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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 is a cofactor for enzymes necessary for the metabolism of sulfur-containing amino acid and nitrogen-containing compounds present in DNA and RNA, the production of uric acid, and the oxidation and detoxification of various other compounds (8). Both molybdenum deficiency and toxicity are rare (4, 9). Dietary Mo affects copper metabolism in the human body and its high doses inhibit copper absorption (4, 8). This property has been used for the treatment of Wilson’s disease, which causes elevated concentrations of copper in the body (4). The amount of Mo in the body is regulated by excretion in the urine and bile. Low Mo intake is a predisposing cause of renal xanthine calculi and gout. Deficiency diseases are secondary to parenteral nutrition (8). However, high intakes of Mo (10–15 mg/day) also cause gout. Mo intake at this level may also be associated with altered metabolism of nucleotides and impaired copper bioavailability (9).
Teace Elements in Parenteral Nutrition*
Published in Fima Lifshitz, Childhood Nutrition, 2020
Adib A. Moukarzel, Marvin E. Ament
Molybdenum in the diet is absorbed as molybdate in its hexavalent form and is easily absorbed from salts and vegetables. Excretion is mainly in the urine, but urinary excretion rises as sulfate intake or endogenous sulfate production increases. It has been found that patients with large volume diarrhea such as Crohn’s disease may have excessive molybdenum losses in their stool.111 The minimum requirements for molybdenum are really unknown. Limited balanced studies have shown that between 48 to 96 mcg/day may be required. Larger supplementation may be required in the patient with extra-gastrointestinal losses. Normally, patients with acute stress-like illnesses may have greater requirements. Intravenous data in children is not available. A single case of molybdenum deficiency has been recognized. The patient developed a coma-like syndrome which was reversed with 300 mg of molybdenum per day.112
Liver Diseases
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Alcoholics show deficiencies of essential trace elements such as iron, magnesium, and zinc.182,287,536 Zinc deficiency has been associated with esophageal carcinoma in Iran.314 Molybdenum deficiency is also connected with increased incidence of this tumor.558
Aldehyde oxidase mediated drug metabolism: an underpredicted obstacle in drug discovery and development
Published in Drug Metabolism Reviews, 2022
Siva Nageswara Rao Gajula, Tanaaz Navin Nathani, Rashmi Madhukar Patil, Sasikala Talari, Rajesh Sonti
The enzymatic activity of AO is associated with homogenization and storage procedure. Hence, different liver tissue preparations may cause observed variations in the activity. Hutzler et al. showed an average of 42% loss in AO activity within 24 h after isolation of hepatocytes. In addition, significant interindividual variability of five- to eight-fold in intrinsic clearance in fresh and cryopreserved hepatocytes. The magnitude of this variability depends on the substrate and method, that is, whether the metabolite formation or substrate depletion was monitored (Hutzler et al. 2014). The contributing factors to inter-subject variations are genetic polymorphism, molybdenum deficiency, de-dimerization of the enzyme, and diet (Cheshmazar et al. 2019). In the quantitative characterization of AOX1 on 20 donors (10 male and female), AOX activity was higher in male than female donors (Fu et al. 2013).
Aldehyde oxidase at the crossroad of metabolism and preclinical screening
Published in Drug Metabolism Reviews, 2019
Narges Cheshmazar, Siavoush Dastmalchi, Mineko Terao, Enrico Garattini, Maryam Hamzeh-Mivehroud
Inter-subject variability in AOX-dependent drug metabolism is a final problem to be considered, as the levels of hepatic AOX activity vary in different individuals because of several factors. In fact, genetic polymorphisms, molybdenum deficiency, diet, and potential AOX de-dimerization are the most common reasons proposed for inter-individual variability in AOX activity. With respect to this, we suggest that metabolic clearance prediction studies using cellular or cell-free samples obtained from individual donors must be preceded by prescreening experiment aimed at selecting high AOX activity donors before isolation and pooling of cytosol, S9 fraction or cryopreserved hepatocytes. This is likely to reduce the possibility of any underestimation of AOX metabolic clearance to a minimum (Argikar et al. 2016).