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In enzymology, a L-glutamate oxidase (EC 1.4.3.11) is an enzyme that catalyzes the chemical reaction L-glutamate + O 2 + H 2 O ⇌ {\displaystyle \rightleftharpoons } 2-oxoglutarate + NH 3 + H 2 O 2 The 3 substrates of this enzyme are L-glutamate , O 2 , and H 2 O , whereas its 3 products are 2-oxoglutarate , NH 3 , and H 2 O 2 .
Glutathione reductase (GR) also known as glutathione-disulfide reductase (GSR) is an enzyme that in humans is encoded by the GSR gene.Glutathione reductase (EC 1.8.1.7) catalyzes the reduction of glutathione disulfide to the sulfhydryl form glutathione (), which is a critical molecule in resisting oxidative stress and maintaining the reducing environment of the cell.
Coenzyme Q 10 (CoQ 10 / ˌ k oʊ k j uː ˈ t ɛ n /), also known as ubiquinone, is a naturally occurring biochemical cofactor (coenzyme) and an antioxidant produced by the human body. [1] [2] [3] It can also be obtained from dietary sources, such as meat, fish, seed oils, vegetables, and dietary supplements.
Curb food cravings. Change unhealthy eating habits. Reduce food noise. Lower blood sugar. These medications can be an effective treatment if you’re struggling with how to not be hungry all the time.
The manifestations of histamine intolerance, or, adverse reactions to ingested histamine, are not confined to the gastrointestinal system, and are usually systemic, affecting the entire body; still, these symptoms are often sporadic and non-specific: [5] [6] [7] symptoms attributed to histamine intolerance are wide-ranging and may affect various physiological systems, including the skin ...
The exogenous amines are directly absorbed from food in the intestine. Alcohol can increase the absorption rate. Monoamine oxidase breaks down biogenic amines and prevents excessive resorption. MAO inhibitors (MAOIs) are also used as medications for the treatment of depression to prevent MAO from breaking down amines important for positive mood.
Glutaric acidemia type 2 has an autosomal recessive pattern of inheritance. Mutations in the ETFA, ETFB, and ETFDH genes cause glutaric acidemia type II. Mutations in these genes result in a deficiency in one of two enzymes that normally work together in the mitochondria, which are the energy-producing centers of cells.
The first committed step is the reaction of PRPP, glutamine and water to 5'-phosphoribosylamine (PRA), glutamate, and pyrophosphate - catalyzed by amidophosphoribosyltransferase, which is activated by PRPP and inhibited by AMP, GMP and IMP. PRPP + L-Glutamine + H 2 O → PRA + L-Glutamate + PPi