Effect of S-adenosyl-l-methionine on rat brain oxidative stress damage in a combined model of permanent focal ischemia and global ischemia-reperfusion

Villalobos, M.A.; Cruz, J. P. De La; Cuerda, M.A.; Ortiz, Pablo; Smith-Agreda, J; Cuesta, Felipe Sánchez de la

doi:10.1016/s0006-8993(00)02873-0

Cited by 29 publications

(23 citation statements)

References 29 publications

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“…Note further the increase in attack latency, decline in attack frequency and increase in cognitive performance beyond that of baseline levels, when these mice were maintained on the deficient diet supplemented with NAC, ALCAR, and SAM. Values represent the mean ± standard error recorded for all mice in both experiments; values accompanied by an asterisk differed statistically from value obtained for mice on the complete diet (''start'') more permanent decline in cognitive performance (e.g., Smolkova et al 2004;Tchantchou et al 2004Tchantchou et al , 2005Tchantchou et al a, b, 2006Troen 2005), the findings of the present study, coupled with prior studies of suggest that supplementation with NAC, ALCAR, and SAM may exert multiple neuroprotective effects in Alzheimer's disease, which encompass neurotransmitter balance, antioxidant protection, energy maintenance, buffering against Abeta neurotoxicity, and prevention of presenilin overexpression (Barnes et al 1990;Chan and Shea 2006;Chan et al 2007;De La Cruz et al 2002;Dhitavat et al 2001Dhitavat et al , 2002Dhitavat et al , 2005Farr et al 2003;Fu et al 2006;Fuso et al 2005;Ho et al 2003;Markowska and Olton 1990;Tchantchou et al 2004Tchantchou et al , 2005aTchantchou et al , b, 2006Villalobos et al 2000).…”

Section: Discussionsupporting

confidence: 63%

“…This combination included N-acetyl cysteine (NAC; an antioxidant and glutathione precursor that buffers Abeta neurotoxicity and prevents cognitive decline; Dhitavat et al 2001;Farr et al 2003;Fu et al 2006;Tchantchou et al 2005a, b), acetyl-L-carnitine (ALCAR; which raises ATP levels, protects neuronal mitochondria, buffers Abeta neurotoxicity and supports cognitive performance; Barnes et al 1990;Dhitavat et al 2001Dhitavat et al , 2002Dhitavat et al , 2005Markowska and Olton 1990) and S-adenosylmethionine (which facilitates glutathione usage, reduces oxidative damage to brain tissue, prevents cognitive decline and maintains acetylcholine levels; Chan and Shea 2006;Chan et al 2007;De la Cruz et al 2002;Tchantchou et al 2006;Villalobos et al 2000).…”

Section: Introductionmentioning

confidence: 99%

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Effects of Dietary Supplementation with N-Acetyl Cysteine, Acetyl-l-Carnitine and S-Adenosyl Methionine on Cognitive Performance and Aggression in Normal Mice and Mice Expressing Human ApoE4

Chan

Shea

2007

Neuromol Med

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In addition to cognitive impairment, behavioral changes such as aggressive behavior, depression, and psychosis accompany Alzheimer's Disease. Such symptoms may arise due to imbalances in neurotransmitters rather than overt neurodegeneration. Herein, we demonstrate that combined administration of N-acetyl cysteine (an antioxidant and glutathione precursor that protects against A beta neurotoxicity), acetyl-L-carnitine (which raises ATP levels, protects mitochondria, and buffers A beta neurotoxicity), and S-adenosylmethionine (which facilitates glutathione usage and maintains acetylcholine levels) enhanced or maintain cognitive function, and attenuated or prevented aggression, in mouse models of aging and neurodegeneration. Enhancement of cognitive function was rapidly reversed upon withdrawal of the formulation and restored following additional rounds supplementation. Behavioral abnormalities correlated with a decline in acetylcholine, which was also prevented by this nutriceutical combination, suggesting that neurotransmitter imbalance may contribute to their manifestation. Treatment with this nutriceutical combination was able to compensate for lack of dietary folate and vitamin E, coupled with administration of dietary iron as a pro-oxidant (which collectively increase homocysteine and oxidative damage to brain tissue), indicating that it provided antioxidant neuroprotection. Maintenance of neurotransmitter levels and prevention of oxidative damage underscore the efficacy of a therapeutic approach that utilizes a combination of neuroprotective agents.

