species and elimination of toxic xenobiotics by forming GSH conjugates, often reduced in AD. In this work SAM supplementation restored impaired GST activity, lowering ROS levels [101].…”

Section: Involvement Of Sam In Oxidative Stress and Neurodegenerationmentioning

confidence: 93%

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Role of S-adenosylmethionine in the Modulation of Oxidative Stress- Related Neurodegeneration

Cavallaro¹,

Fuso²,

D’Erme³

et al. 2016

Int J Clin Nutr Diet

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S-adenosyl-L-methionine (SAM) is the main biological methyl donor in transmethylation reactions, consisting in the transferring of a methyl moiety to different substrates including DNA, proteins, lipids and RNA. SAM level in the organism decreases with aging and restoring the original levels through exogenous supplementation is an important tool for the improvement of many vital functions. Indeed, SAM deficiency may contribute to the onset of several diseases, i.e. depression, liver diseases, osteoarthritis and senile neurological disorders such as Alzheimer's and Parkinson's diseases. Recent evidences indicate that SAM may have an involvement in oxidative stress, a process which typically involves an alteration of cellular sulfur amino acids homeostasis. SAM is not only the principal methyl donor, but also a precursor of glutathione, the major endogenous antioxidant, whose role in counteracting oxidative stress is well known. In this review we will highlight the role of SAM not just as a methyl-donor but also as a regulator of different metabolic pathways involved in the antioxidant response in brain related disorders. Role of S-adenosylmethionine in the Modulation of Oxidative StressRelated Neurodegeneration Review ArticleOpen Access IntroductionThe interaction between environmental and genetic factors plays a fundamental role in inducing and modulating the aging processes towards brain disorders. Among environmental factors, diet and nutritional lifestyle have a key role in brain health through the alteration of the intake or the bioavailability of metabolites and cofactors. Specific nutritional factors have particular impact on one-carbon metabolism, which is a complex biochemical pathway regulated by the presence of folate, vitamin B12 and B6 (among other metabolites) and leading to the production of S-adenosyl-L-methionine (SAM), the main biological methyl donor in transmethylation reactions, consisting in the transferring of a methyl moiety to different substrates including DNA, proteins, lipids and RNA. This metabolism involves three interrelated biochemical pathways: folate cycle, transsulfuration pathway and methionine cycle. These three metabolic sequences were first combined and correlated in 1964 by Laster's group [1][2][3] giving the integrated point of view of transmethylation and transsulfuration pathways, linking sulfur amino acid metabolism to the provision of methyl groups for many biochemical processes. Normal functioning of this metabolic cycle is essential for growth and development and impairment of this metabolism; transmethylation efficiency is associated with many diseases like cardiovascular diseases [4][5], liver diseases [6-9], neural tube defects [10] and brain diseases [11][12][13][14][15][16]. One-carbon metabolism alterations, low methylation and oxidative stress are all linked to Late Onset Alzheimer's Disease (LOAD) [17][18][19][20][21][22][23][24] Moreover, wide confirmed reports underline the role of SAM dependent reactions in age related neurodegeneration also showi...

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Section: Involvement Of Sam In Oxidative Stress and Neurodegenerationsupporting

confidence: 82%

Section: Involvement Of Sam In Oxidative Stress and Neurodegenerationmentioning

confidence: 93%

Role of S-adenosylmethionine in the Modulation of Oxidative Stress- Related Neurodegeneration

Cavallaro¹,

Fuso²,

D’Erme³

et al. 2016

Int J Clin Nutr Diet

View full text Add to dashboard Cite

show abstract

“…Cellular methylation processes are ubiquitous metabolic events (29 -32) that are linked to redox status (33) and involved in immune processes (34), both processes known to be involved in obesity and the progression of type II diabetes (35,36). SAM and SAH levels as well as protein-arginine methylation are altered in diabetic models (5-9) and in humans (10, 11).…”

Section: Discussionmentioning

confidence: 99%

S-Adenosylmethionine-dependent Protein Methylation Is Required for Expression of Selenoprotein P and Gluconeogenic Enzymes in HepG2 Human Hepatocytes

Jackson

Cao

Zeng

et al. 2012

Journal of Biological Chemistry

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Background: Protein methylation is required for gluconeogenic enzyme expression. Selenoprotein P is transcriptionally controlled similarly to gluconeogenenic enzymes. S-adenosylhomocysteine is an inhibitor of methylation. Results: S-Adenosylhomocysteine decreases selenoprotein P and gluconeogenic enzyme expression. Conclusion: Hepatocellular methylation is a nexus of control over selenoprotein P and gluconeogenic enzyme expression. Significance: Determination of how methylation affects proteins involved in type II diabetes may aid in development of therapeutics.

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“…Spot b11 (Fig. 2), S-adenosylmethionine (SAM) synthetase, can be determined through its action as a precursor for intracellular glutathione (GSH, a major cellular antioxidant) or direct radical scavenging (Evans et al 1997;Tchantchou et al 2008). Ascorbate peroxidase (APX) (Fig.…”

Section: Proteins Related To Ros Regulationmentioning

confidence: 99%

Proteomics-based analysis reveals that Verticillium dahliae toxin induces cell death by modifying the synthesis of host proteins

Xie

Wang

et al. 2013

J Gen Plant Pathol

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Verticillium dahliae is one of the most destructive soil-borne fungal pathogens that cause vascular wilt diseases in a wide range of important crop plants, including cotton. However, the mechanisms used by this pathogen to infect cotton have not been fully elucidated. In the present study, we first investigated changes in protein abundance during the initial interaction between cotton roots and V. dahliae. Among the proteins that were upregulated upon infection, some were related to reactive oxygen species (ROS); among those downregulated upon infection were proteins involved in normal metabolism or cell structure. Further experiments confirmed that a sudden release of ROS and cell death accompany V. dahliae infection in the cotton vasculature. Further analysis indicated that a culture supernatant of V. dahliae induced lesion formation in tobacco leaves; de novo protein synthesis not active gene expression was required for this induction. Lesion formation was dependent on the age of leaves, but neither the known ROS burst nor the ubiquitin/ 26S proteasome system are prerequisites.

show abstract

S-Adenosylmethionine Mediates Glutathione Efficacy by Increasing Glutathione S-Transferase Activity: Implications for S-Adenosyl Methionine as A Neuroprotective Dietary Supplement

Cited by 63 publications

References 33 publications

Role of S-adenosylmethionine in the Modulation of Oxidative Stress- Related Neurodegeneration

Role of S-adenosylmethionine in the Modulation of Oxidative Stress- Related Neurodegeneration

S-Adenosylmethionine-dependent Protein Methylation Is Required for Expression of Selenoprotein P and Gluconeogenic Enzymes in HepG2 Human Hepatocytes

Proteomics-based analysis reveals that Verticillium dahliae toxin induces cell death by modifying the synthesis of host proteins

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