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hair related research references ||
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melanin related research references
Neurotox Res. 2000 Feb;1(3):153-69.
Neurotoxicity due to o-quinones: neuromelanin formation and possible mechanisms for o-quinone detoxification.
Solano F, Hearing VJ, Garcia-Borron JC.
Department of Biochemistry and Molecular Biology B, School of Medicine, University of Murcia, Spain. psolancu.um.es
o-Quinones are easily formed by oxidation of physiologically relevant catechols. These reactions mainly occur in two specialized cells, catecholaminergic neurons and melanocytes. Both types of cells are related ontogenetically, as they arise from the neural crest during the developmental differentiation. o-Quinones are used to form melanin, a protective pigment formed by different mechanisms in melanocytes and catecholaminergic neurons. However, the reactivity of these quinones makes their presence in the cytosol dangerous for the cell survival and these compounds have been proposed as degenerative and apoptotic agents. Thus, melanin-producing cells show several potential mechanisms to protect themselves against the noxious effects of o-quinones. In melanocytes, the most effective autoprotecting mechanisms are the existence of malanosomes as a confined site for melano-synthesis and the action of tyrosinase-related protein 2 (TRP2) to drive L-dopachrome to 5,6-dihydroxyindole-2-carboxylic acid minimizing the formation of 5,6-dihydroxyindole. In catecholaminergic neurons, recent data suggest that glutathione transferase (GST M2-2 isoenzyme) and macrophage migration inhibitory factor (MIF) are very effective in preventing long-lived formation of dopaminechrome and noradrenochrome, although the detoxification reactions are different (conjugation to GSH or isomerization respectively). These mechanisms are less efficient for adrenochrome, although MIF and GST M1-1 could also catalyze similar reactions using this compound as substrate. In addition, the formation of adrenochrome is still under discussion, and adrenolutin formation could contribute to deactivate its harmful effects. The contribution of D-dopachrome tautomerase to these mechanisms is yet unknown, although in contrast to MIF, that enzyme does not recognize catecholaminechromes as substrates. Diaphorase could also be protective against quinones, since this enzyme catalyzes their bielectronic reduction back to catechols, thus preventing the formation of chrome species. This activity has been described in melanocytes and neurons, so that its contribution should be further investigated. In contrast to diaphorase, cytochrome P450 reductase should not be considered a protective enzyme, since its monoelectronic reduction of quinones leads to formation of semiquinones, that is, even more noxious than the quinones.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12835099&dopt=Abstract [PubMed]
columbia.edu
Dopamine-quinone is synthesized by oxidation of the catechol ring of dopamine. If this occurs within the neuronal cytosol, the quinone may react with cytosolic components, particularly with cysteine residues. In contrast, if quinone is produced within neuronal lysosomes it may provide the fundamental building block for neuromelanin. Since the population of neurons that die in Parkinson's disease are those that display obvious intralysosomal neuromelanin and since cytosolic dopamine-dependent oxyradical formation may underlie methamphetamine toxicity and other specific forms of neurodegeneration in dopaminergic neurons, it is important to elucidate the pathways leading to production of dopamine-quinone. Here we review pathways by which intracellular catechols may be oxidized to quinones, either enzymatically or via reduction of ferric iron or other metals. These metabolites can be adduced by cysteine, could underlie aberrant metabolism and ubiquitination pathways, may induce Lewy body formation, and mediate the synthesis of hydroxyl radical and oxyradical species. Finally, we suggest that by accumulating excess cytosolic catecholamine, neuromelanin synthesis may safely sequester quinones that would otherwise be produced in the neuronal cytosol.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12835101&dopt=Abstract [PubMed]
Neurotox Res. 1999 Dec;1(2):141-7.
Model neuromelanins as antioxidative agents during lipid peroxidation.
Wilczok T, Stepien K, Dzierzega-Lecznar A, Zajdel A, Wilczok A.
Department of Molecular Biology, Biochemistry and Biopharmacy, Medical University of Silesia, Narcyzow 1, 41-200 Sosnowiec, Poland.
The oxidative pathway of dopamine metabolism in the human brain leads to formation and accumulation of neuromelanin in the cytoplasm of most nigrostriatal dopaminergic neurons. The physiological significance of neuromelanin and its contribution to the neurodegenerative processes underlying Parkinson's disease are still controversial. The effect of model neuromelanins on Fe(II)/ascorbate-induced lipid peroxidation in micelles of linoleic acid and in lecithin liposomes was determined. Synthetic neuromelanins were obtained from dopamine (DA), 5-S-cysteinyldopamine (CysDA) or from equimolar mixture of these precursors. Thiobarbituric acid test and reverse-phase HPLC, used for measurements of primary and secondary oxidation products, showed that all melanins tested significantly suppressed peroxidation of both, linoleic acid and liposomal lecithin. The inhibitory effect of CysDA-melanin was lower than of DA/CysDA-melanin and DA-melanin. All the melanins were able to reduce linoleic acid hydroperoxides to their stable hydroxy derivatives. The results obtained suggest that neuromelanin can act as natural antioxidant. The fatty acid hydroperoxide-reducing ability demonstrated for the model neuromelanins appears to be involved in the mechanism of antioxidative activity of neuromelanin.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12835109&dopt=Abstract [PubMed]
Like developmental biology of any part of our body, hair growth is a complicated process. Hence the homework for
modern science to yet unravel the process and mechanism to a completion. There exist a number of traditional and alternative therapeutic methods that include drugs, surgery, suppelements, and even snake oils that have been developed and used for those who lose hair.
No understanding, and there is no solution. Of course, none of these approaches are perfect for all hair loss problems, especially due to the heterogeneity of the causes underlying hair losses. Most of chemical drugs and hair transplantation surgeries are accompanied by undesirable side effects.
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