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Micronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
The flavin coenzymes including flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) are derivatives of riboflavin (vitamin B2). Like the nicotinamide coenzymes, the flavin coenzymes participate in redox reactions that affect energy nutrients in the citric acid cycle and in the electron transport system.
Molecular Aspects of the Activity and Inhibition of the FAD-Containing Monoamine Oxidases
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Supported by extensive molecular model chemistry and recent thermodynamic calculations, three mechanisms have been considered for MAO catalysis: the polar nucleophilic mechanism (Orru et al., 2013), the radical (Silverman, 1995), and the hydride transfer mechanism (Kay et al., 2007). The hydride transfer mechanism (Fig. 10.5) is found in other oxidases and is supported by theoretical studies based on transition state theory (Vianello et al., 2016). However, the versatility of flavin catalysis could allow alternative mechanisms with specific chemicals, for example with the cyclopropylamines.
The Iodotyrosine Deiodinase Defect
Published in Geraldo Medeiros-Neto, John Bruton Stanbury, Inherited Disorders of the Thyroid System, 2019
Geraldo Medeiros-Neto, John Bruton Stanbury
Activity is stimulated by sodium dithionate in the absence of NADPH,118 and the rate of deiodination is dependent on the quantity of NADPH.114 The dithionate might reduce the flavins. Kusakabe and Miyaki observed that the fraction from a supernatant of homogenate of thyroid migrated toward the anode on electrophoresis, while that solubi-lized from the particulate fraction migrated toward the cathode.115 This suggested that the iodotyrosine deiodinase existed in two isoforms. The removal of the first iodine from diidotyrosine occurs less rapidly than does the deiodination of monoiodotyrosine. Substances such as menadione, methelene blue, and phenazine methosulfate inhibit deiodination even when supplemented with NADPH, probably by accelerating NADPH oxidation.116 Serotonin, acetylcholine, epinephrin, and ferricyanide also inhibit deiodination. Prior injection of nicotinamide into rats stimulates the capacity of liver homogenates to deiodinate DIT, probably by stimulating the concentration of NADPH in the tissue.124 MIT and DIT block tyrosine hydroxylase, but it is not clear what function this might serve, if any.119 It also inhibits dopamine synthesis and induces hyperprolactinemia and hyperaldosteronemia.125-127
A case report of sudden-onset auditory neuropathy spectrum disorder associated with Brown-Vialetto-Van Laere syndrome (riboflavin transporter deficiency)
Published in International Journal of Audiology, 2022
Ozlem Gedik Soyuyuce, Elif Ayanoglu Aksoy, Zuhal Yapici
The flavin deficiencies associated with BVVL may cause dysfunction in auditory neuron firing and thus auditory dyssynchrony (Chandran et al. 2015). The time between the onset of deafness and the development of other manifestations varies but is usually one to two years. An intercurrent event (usually an injury or infection) appears to precipitate the initial manifestations or worsen existing findings (Summers et al. 1987). Since no intercurrent event was reported by the parents of our case, it remains unclear what caused the fluctuations and worsening in auditory findings, as well as the progression of disease with additional severe neurological symptoms within months. However, the fluctuations with the ABR wave presentation due to a probable gradual loss of function of riboflavin transporter proteins early in disease course might be associated with the dyssynchrony at the periphery of the auditory system similar to fluctuations observed in temperature-sensitive ANSD (Moser and Starr 2016). Fluctuations with the ABR wave presentation might indicate that the nerves were still recoverable during the earliest stage. However, after a long duration of illness, total nerve dyssynchrony sets in, and a total absence of waveforms suggests complete damage (Chandran et al. 2015).
Exploring the contribution of mitochondrial dynamics to multiple acyl-CoA dehydrogenase deficiency-related phenotype
Published in Archives of Physiology and Biochemistry, 2021
Sofia R. Brandão, Rita Ferreira, Hugo Rocha
Riboflavin-responsive multiple acyl-CoA dehydrogenase deficiency (RR-MADD) is a variant of MAD defects, which benefit from riboflavin treatment, with a clinical improvement and an almost normalization of biochemical abnormalities (Gregersen et al.1982). Riboflavin is the precursor of FAD, which is a cofactor for many enzymes such as acyl-CoA dehydrogenases, ETFDH and other mitochondrial enzymes, being also essential for the folding and stability of these flavoproteins (Olsen et al.2003, Ho et al.2011). Patients with RR-MADD showed milder folding defects of ETFDH variants, with a significant increase in protein stability and activity after riboflavin treatment (Cornelius et al.2013). In addition of ETFDH mutations, other RR-MADD phenotype-like may be caused by defects in flavin metabolism and transport (Olsen et al.2007, 2016). Most of the patients with late-onset MADD are clearly responsive to riboflavin, since they usually present a missense mutation on the ETFDH gene which is more commonly associated with RR-MADD phenotypes (Grünert 2014). However, severe MADD forms may also be associated to ETFDH mutations (Rocha et al.2011, Alves et al.2012).
Differential effects of C-reactive protein levels on voriconazole metabolism at three age groups in allogeneic hematopoietic cell transplant recipients
Published in Journal of Chemotherapy, 2021
Xingxian Luo, Taifeng Li, Lei Hu, Silu Liu, Haiyan Zhao, Jiaqi Zhang, Yufei Feng, Lin Huang
In the present study, the median concentration of VRCZ was highest in adults (1.48 mg/L), followed by children aged 10–18 (0.85 mg/L), and the lowest was children aged 2–10 years (0.65 mg/L), which were partly consistent with wei et al reported.10 Conversely, the order of the magnitude of the MR values was aged in 2–10 years (1.72), then in 11–18 years (1.21) and followed in 19–60 years (0.95), further verifying that metabolic rate of VRCZ exhibits negative relationship with age groups. Mann–Whitney U test suggested that MR values in 11–18 and 19–60 years were significantly lower in age 2–10 years (p < .05), indicating a higher activity of CYP2C19 enzyme in age 2–10 years. Existing evidence support that higher metabolic activity of flavin-containing monooxygenase 3 (FMO3) and CYP2C19 are found in children compared with adults.23 A higher metabolic intensity of VRCZ in younger children would reduce the impact of inflammation on liver microsomal enzyme activity. With the increase of age, the impact of inflammation on VRCZ metabolism seemed to be more and more prominent.