Vitamin B12 deficiency.

Among the numerous functions of melatonin, the control of survival and differentiation of mesenchymal stem cells (MSCs) has been recently proposed. MSCs are a heterogeneous population of multipotent elements resident in tissues such as bone marrow, muscle, and adipose tissue, which are primarily involved in developmental and regeneration processes, gaining thus increasing interest for tissue repair and restoration therapeutic protocols. Receptor-dependent and receptor-independent responses to melatonin are suggested to occur in these cells. These involve antioxidant or redox-dependent functions of this indolamine as well as secondary effects resulting from autocrine and paracrine responses. Inflammatory cytokines and adipokines, proangiogenic/mitogenic stimuli, and other mediators that influence the differentiation processes may affect the survival and functional integrity of these mesenchymal precursor cells. In this scenario, melatonin seems to regulate signaling pathways that drive commitment and differentiation of MSC into osteogenic, chondrogenic, adipogenic, or myogenic lineages. Common pathways suggested to be involved as master regulators of these processes are the Wnt/β-catenin pathway, the MAPKs and the, TGF-β signaling. In this respect melatonin emerges a novel and potential modulator of MSC lineage commitment and adipogenic differentiation. These and other aspects of the physiological and pharmacological effects of melatonin as regulator of MSC are discussed in this review.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/jpi.12133

Melatonin regulates mesenchymal stem cell differentiation: a review

Counteraction of urea by trimethylamine N-oxide is due to direct interaction. Biophys J. 97:2559―2566

Among contrasting anions, CN− ion is extremely toxic and dangerous pollutant. Consequently, there is considerable interest in the colorimetric and fluorescent detection of CN− ions at trace level by using simple methods In this critical review begins with a brief discussion of the source, applications, toxicity of cyanide and mechanism of CN− ion sensor. Further, the fluorescent and colorimetric CN− ion sensors are classified according to their receptors into several categories like azine, azo, benzimidazole, benzothiazole, bisthiazole, BODIFY, coumarin, nanoparticles, hemicyanine, imine, indoline, malononitrile, naphthalene, naphthalimide, phenazine, pyrene, quinoline, rhodamine and thiazolidine functionalized sensing system in the year 2016.

Chromogenic and fluorogenic chemosensors for lethal cyanide ion. A comprehensive review of the year 2016

Methylcobalamin (MeCbl) and adenosylcobalamin (AdoCbl) are coenzymes for methionine synthase and methylmalonyl-CoA mutase, respectively. Hydroxylcobalamin (HOCbl) and cyanocobalamin (CNCbl) are frequently used for supplementation. MeCbl and AdoCbl have recently emerged as alternative forms in supplements. In the light of metabolic transformation of Cbl into its cofactor forms, this review discusses current evidence on efficacy and utility of different Cbl forms in preventing or treating Cbl deficiency. Cbl-transporting proteins bind and mediate the uptake of all aforementioned forms of Cbl. After internalization and lysosomal release, Cbl binds to the cytosolic chaperon MMACHC that is responsible for (i) flavin-dependent decyanation of [CN-Co3+]Cbl to [Co2+]Cbl; (ii) glutathione-dependent dealkylation of MeCbl and AdoCbl to [Co2+/1+]Cbl; and (iii) glutathione-dependent decyanation of CNCbl or reduction of HOCbl under anaerobic conditions. MMACHC shows a broad specificity for Cbl forms and supplies the Cbl2+ intermediate for synthesis of MeCbl and AdoCbl. Cobalamin chemistry, physiology, and biochemistry suggest that MeCbl and AdoCbl follow the same route of intracellular processing as CNCbl does. We conclude that supplementing MeCbl or AdoCbl is unlikely to be advantageous compared to CNCbl. On the other hand, there are obvious advantages of high parenteral doses (1–2 mg) of HOCbl in treating inborn errors of Cbl metabolism.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/mnfr.201500019

Cobalamin coenzyme forms are not likely to be superior to cyano- and hydroxyl-cobalamin in prevention or treatment of cobalamin deficiency

Adipocyte differentiation is a complex developmental process forming adipocytes from various precursor cells. The murine 3T3-L1 preadipocyte cell line has been most frequently used in the studies of adipocyte differentiation. Differentiation of 3T3-L1 preadipocytes includes a medium containing fetal bovine serum (FBS) with hormonal induction. In this study, we observed that differentiation medium containing adult bovine serum (ABS) instead of FBS did not support differentiation of preadipocytes. Impaired adipocyte differentiation was due to the presence of a serum protein factor in ABS that suppresses differentiation of preadipocytes. Using a proteomic analysis, alpha-2-macroglobulin and paraoxonase/arylesterase 1, which were previously shown to suppress differentiation of preadipocytes, were identified as anti-adipogenic proteins. Although their functional mechanisms have not yet been elucidated, the anti-adipogenic effects of these proteins are discussed. [BMB Reports 2013; 46(12): 582-587]

Jihyun Park

Papers

Identification of anti-adipogenic proteins in adult bovine serum suppressing 3T3-L1 preadipocyte differentiation.

Processing of glutathionylcobalamin by a bovine B12 trafficking chaperone bCblC involved in intracellular B12 metabolism.

Destabilization of a bovine B12 trafficking chaperone protein by oxidized form of glutathione

Identification of tetranectin as adipogenic serum protein.

Adipogenic function of mouse tetranectin and identification of its functional domain.