S-adenosylmethionine blood levels in major depression: changes with drug treatment

Bell, Kate M.; Potkin, S.G.; Carreon, Daisy C.; Plon, Lawrence

doi:10.1111/j.1600-0404.1994.tb05404.x

Cited by 64 publications

(31 citation statements)

References 13 publications

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“…The difference between our results and the reported ones could be due to differences in extraction and detection methodology. SAM concentration has also been shown to be affected by other medications, such as vitamins, anti-depression drugs and levodopa [15][16][17]. These drugs, together with dietary intake of methionine, could have influenced SAM levels in our study.…”

mentioning

confidence: 65%

A hydrophilic-interaction chromatography tandem mass spectrometry method for quantitation of serum s-adenosylmethionine in patients infected with human immunodeficiency virus

Wang

Huang

Davis

et al. 2008

Clinica Chimica Acta

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mentioning

confidence: 65%

A hydrophilic-interaction chromatography tandem mass spectrometry method for quantitation of serum s-adenosylmethionine in patients infected with human immunodeficiency virus

Wang

Huang

Davis

et al. 2008

Clinica Chimica Acta

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“…It has been previously reported that serum and cerebrospinal fluid levels of SAM are low in depressed patients [59] and that increases in serum SAM levels correlate with improved treatment response [60]. Besides the stimulatory effect of SAM on central monoaminergic neurotransmitters, alternative mechanisms may exist in which increased or restored membrane phospholipids methylation plays a role in the antidepressant effect.…”

Section: Sam and The Blood Brain Barriermentioning

confidence: 99%

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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“…Of note, SAM participates in transmethylation, transsulfuration, and aminopropylation anabolic reactions. Accordingly, SAM constitutes the main biological methyl donor molecule involved in the methylation of DNA, proteins, and phospholipids [19][20][21]. Interestingly, a previous report showed that parenteral and oral SAM treatments promoted an increase in SAM levels in the cerebrospinal fluid of depressed patients, indicating that SAM crosses the blood-brain barrier [22].…”

Section: Introductionmentioning

confidence: 99%

Striatal adenosine A2A receptor expression is controlled by S-adenosyl-L-methionine-mediated methylation

Villar-Menéndez

Núñez

Díaz-Sánchez

et al. 2014

Purinergic Signalling

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Adenosine A 2A receptor (A 2A R) is a G proteincoupled receptor enriched in the striatum for which an increased expression has been demonstrated in certain neurological diseases. Interestingly, previous in vitro studies demonstrated that A 2A R expression levels are reduced after treatment with S-adenosyl-L-methionine (SAM), a methyl donor molecule involved in the methylation of important biological structures such as DNA, proteins, and lipids. However, the in vivo effects of SAM treatment on A 2A R expression are still obscure. Here, we demonstrated that 2 weeks of SAM treatment produced a significant reduction in the rat striatal A 2A R messenger RNA (mRNA) and protein content as well as A 2A R-mediated signaling. Furthermore, when the content of 5-methylcytosine levels in the 5′UTR region of ADORA2A was analyzed, this was significantly increased in the striatum of SAM-treated animals; thus, an unambiguous correlation between SAM-mediated methylation and striatal A 2A R expression could be established. Overall, we concluded that striatal A 2A R functionality can be controlled by SAM treatment, an issue that might be relevant for the management of these neurological conditions that course with increased A 2A R expression.

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S-adenosylmethionine blood levels in major depression: changes with drug treatment

Cited by 64 publications

References 13 publications

A hydrophilic-interaction chromatography tandem mass spectrometry method for quantitation of serum s-adenosylmethionine in patients infected with human immunodeficiency virus

A hydrophilic-interaction chromatography tandem mass spectrometry method for quantitation of serum s-adenosylmethionine in patients infected with human immunodeficiency virus

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

Striatal adenosine A2A receptor expression is controlled by S-adenosyl-L-methionine-mediated methylation

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