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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
Molybdenum (Mo) is an essential micro-mineral and acts as a cofactor for the activities of several enzymes in the human body including xanthine oxidase, aldehyde oxidase, sulfite oxidase, nitrate reductase, and hydrogenase (4, 6, 8–9). Xanthine oxidase and aldehyde oxidase play a role in iron utilization as well as in cellular metabolism and electron transport. Xanthine oxidase is also used in the uptake and release of iron from ferritin in the intestinal mucosa and in the release of iron from ferritin in the liver, placenta, and erythropoietic tissues to the ferrous form (8). Xanthine oxidase and hydrogenase play a role in the production of uric acid from hypoxanthine and xanthine (4). Aldehyde oxidase oxidizes and detoxifies purines and pyrimidines, while sulfite oxidase containing molybdenum incorporated as part of the molecule, is used for the conversion of sulfite to sulfate (4).
Mechanisms of Airway Responses to Inhaled Sulfur Dioxide
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Most absorbed 35SO2 is eventually excreted in the urine as sulfate (SO4) (Yokohama et al, 1971), but the mechanism of bioconversion to sulfate is not determined (Neta and Huie, 1985; Petering and Shih, 1975). Bisulfite ion is converted to sulfate by sulfite oxidase, an enzyme found in lung, liver, and a variety of other tissues. Since thiosulfates, not bisulfite, are the principal chemical form of absorbed SO2 in the bloodstream, the importance of sulfite oxidase in SO2 clearance remains uncertain (Petering and Shih, 1975). Sulfite can also be converted to sulfate by nonenzymatic autooxidation that occurs in the presence of oxygen. Although this reaction is usually slow, it can be catalyzed by trace metal ions (Hoffmann and Boyce, 1983). This reaction is also a source of free radicals that could contribute to the tissue toxicity of SO2 (Neta and Huie, 1985).
The minerals
Published in Geoffrey P. Webb, Nutrition, 2019
Experimental molybdenum deficiency can be induced in animals but just one verified case of molybdenum deficiency has been reported in a single TPN patient. Molybdenum is a cofactor for the following: Xanthine oxidase, an enzyme involved in purine breakdown. Aldehyde oxidase, an enzyme involved in nucleotide breakdown from nucleic acids. Sulphite oxidase involved in the breakdown of sulphur-containing amino acids. The mitochondrial component mARC is a relatively recently discovered molybdenum enzyme in mammals. Neither its exact functions nor physiological significance are completely clear. It may play a role in drug metabolism and the detoxification of foreign substances (Havemeyer et al. 2011).
Inosine supplements only reach the CNS in molybdenum deficient humans and may cause astrocyte degeneration and bulbar–respiratory disease
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2022
A 12-week pilot trial of oral inosine in ALS patients was published after the ALS untangled review (5). The rationale for the trial was that oxidative stress is implicated in the pathogenesis of ALS and inosine is metabolized to urate, and urate is a potent antioxidant. The 25 participants had a baseline serum urate level of 4.1 mg/dL. Oral inosine loading, up to 3000 mg per day, lifted this to 7–8 mg/dL over 6 weeks. These figures are consistent with only partial metabolization of inosine to urate, the remaining inosine would have reached the CNS. Three biomarkers of oxidative stress were measured, 3-nitrotyrosine, ferric-reducing antioxidant power, and glutathione. Plasma levels for the first two changed in a predictable manner in response to the urate increase, CSF levels were not determined. More significantly, urate did not trigger an increase in plasma or brain glutathione, almost as though some other factor was preventing this, for example, concurrent sulfite oxidase deficiency. SO is a Mo-dependent enzyme.
Heterozygote MTHFR A1298C mutation in a case of autosomal recessive bestrophinopathy with branch retinal vein occlusion
Published in Ophthalmic Genetics, 2022
Sara Hemmati, Golnaz Khakpour, Fatemeh Nadjafi-Semnani, Arzhang Gordiz, Masoome Sajadi, Fatemeh Abdi
Bilateral lens subluxation without a history of trauma also requires a full workup. Some of the causes include homocystinuria, Marfan syndrome, Weill-Marchesani syndrome, and sulfite oxidase deficiency (10). Elevated serum homocysteine can influence the development of zonular fibers and lead to lens subluxation or even dislocation, usually, inferiorly (10). The occurrence of bilateral inferior lens dislocation in our patient at 3 years of age should have prompted investigations about its cause and starting treatment at that point would probably have prevented the present vascular occlusion.
Neonatal seizures treatment based on conventional multichannel EEG monitoring: an overview of therapeutic options
Published in Expert Review of Neurotherapeutics, 2022
Isotta Guidotti, Licia Lugli, Luca Ori, Maria Federica Roversi, Elisa Della Casa Muttini, Luca Bedetti, Marisa Pugliese, Francesca Cavalleri, Francesca Stefanelli, Fabrizio Ferrari, Alberto Berardi
No specific therapy exists for sulfite oxidase deficiency; however, a narrow temporal window of intervention with daily infusions of cyclic pyranopterin may exist in children with molybdenum cofactor deficiency prior to the onset of brain injury.