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Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations

Vitamin B(12) deficiency causes significant changes in cellular metabolism leading to various clinical symptoms, such as hematological, psychiatric, and neurological disorders. We hypothesize that skin pigmentation disorders may be a diagnostically important manifestation of vitamin B(12) deficiency...

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Autores principales: Rzepka, Zuzanna, Respondek, Michalina, Rok, Jakub, Beberok, Artur, ó Proinsias, Keith, Gryko, Dorota, Wrześniok, Dorota
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163934/
https://www.ncbi.nlm.nih.gov/pubmed/30235895
http://dx.doi.org/10.3390/ijms19092845
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author Rzepka, Zuzanna
Respondek, Michalina
Rok, Jakub
Beberok, Artur
ó Proinsias, Keith
Gryko, Dorota
Wrześniok, Dorota
author_facet Rzepka, Zuzanna
Respondek, Michalina
Rok, Jakub
Beberok, Artur
ó Proinsias, Keith
Gryko, Dorota
Wrześniok, Dorota
author_sort Rzepka, Zuzanna
collection PubMed
description Vitamin B(12) deficiency causes significant changes in cellular metabolism leading to various clinical symptoms, such as hematological, psychiatric, and neurological disorders. We hypothesize that skin pigmentation disorders may be a diagnostically important manifestation of vitamin B(12) deficiency, however the cellular and molecular mechanisms underlying these effects remain unknown. The aim of this study was to examine the effect of vitamin B(12) deficiency on melanocytes homeostasis. Hypocobalaminemia in vitro model was developed by treating epidermal melanocytes with synthesized vitamin B(12) antagonist—hydroxycobalamin(c-lactam). The cells were examined using immunoenzymatic, spectrophotometric, and fluorimetric assays as well as image cytometry. Significant melanogenesis stimulation—the increase of relative melanin content and tyrosinase activity up to 131% and 135%, respectively—has been indicated. Cobalamin-deficient cells displayed the elevation (by 120%) in reactive oxygen species level. Moreover, the redox status imbalance was stated. The study provided a scientific evidence for melanocytes homeostasis disturbance under hypocobalaminemia, thus indicating a significant element of the hyperpigmentation mechanism due to vitamin B(12) deficiency. Furthermore, the implication between pigmentary and hematological and/or neuropsychiatric symptoms in cobalamin-deficient patients may be an important issue.
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spelling pubmed-61639342018-10-10 Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations Rzepka, Zuzanna Respondek, Michalina Rok, Jakub Beberok, Artur ó Proinsias, Keith Gryko, Dorota Wrześniok, Dorota Int J Mol Sci Article Vitamin B(12) deficiency causes significant changes in cellular metabolism leading to various clinical symptoms, such as hematological, psychiatric, and neurological disorders. We hypothesize that skin pigmentation disorders may be a diagnostically important manifestation of vitamin B(12) deficiency, however the cellular and molecular mechanisms underlying these effects remain unknown. The aim of this study was to examine the effect of vitamin B(12) deficiency on melanocytes homeostasis. Hypocobalaminemia in vitro model was developed by treating epidermal melanocytes with synthesized vitamin B(12) antagonist—hydroxycobalamin(c-lactam). The cells were examined using immunoenzymatic, spectrophotometric, and fluorimetric assays as well as image cytometry. Significant melanogenesis stimulation—the increase of relative melanin content and tyrosinase activity up to 131% and 135%, respectively—has been indicated. Cobalamin-deficient cells displayed the elevation (by 120%) in reactive oxygen species level. Moreover, the redox status imbalance was stated. The study provided a scientific evidence for melanocytes homeostasis disturbance under hypocobalaminemia, thus indicating a significant element of the hyperpigmentation mechanism due to vitamin B(12) deficiency. Furthermore, the implication between pigmentary and hematological and/or neuropsychiatric symptoms in cobalamin-deficient patients may be an important issue. MDPI 2018-09-19 /pmc/articles/PMC6163934/ /pubmed/30235895 http://dx.doi.org/10.3390/ijms19092845 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Rzepka, Zuzanna
Respondek, Michalina
Rok, Jakub
Beberok, Artur
ó Proinsias, Keith
Gryko, Dorota
Wrześniok, Dorota
Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations
title Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations
title_full Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations
title_fullStr Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations
title_full_unstemmed Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations
title_short Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations
title_sort vitamin b(12) deficiency induces imbalance in melanocytes homeostasis—a cellular basis of hypocobalaminemia pigmentary manifestations
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163934/
https://www.ncbi.nlm.nih.gov/pubmed/30235895
http://dx.doi.org/10.3390/ijms19092845
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