Nervous system cobalamins

J Metz. Pathogenesis of cobalamin neuropathy deficiency of nervous system S-adenosylmethionine Nutr Rev 51 12-15, 1993. 

Regulation of homocysteine metabolism appears to be especially important in the central nervous system, presumably because of the critical role of methyl transfer reactions in the production of neurotransmitters and other methylated products. It has been known for decades that mental retardation is a feature of the genetic diseases, such as CBS deficiency, that cause severe hyperhomocysteinemia and ho-mocystinuria. Impaired cognitive function is also seen in pernicious anemia, which causes hyperhomocysteinemia due to deficiency of cobalamin (see Chapter 28). Hyperhomocysteinemia also may be linked to depression, schizophrenia, multiple sclerosis, and Alzheimer s disease. The molecular mechanisms underlying these clinical associations have not yet been delineated. 

Metz J Cobalamin deficiency and the pathogenesis of nervous system disease. Annu Rev Nutr 12 59-79,1992. 

Vitamin B12 (cyancobali-min, cobalamin) Protein and fatty acid metabolism production of red blood cells maintenance of nervous system, concentration and memory. Clams, oysters, beef, eggs and dairy products. Not found in many plant products strict vegetarians may need to consider Bi2 supplements. 2 mg No... 

Scalabrino G, Tredici G, Buccellato ER, and Manfridi A (2000) Further evidence for the involvement of epidermal growth factor in the signalingpathway ofvitamin B u (cobalamin) in the rat central nervous system. Journal of Neuropathology and Experimental Neurology 59, 808-14. 

There are two major clinical manifestations of cobalamin (B12) deficiency. One such presentation is hematopoietic (caused by the adverse effects of a B12 deficiency on folate metabolism), and the other is neurologic (caused by hypomethylation in the nervous system). 

Sea lettuces are a source of vitamins from group B (MacArtain et al, 2007 McDermid and Stuercke, 2003). For instances, Ulva lactuca contain high amount of cobalamin or vitamin B12. Vitamin B12 plays a key role in homeostasis of the brain and nervous system, and for the formation of blood (Scalabrino, 2009). Daily ingestion of 1.4 g/day of Ulva lactuca will be enough to meet the daily requirements of vitamin B12 (MacArtain et al, 2007). One of the most important vitamins B occurring in Ulva reticulata is riboflavin (vitamin B2). Vitamin B2 deficiency is often endemic in human... 

Scalabrino, G. (2009). The multi-faceted basis of vitamin B12 (cobalamin) neurotrophism in adult central nervous system Lessons learned from its deficiency. Prog. Neurobiol. 88, 203-220. 

NO is known to react with the cobalt of cobalamins (Cbl). The structure of cobalamin is presented in Scheme 7. Cobalamins containing various axial ligands tram to dimethylbenzimidazole moiety are known as vitamin B12 and are important cofactors for 5-methyltetrahydrofolate-homocysteine methyltransferase and methylmalonyl-coA mutase playing a key role in the normal functioning of the brain and nervous system and in red blood cell formation [330, 331]. 

The deficiencies of cystathionine )5-synthase (CBS), sulfite oxidase, and methylenetetrahydrofolate reductase (MTHFR) may all result in central nervous system dysfunction, in particular mental retardation [1-3]. Defects of CBS and sulfite oxidase both cause dislocated lenses of the eyes, but the phenotypes are different otherwise. The manifestations of CBS deficiency, the most common of these disorders, and MTHFR deficiency range from severely affected to asymptomatic patients both may cause vascular occlusion. Deficiency of sulfite oxidase is clinically uniform, but genetically heterogeneous, and functional deficiency of the enzyme can result from several inherited defects of molybdenum cofactor biosynthesis [2, 4]. Hereditary folate malabsorption and defects of cobalamin transport (transcobala-min II deficiency) or cobalamin cofactor biosynthesis (cblC-G diseases) may cause megaloblastic anemia, in addition to CNS dysfunction [3, 5, 6]. 

Cobalamln Cobalamin or vitamin Bj2 is another vitamin required for the metabolism of amino acids, fatty acids, nucleic acids, and carbohydrates. Cobalamin deficiency can cause severe and irreversible damage in the brain, nervous, cardiovascular, and hematopoietic (pernicious anemia) systems [4]. Animals, plants, and fungi do not synthesize vitamin Bj2, which can only be produced by some microorganisms. To date, the best cobalamin producer is Propionibacterium freudenreichii, which is currently applied for industrial production. 

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