Effects of S-Adenosylmethionine and Its Combinations With Taurine and/or Betaine on Glutathione Homeostasis in Ethanol-induced Acute Hepatotoxicity

Lee, Seo Yeon; Ko, Kwang Suk

doi:10.15430/jcp.2016.21.3.164

Cited by 15 publications

(6 citation statements)

References 48 publications

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“…The imbalance in HCY metabolism can modulate autophagy, which is involved in the pathogenesis of diseases such as cardiovascular diseases and neurological and psychiatric disorders 92 . Moreover, the availability of SAM is a limiting factor of the synthesis of the endogenous antioxidant GSH 93 . GSH and cysteine are critical for attenuating much of the oxidative damage generated 91 .…”

Section: Sam As the Mediator Of Sulphur‐containing Molecules Modulamentioning

confidence: 99%

S‐adenosylmethionine: A metabolite critical to the regulation of autophagy

Ouyang

et al. 2020

Cell Proliferation

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Autophagy is a mechanism that enables cells to maintain cellular homeostasis by removing damaged materials and mobilizing energy reserves in conditions of starvation. Although nutrient availability strongly impacts the process of autophagy, the specific metabolites that regulate autophagic responses have not yet been determined. Recent results indicate that S‐adenosylmethionine (SAM) represents a critical inhibitor of methionine starvation–induced autophagy. SAM is primarily involved in four key metabolic pathways: transmethylation, transsulphuration, polyamine synthesis and 5′‐deoxyadenosyl 5′‐radical–mediated biochemical transformations. SAM is the sole methyl group donor involved in the methylation of DNA, RNA and histones, modulating the autophagic process by mediating epigenetic effects. Moreover, the metabolites of SAM, such as homocysteine, glutathione, decarboxylated SAM and spermidine, also exert important influences on the regulation of autophagy. From our perspective, nuclear‐cytosolic SAM is a conserved metabolic inhibitor that connects cellular metabolic status and the regulation of autophagy. In the future, SAM might be a new target of autophagy regulators and be widely used in the treatment of various diseases.

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Section: Sam As the Mediator Of Sulphur‐containing Molecules Modulamentioning

confidence: 99%

S‐adenosylmethionine: A metabolite critical to the regulation of autophagy

Ouyang

et al. 2020

Cell Proliferation

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“…Patients with alcoholic liver disease (ALD) or non-alcoholic liver disease (NAFLD) were found to exhibit low hepatic GSH levels, which were replenished after oral AdoMet treatment (1.2 g/day for 6 months) [77]. Rodent studies have supported this finding, concluding that AdoMet supplementation is effective at attenuating liver injury by increasing GSH levels [80,81,82,83,84].…”

Section: Effect Of Individual Amino Acid Supplementationmentioning

confidence: 99%

Impact of Supplementary Amino Acids, Micronutrients, and Overall Diet on Glutathione Homeostasis

Gould

Pazdro

2019

Nutrients

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Glutathione (GSH) is a critical endogenous antioxidant found in all eukaryotic cells. Higher GSH concentrations protect against cellular damage, tissue degeneration, and disease progression in various models, so there is considerable interest in developing interventions that augment GSH biosynthesis. Oral GSH supplementation is not the most efficient option due to the enzymatic degradation of ingested GSH within the intestine by γ-glutamyltransferase, but supplementation of its component amino acids—cysteine, glycine, and glutamate—enhances tissue GSH synthesis. Furthermore, supplementation with some non-precursor amino acids and micronutrients appears to influence the redox status of GSH and related antioxidants, such as vitamins C and E, lowering systemic oxidative stress and slowing the rate of tissue deterioration. In this review, the effects of oral supplementation of amino acids and micronutrients on GSH metabolism are evaluated. And since specific dietary patterns and diets are being prescribed as first-line therapeutics for conditions such as hypertension and diabetes, the impact of overall diets on GSH homeostasis is also assessed.

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“…S-adenosylmethionine (SAM) functions as a conserved metabolic switch that regulates autophagy by controlling methylation [ 187 , 216 , 217 ], sulphuration [ 218 , 219 , 220 ], and synthesis of polyamines [ 221 , 222 ]. Furthermore, SAM also controls the availability of natural antioxidant GSH and other sulfur-containing metabolites like cysteine [ 223 ]. GSH and cysteine are essential to reduce cancer-related oxidative damage [ 224 ].…”

Section: Mechanisms Relating One-carbon and Polyamine Metabolism To C...mentioning

confidence: 99%

One-Carbon and Polyamine Metabolism as Cancer Therapy Targets

et al. 2022

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Cancer metabolic reprogramming is essential for maintaining cancer cell survival and rapid replication. A common target of this metabolic reprogramming is one-carbon metabolism which is notable for its function in DNA synthesis, protein and DNA methylation, and antioxidant production. Polyamines are a key output of one-carbon metabolism with widespread effects on gene expression and signaling. As a result of these functions, one-carbon and polyamine metabolism have recently drawn a lot of interest for their part in cancer malignancy. Therapeutic inhibitors that target one-carbon and polyamine metabolism have thus been trialed as anticancer medications. The significance and future possibilities of one-carbon and polyamine metabolism as a target in cancer therapy are discussed in this review.

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Effects of S-Adenosylmethionine and Its Combinations With Taurine and/or Betaine on Glutathione Homeostasis in Ethanol-induced Acute Hepatotoxicity

Cited by 15 publications

References 48 publications

S‐adenosylmethionine: A metabolite critical to the regulation of autophagy

S‐adenosylmethionine: A metabolite critical to the regulation of autophagy

Impact of Supplementary Amino Acids, Micronutrients, and Overall Diet on Glutathione Homeostasis

One-Carbon and Polyamine Metabolism as Cancer Therapy Targets

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