Homocysteine effect on protein degradation rates

Stern, Felicia; Berner, Yitshal; Polyak, Zeev; Komarnitsky, Margarita; Sela, Ben‐Ami; Hopp, Micha; Dror, Yosef

doi:10.1016/j.clinbiochem.2004.07.011

Cited by 13 publications

(5 citation statements)

References 39 publications

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“…It is well known that SOD and CAT own sequential functions in ROS removing, by O 2 À dismutation, followed by H 2 O 2 conversion to H 2 O and O 2 , respectively (Halliwell and Gutteridge, 2007), thus we believe that CAT activity was increased by a compensatory effect, to remove the H 2 O 2 in excess generated by SOD increases in blood. On the other hand, it has been reported that Hcy can regulate protein turnover and gene expression, including antioxidant enzymes (Stern et al, 2004;Sharma et al, 2006). These effects of Hcy could be responsible, at least in part, by alterations in the activities of antioxidant enzymes observed in our study.…”

Section: Discussionmentioning

confidence: 97%

Chronic hyperhomocysteinemia alters antioxidant defenses and increases DNA damage in brain and blood of rats: Protective effect of folic acid

Matté

Mackedanz

Stefanello

et al. 2009

Neurochemistry International

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Section: Discussionmentioning

confidence: 97%

Chronic hyperhomocysteinemia alters antioxidant defenses and increases DNA damage in brain and blood of rats: Protective effect of folic acid

Matté

Mackedanz

Stefanello

et al. 2009

Neurochemistry International

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“…Conversely, homocysteine may also affect the metabolism of ADMA. First, homocysteine may, either by destabilizing protein structure or by increasing oxidative stress, accelerate protein degradation (29), resulting in an increased release of free ADMA from methylated proteins. Second, the enzymatic activity of DDAH, which is responsible for the breakdown of ADMA, is inhibited by homocysteine (30).…”

Section: Possible Links Between the Metabolic Pathways Of Adma And Homentioning

confidence: 99%

Measurement of asymmetric dimethylarginine in plasma: methodological considerations and clinical relevance

Teerlink¹

2005

Clinical Chemistry and Laboratory Medicine (CCLM)

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Asymmetric dimethylarginine (ADMA) is a potent inhibitor of nitric oxide synthase and is regarded as a novel risk factor for cardiovascular disease. The metabolic pathways of ADMA and homocysteine are strongly intertwined. First, during synthesis of ADMA, two equivalents of homocysteine are formed. Second, homocysteine has been shown to inhibit the ADMA-degrading enzyme dimethylarginine dimethylaminohydrolase. Finally, homocysteine, either directly or by increasing oxidative stress, may promote release of free ADMA by accelerating protein degradation. Currently used techniques for the quantification of ADMA in plasma are mostly based on liquid chromatography with fluorimetric or mass spectrometric detection. Plasma ADMA has a very narrow concentration distribution, with an inter-individual coefficient of variation of approximately 12%, and even slightly elevated ADMA concentrations are associated with increased cardiovascular disease risk. Therefore, to generate useful results in clinical research, high precision of the assay used for the quantification of ADMA assay is a matter of prime importance. Assays with a high coefficient of variation may lead to low statistical power in clinical trials and to a severe underestimation of the strength of associations in epidemiological studies.

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“…Folic acid, mainly in the active form of tetrahydrofolate, plays a role as one-carbon carrier to contribute to the synthesis of pyrimidine and purine, and, thereby, protein synthesis through central dogma. Second, Stern et al (2004) elucidated that homocysteine had detrimental effects on protein metabolism, and it would accelerate protein degradation rates, and homocysteine might interact with nucleic acid thus disturbed protein synthesis. Herein, we observed that GH and IGF-1, hormones that maintain protein synthesis, differed in response to folate supplemental levels.…”

Section: Discussionmentioning

confidence: 99%

Effects of folic acid supplementation on growth performance and hepatic folate metabolism-related gene expressions in weaned piglets

Yang

Liu

et al. 2010

Front. Agric. China

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The present study was conducted to evaluate the effects of different folic acid supplemental levels on growth performance, serum biochemical indicators, and hepatic folate metabolism-related gene expressions in weaned piglets. There were 160 piglets with initially average bodyweight of 7.33 kg randomly assigned to diets containing five levels of folic acid: basal diets (C), 0.5 mg$kg -1 folic acid (FS 0.5), 2.5 mg$kg -1 folic acid (FS 2.5), 5.0 mg$kg -1 folic acid (FS 5.0), or 10.0 mg$kg -1 folic acid (FS 10.0). Blood samples were collected from a subset (n = 20; 4 pigs per treatment) of the piglets on day 0, 14, and 28. Liver samples were collected from the blood-taken piglets on day 28 of the experiment. Pigs fed basal diet supplemented with 2.5 mg$kg -1 folic acid grew faster (P < 0.05) and consumed more feed (P < 0.01) than groups of C, FS 5.0, and FS 10.0 during the last two weeks. Dietary treatment had no effect on F/G throughout the experiment. Pigs in the FS 2.5 group showed greater concentrations of Growth Hormone (GH) (P < 0.05) and Insulin-like Growth Factors (IGF-1) (P < 0.01) in serum than C and FS 10.0 on day 28. RT-PCR analysis revealed that FS 0.5, FS 2.5, and FS 5.0 had a greater abundance of the mRNA encoding 5,10-methylenetetrahydrofolate reductase than C and FS 10.0 (P < 0.01). The mRNA expressions of folate binding protein in FS 0.5 and FS 2.5 were upregulated compared with pigs fed with basal diet (P < 0.05). These results demonstrated that folate supplemental level of 2.5 mg$kg -1 significantly enhanced the growth performance of piglets. Folic acid had an impact on folate metabolism and the homocysteine concentrations. No folate supplementation or folate supplemental level of 10 mg$kg -1 could not increase the growth performance to the greatest degree.

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Homocysteine effect on protein degradation rates

Cited by 13 publications

References 39 publications

Chronic hyperhomocysteinemia alters antioxidant defenses and increases DNA damage in brain and blood of rats: Protective effect of folic acid

Chronic hyperhomocysteinemia alters antioxidant defenses and increases DNA damage in brain and blood of rats: Protective effect of folic acid

Measurement of asymmetric dimethylarginine in plasma: methodological considerations and clinical relevance

Effects of folic acid supplementation on growth performance and hepatic folate metabolism-related gene expressions in weaned piglets

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