Conversion of Methionine to Cystine: Experiments with Radioactive Sulfur (S35)

Tarver, Harold; Schmidt, Carl L. A.

doi:10.3181/00379727-41-10703p

Cited by 19 publications

(20 citation statements)

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“…In the majority of tissues, cysteine content depends on several factors including cysteine supply in the diet, by cysteine synthesizing organs, mainly the liver, membrane transport of extracellular cystine converting intracellularly to cysteine, protein breakdown, and cysteine catabolism to taurine and inorganic sulfur (Lu 1999, Stipanuk & Ueki 2011. Cysteine is also connected with Hcy by the transsulfuration pathway (Tarver & Schmidt 1939) restricted to several organs (Finkelstein 1990(Finkelstein , 2000, but to our knowledge, there was no comprehensive evidence showing that this reaction is active in the human placenta.…”

Section: Discussionmentioning

confidence: 98%

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Placental markers of folate-related metabolism in preeclampsia

Mislanova¹,

Martsenyuk²,

Huppertz³

et al. 2011

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The etiology and degree of clinical symptoms of preeclampsia depend on genotypic and phenotypic maternal and trophoblast factors, and elevated levels of plasma homocysteine (Hcy) are one of the pathogenetic factors of preeclampsia. To assess the impact of the folate-related metabolism, we characterized the indices of this metabolism in 40 samples from uncomplicated term placentas and 28 samples from preeclamptic pregnancies by quantifying the total content of folate, methionine (Met), Hcy and related cysteine, and glutathione (GSH) in compliance with the 677 C/T genotype of methylene tetrahydrofolate reductase (MTHFR). The prevalence of MTHFR genotypes was not significantly different between the two groups. The polymorphism of MTHFR was not unambiguously connected with the content of total placental Met, Hcy and related cysteine, and GSH either in uncomplicated or in complicated pregnancies. By contrast, the combination of the heterozygous MTHFR genotype with folate deficiency in the samples from preeclamptic pregnancies was characterized by a statistically significant decrease in the Met content, a trend toward increased Hcy levels and a tight association between metabolically directly and indirectly related compounds, e.g. positive relation between Hcy versus cysteine and folate versus GSH and negative relation between folate versus Hcy and both Hcy and cysteine versus GSH. We demonstrated the expression of cystathionine-b-synthase (CBS) in human placenta at term by RT-PCR and western blot analysis, for the first time, and confirmed its catalytic activity and the accumulation of cysteine and CBS in placental explants cultivated in the presence of elevated Hcy concentrations. We suggest that disturbance in placental folate-related metabolism may be one of the pathogenetic factors in preeclampsia.

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Section: Discussionmentioning

confidence: 98%

“…Hcy, a thiol-containing amino acid, is the demethylated derivative of the essential amino acid Met and an intermediate in the Met cycle and transsulfuration pathway (Tarver & Schmidt 1939, Mudd & Levy 1989. It may be remethylated to Met or eliminated from the cycle by formation of cysteine in the transsulfuration pathway.…”

Section: Introductionmentioning

confidence: 99%

Placental markers of folate-related metabolism in preeclampsia

Mislanova¹,

Martsenyuk²,

Huppertz³

et al. 2011

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“…That cysteine can be synthesized from methionine was first demonstrated by Tarver andSchmidt in 1939 (Tarver andSchmidt, 1939). This pathway is termed the transsulfuration or the cystathionine pathway (Fig.…”

Section: Methionine Metabolism and The Transsulfuration Pathway-mentioning

confidence: 99%

Regulation of glutathione synthesis

Lu¹

2009

Molecular Aspects of Medicine

1,648

765

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Glutathione (GSH) is a ubiquitous intracellular peptide with diverse functions that include detoxification, antioxidant defense, maintenance of thiol status, and modulation of cell proliferation. GSH is synthesized in the cytosol of all mammalian cells in a tightly regulated manner. The major determinants of GSH synthesis are the availability of cysteine, the sulfur amino acid precursor, and the activity of the rate-limiting enzyme, glutamate cysteine ligase (GCL). GCL is composed for a catalytic (GCLC) and modifier (GCLM) subunit and they are regulated at multiple levels and at times differentially. The second enzyme of GSH synthesis, GSH synthase (GS) is also regulated in a coordinated manner as GCL subunits and its up-regulation can further enhance the capacity of the cell to synthesize GSH. Oxidative stress is well known to induce the expression of GSH synthetic enzymes. Key transcription factors identified thus far include Nrf2/Nrf1 via the antioxidant response element (ARE), activator protein-1 (AP-1) and nuclear factor κ B (NFκB). Dysregulation of GSH synthesis is increasingly being recognized as contributing to the pathogenesis of many pathological conditions. These include diabetes mellitus, pulmonary fibrosis, cholestatic liver injury, endotoxemia and drug-resistant tumor cells. Manipulation of the GSH synthetic capacity is an important target in the treatment of many of these disorders.

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“…Abbreviations TPN, total parenteral nutrition; US-TPN, unsupplemented total parenteral nutrition; S-TPN, cysteine-supplemented total parenteral nutrition Cysteine is a sultbydryl-containing compound that in adult man may be synthesized from methionine via the transsulfuration pathway (19). In the newborn, cysteine may be an essential amino acid (6).…”

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confidence: 99%