2-01-02 S-adenosyl-methionine and I-methionine in AIDS-associated vascular myelopathy

1997 ◽  
Vol 150 ◽  
pp. S69
Author(s):  
Alessandro Di Rocco ◽  
Peter Werner ◽  
Teodoro Bottiglieri ◽  
M. Tagliati ◽  
Madhau Sunkara ◽  
...  
Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 130
Author(s):  
Munehiro Kitada ◽  
Yoshio Ogura ◽  
Itaru Monno ◽  
Jing Xu ◽  
Daisuke Koya

Enhanced oxidative stress is closely related to aging and impaired metabolic health and is influenced by diet-derived nutrients and energy. Recent studies have shown that methionine restriction (MetR) is related to longevity and metabolic health in organisms from yeast to rodents. The effect of MetR on lifespan extension and metabolic health is mediated partially through a reduction in oxidative stress. Methionine metabolism is involved in the supply of methyl donors such as S-adenosyl-methionine (SAM), glutathione synthesis and polyamine metabolism. SAM, a methionine metabolite, activates mechanistic target of rapamycin complex 1 and suppresses autophagy; therefore, MetR can induce autophagy. In the process of glutathione synthesis in methionine metabolism, hydrogen sulfide (H2S) is produced through cystathionine-β-synthase and cystathionine-γ-lyase; however, MetR can induce increased H2S production through this pathway. Similarly, MetR can increase the production of polyamines such as spermidine, which are involved in autophagy. In addition, MetR decreases oxidative stress by inhibiting reactive oxygen species production in mitochondria. Thus, MetR can attenuate oxidative stress through multiple mechanisms, consequently associating with lifespan extension and metabolic health. In this review, we summarize the current understanding of the effects of MetR on lifespan extension and metabolic health, focusing on the reduction in oxidative stress.


2021 ◽  
Vol 89 (3) ◽  
pp. 127-133 ◽  
Author(s):  
Aaron D. Goldman ◽  
Betul Kacar

AbstractThe RNA World is one of the most widely accepted hypotheses explaining the origin of the genetic system used by all organisms today. It proposes that the tripartite system of DNA, RNA, and proteins was preceded by one consisting solely of RNA, which both stored genetic information and performed the molecular functions encoded by that genetic information. Current research into a potential RNA World revolves around the catalytic properties of RNA-based enzymes, or ribozymes. Well before the discovery of ribozymes, Harold White proposed that evidence for a precursor RNA world could be found within modern proteins in the form of coenzymes, the majority of which contain nucleobases or nucleoside moieties, such as Coenzyme A and S-adenosyl methionine, or are themselves nucleotides, such as ATP and NADH (a dinucleotide). These coenzymes, White suggested, had been the catalytic active sites of ancient ribozymes, which transitioned to their current forms after the surrounding ribozyme scaffolds had been replaced by protein apoenzymes during the evolution of translation. Since its proposal four decades ago, this groundbreaking hypothesis has garnered support from several different research disciplines and motivated similar hypotheses about other classes of cofactors, most notably iron-sulfur cluster cofactors as remnants of the geochemical setting of the origin of life. Evidence from prebiotic geochemistry, ribozyme biochemistry, and evolutionary biology, increasingly supports these hypotheses. Certain coenzymes and cofactors may bridge modern biology with the past and can thus provide insights into the elusive and poorly-recorded period of the origin and early evolution of life.


2020 ◽  
Vol 07 (03) ◽  
pp. 080-086
Author(s):  
Syed Aaquil Hasan Syed Javid Hasan ◽  
Raisa Arifanie O'Zelian Pawirotaroeno ◽  
Syed Abrar Hasan Syed Javid Hasan ◽  
Elene Abzianidze

AbstractOne of the significant consequences of alcohol consumption is cancer formation via several contributing factors such as action of alcohol metabolites, vitamin deficiencies, and oxidative stress. All these factors have been shown to cause epigenetic modifications via DNA hypomethylation, thus forming a basis for cancer development. Several published reviews and studies were systematically reviewed. Omnivores and vegetarians differ in terms of nutritional intake and deficiencies. As folate deficiency was found to be common among the omnivores, chronic alcoholism could possibly cause damage and eventually cancer in an omnivorous individual via DNA hypomethylation due to folate deficiency. Furthermore, as niacin was found to be deficient among vegetarians, damage in vegetarian chronic alcoholics could be due to increased NADH/NAD+ ratio, thus slowing alcohol metabolism in liver leading to increased alcohol and acetaldehyde which inhibit methyltransferase enzymes, eventually leading to DNA hypomethylation. Hence correcting the concerned deficiency and supplementation with S-adenosyl methionine could prove to be protective in chronic alcohol use.


2013 ◽  
Vol 49 (5) ◽  
pp. 342-346 ◽  
Author(s):  
Lionel Sebbag ◽  
Nicole Smee ◽  
Deon van der Merwe ◽  
Dustin Schmid

A 2.5 yr old spayed female Weimaraner presented after ingestion of blue-green algae (Microcystis spp.). One day prior to presentation, the patient was swimming at a local lake known to be contaminated with high levels of blue-green algae that was responsible for deaths of several other dogs the same summer. The patient presented 24 hr after exposure with vomiting, inappetence, weakness, and lethargy. Blood work at the time of admission was consistent with acute hepatic failure, characteristic findings of intoxication by Microcystis spp. Diagnosis was suspected by analyzing a water sample from the location where the patient was swimming. Supportive care including fluids, fresh frozen plasma, whole blood, vitamin K, B complex vitamins, S-adenosyl methionine, and Silybum marianum were started. The patient was discharged on supportive medications, and follow-up blood work showed continued improvement. Ingestion is typically fatal for most patients. This is the first canine to be reported in the literature to survive treatment after known exposure.


1986 ◽  
Vol 17 (2) ◽  
pp. 111-118 ◽  
Author(s):  
Michael A. Sherer ◽  
Giulio L. Cantoni ◽  
Robert N. Golden ◽  
Matthew V. Rudorfer ◽  
William Z. Potter

2003 ◽  
Vol 5 (6) ◽  
pp. 460-466 ◽  
Author(s):  
George I. Papakostas ◽  
Jonathan E. Alpert ◽  
Maurizio Fava

1996 ◽  
Vol 10 (5) ◽  
pp. 903-912 ◽  
Author(s):  
Emeline Teyssier ◽  
Maryse A. Block ◽  
Roland Douce ◽  
Jacques Joyard

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