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Section: Discussionsupporting

confidence: 63%

Section: Introductionmentioning

confidence: 99%

Effects of Dietary Supplementation with N-Acetyl Cysteine, Acetyl-l-Carnitine and S-Adenosyl Methionine on Cognitive Performance and Aggression in Normal Mice and Mice Expressing Human ApoE4

Chan

Shea

2007

Neuromol Med

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“…SAM treatment protects the neurons from degeneration by several mechanisms (38,39 ). The protective effect of SAM was suppressed by simultaneous administration of SAH (40 ).…”

Section: Discussionmentioning

confidence: 99%

Folate and Methylation Status in Relation to Phosphorylated Tau Protein(181P) and β-Amyloid(1–42) in Cerebrospinal Fluid

Obeid¹,

Kasoha²,

Knapp³

et al. 2007

Clinical Chemistry

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Background: Increased plasma total homocysteine (tHcy) is a risk factor for neurological diseases, but the underlying pathophysiology has not been adequately explained. Methods: We evaluated concentrations of tHcy, S-adenosyl homocysteine (SAH), S-adenosyl methionine (SAM), folate, and vitamin B 12 in cerebrospinal fluid (CSF) and plasma or serum from 182 patients with different neurological disorders. We measured concentrations of phosphorylated tau protein (P-tau) (181P) and ␤-amyloid(1-42) in the CSF. Results: Aging was associated with higher concentrations of tHcy and SAH in the CSF, in addition to lower concentrations of CSF folate and lower SAM:SAH ratio. Concentrations of CSF SAH and CSF folate correlated significantly with those of P-tau (r ‫؍‬ 0.46 and r ‫؍‬ ؊0.28, respectively). Moreover, P-tau correlated negatively with SAM:SAH ratio (r ‫؍‬ ؊0.40, P <0.001). The association between SAH and higher P-tau was observed in 3 age groups (<41, 41-60, and >60 years). CSF tHcy was predicted by concentrations of CSF cystathionine (␤ ‫؍‬ 0.478), folate (␤ ‫؍‬ ؊0.403), albumin (␤ ‫؍‬ 0.349), and age (␤ ‫؍‬ 0.298). Conclusions: tHcy concentration in the brain is related to age, B vitamins, and CSF albumin. Increase of CSF SAH is related to increased CSF P-tau; decreased degradation of P-tau might be a plausible explanation. Disturbed methyl group metabolism may be the link be-

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“…In a rat model of brain ischemia/reperfusion, SAM inhibits brain lipid peroxidation, together with increased mitochondrial function [99][100]. Several experimental findings underscored the critical role of SAM in maintenance of neuronal health, suggesting a possible role of SAM as a neuroprotective dietary supplement in AD.…”

Section: Involvement Of Sam In Oxidative Stress and Neurodegenerationmentioning

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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Effect of S-adenosyl-l-methionine on rat brain oxidative stress damage in a combined model of permanent focal ischemia and global ischemia-reperfusion

Cited by 29 publications

References 29 publications

Effects of Dietary Supplementation with N-Acetyl Cysteine, Acetyl-l-Carnitine and S-Adenosyl Methionine on Cognitive Performance and Aggression in Normal Mice and Mice Expressing Human ApoE4

Effects of Dietary Supplementation with N-Acetyl Cysteine, Acetyl-l-Carnitine and S-Adenosyl Methionine on Cognitive Performance and Aggression in Normal Mice and Mice Expressing Human ApoE4

Folate and Methylation Status in Relation to Phosphorylated Tau Protein(181P) and β-Amyloid(1–42) in Cerebrospinal Fluid

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

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