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Ascorbate as an Enzyme Cofactor
Published in Qi Chen, Margreet C.M. Vissers, Vitamin C, 2020
Margreet C.M. Vissers, Andrew B. Das
The posttranslational modification of collagen by hydroxylation was first described in the 1940s and 1950s [60–64], and the prolyl hydroxylase enzymes responsible were the first identified 2-OGDDs [65–68]. Since this time, the prevalence of protein hydroxylation has become apparent, and this modification is now recognized as being critical to the regulation of the hypoxic response [69–71] and to protein synthesis by modification of ribosomal proteins [57,72]. In addition, demethylation of histones, DNA, and RNA is initiated by oxidative hydroxylation of methyllysine [73–79], methylarginine [80–83], methylcytosine [84,85], and methyladenosine [86–88]. The number of enzymes identified as 2-OGDDs active in mammalian cells has increased rapidly in this century, and their widespread influence on many fundamental aspects of biology is becoming well recognized. Table 5.1 contains a summary of the more than 50 2-OGDD enzymes identified to date in mammalian cells.
Mesolimbic Interactions with Mesopontine Modulation of Locomotion
Published in Peter W. Kalivas, Charles D. Barnes, Limbic Motor Circuits and Neuropsychiatry, 2019
Robert D. Skinner, E. Garcia-Rill
Another role of NO in the nervous system appears to be that of a neurotoxin. Because NO has free radical chemical properties, it is highly reactive and, thus, toxic. In primary cerebral cortical cultures, NMDA added to the culture medium induced the release of NO from NOS-containing neurons. Neurons adjacent to the extensively branched NOS-containing neurons were killed while NOS-containing neurons survived. This neurotoxicity was prevented by addition of N-nitroarginine or N-methylarginine, two antagonists of arginine, or hemoglobin, which binds extracellular NO.196 The clinical import of NO was heralded recently in a study of experimental stroke in an in vivo rat model in which N-nitroarginine was shown to provide better protection against ischemic-induced damage than the NMDA antagonist MK-801.203 It appears that NOS-containing neurons may have a role in Huntington’s disease in which massive loss of caudate nucleus neurons occurs, but NOS-containing neurons are resistive to the destructive process.204 It even seems possible that in patients with elevated numbers of cholinergic PPN cells (NOS-containing), the onset of puberty, with its increased levels of sex steroids, may bring about increased activity of PPN cells. The consequence of this increased neuronal activity may be, (a) toxic levels of NO are produced due to the additional PPN NOS-containing cells, (b) death of non-NOS-containing neurons in close association with PPN neurons, and (c) the subsequent onset of the symptoms of schizophrenia or narcolepsy at age 20 ± 6 years.
Analysis of Modified Amino Acids
Published in Ajit S. Bhown, Protein/Peptide Sequence Analysis: Current Methodologies, 1988
Since the last comprehensive compilation in 1980,9 the number of proteins which have been reported to contain methylated amino acid residues has steadily grown. We, therefore, updated the original list. Table 1 lists 20 additional new references; they include proteins such as α-amylase, HMG-1 and HMG-2 proteins, nuclear acidic phosphoprotein C-23, citrate synthase, elongation factors, initiation factor, and heat shock proteins. Also included are newly observed amino acids such as S-methylmethionine, S-methylcysteine, and δ-N-methylarginine.
Relationship between exercise intervention and NO pathway in patients with heart failure with preserved ejection fraction
Published in Biomarkers, 2018
Flavia Baldassarri, Edzard Schwedhelm, Dorothee Atzler, Rainer H. Böger, Kathrin Cordts, Bernhard Haller, Axel Pressler, Stephan Müller, Christiane Suchy, Rolf Wachter, Hans-Dirk Düngen, Gerd Hasenfuss, Burkert Pieske, Martin Halle, Frank Edelmann, André Duvinage
As exercise is also closely linked to the nitric oxide (NO) system (Schuster et al.2012), exercise training seems to be a promising way to improve vascular function and NO pathway biomarkers. Endothelial NO release has a vasodilatory effect (Tousoulis et al.2012), whereas oxidative stress or pathophysiological conditions, such as vascular injury, stimulate the production of methylated arginine derivatives, such as asymmetric dimethylarginine (ADMA) (Alter et al.2016). Therefore, methylarginine-mediated NO synthase inhibition leads to secondary endothelial dysfunction (Cardounel et al.2007). In contrast to these methylated arginine derivatives, low circulating L-homoarginine (L-hArg) concentrations are independently associated with mortality (Atzler et al.2013).
Quantification of serum homoarginine, methylated arginine and inhibin-A levels in a high-risk pregnancy
Published in Journal of Obstetrics and Gynaecology, 2022
Hatice Banu Keskinkaya, Sedat Abuşoğlu, Ali Ünlü, Mehmet Nuri Atalar, Setenay Arzu Yilmaz
In addition to the h-Arg, we also evaluated the methylarginine derivatives and biochemical screening tests between groups. According to the statistical results, serum ADMA levels in the control group with quadruple test were found to be higher than in the high-risk group quadruple test and the high-risk group with quadruple test (p < .001, p < .05 respectively). Additionally, higher ADMA level was detected in control group with binary test compared to the high-risk group with quadruple test (p < .001). On the other hand, considering the relationship between high-risk groups, lower ADMA level seen in the high-risk group with quadruple test (p < .001) (Figure 2).
Total methylated arginine load as a risk parameter in subjects with masked hypertension
Published in Clinical and Experimental Hypertension, 2020
Muserref Hosaf, Sedat Abusoglu, Ahmet Avci, Kenan Demir, Ali Unlu, Duygu Eryavuz, Gulsum Abusoglu
Serum symmetric dimethylarginine levels might be useful marker for determining the transition from masked to clinical hypertension. Additionally, this is the first study evaluating the other methylarginine levels in addition to asymmetric dimethylarginine in hypertension groups. However, further studies with larger clinical groups are necessary to identify the possible relation between total methylarginine load and etiopathogenesis of masked hypertension. The number of patient groups and lack of serum nitric oxide analysis were a limitation of this study. This might be explained by the difficulty of diagnosing the patients with masked hypertension.