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Glutathione-S-transferases genes-promising predictors of hepatic dysfunction

One of the most commonly known genes involved in chronic diffuse liver diseases pathogenesis are genes that encodes the synthesis of glutathione-S-transferase (GST), known as the second phase enzyme detoxification system that protects against endogenous oxidative stress and exogenous toxins, through...

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Autores principales: Prysyazhnyuk, Vasyl, Sydorchuk, Larysa, Sydorchuk, Ruslan, Prysiazhniuk, Iryna, Bobkovych, Kateryna, Buzdugan, Inna, Dzuryak, Valentina, Prysyazhnyuk, Petro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Baishideng Publishing Group Inc 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8239493/
https://www.ncbi.nlm.nih.gov/pubmed/34239698
http://dx.doi.org/10.4254/wjh.v13.i6.620
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author Prysyazhnyuk, Vasyl
Sydorchuk, Larysa
Sydorchuk, Ruslan
Prysiazhniuk, Iryna
Bobkovych, Kateryna
Buzdugan, Inna
Dzuryak, Valentina
Prysyazhnyuk, Petro
author_facet Prysyazhnyuk, Vasyl
Sydorchuk, Larysa
Sydorchuk, Ruslan
Prysiazhniuk, Iryna
Bobkovych, Kateryna
Buzdugan, Inna
Dzuryak, Valentina
Prysyazhnyuk, Petro
author_sort Prysyazhnyuk, Vasyl
collection PubMed
description One of the most commonly known genes involved in chronic diffuse liver diseases pathogenesis are genes that encodes the synthesis of glutathione-S-transferase (GST), known as the second phase enzyme detoxification system that protects against endogenous oxidative stress and exogenous toxins, through catalisation of glutathione sulfuric groups conjugation and decontamination of lipid and deoxyribonucleic acid oxidation products. The group of GST enzymes consists of cytosolic, mitochondrial and microsomal fractions. Recently, eight classes of soluble cytoplasmic isoforms of GST enzymes are widely known: α-, ζ-, θ-, κ-, μ-, π-, σ-, and ω-. The GSTs gene family in the Human Gene Nomenclature Committee, online database recorded over 20 functional genes. The level of GSTs expression is considered to be a crucial factor in determining the sensitivity of cells to a broad spectrum of toxins. Nevertheless, human GSTs genes have multiple and frequent polymorphisms that include the complete absence of the GSTM1 or the GSTT1 gene. Current review supports the position that genetic polymorphism of GST genes is involved in the pathogenesis of various liver diseases, particularly non-alcoholic fatty liver disease, hepatitis and liver cirrhosis of different etiology and hepatocellular carcinoma. Certain GST allelic variants were proven to be associated with susceptibility to hepatological pathology, and correlations with the natural course of the diseases were subsequently postulated.
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spelling pubmed-82394932021-07-07 Glutathione-S-transferases genes-promising predictors of hepatic dysfunction Prysyazhnyuk, Vasyl Sydorchuk, Larysa Sydorchuk, Ruslan Prysiazhniuk, Iryna Bobkovych, Kateryna Buzdugan, Inna Dzuryak, Valentina Prysyazhnyuk, Petro World J Hepatol Review One of the most commonly known genes involved in chronic diffuse liver diseases pathogenesis are genes that encodes the synthesis of glutathione-S-transferase (GST), known as the second phase enzyme detoxification system that protects against endogenous oxidative stress and exogenous toxins, through catalisation of glutathione sulfuric groups conjugation and decontamination of lipid and deoxyribonucleic acid oxidation products. The group of GST enzymes consists of cytosolic, mitochondrial and microsomal fractions. Recently, eight classes of soluble cytoplasmic isoforms of GST enzymes are widely known: α-, ζ-, θ-, κ-, μ-, π-, σ-, and ω-. The GSTs gene family in the Human Gene Nomenclature Committee, online database recorded over 20 functional genes. The level of GSTs expression is considered to be a crucial factor in determining the sensitivity of cells to a broad spectrum of toxins. Nevertheless, human GSTs genes have multiple and frequent polymorphisms that include the complete absence of the GSTM1 or the GSTT1 gene. Current review supports the position that genetic polymorphism of GST genes is involved in the pathogenesis of various liver diseases, particularly non-alcoholic fatty liver disease, hepatitis and liver cirrhosis of different etiology and hepatocellular carcinoma. Certain GST allelic variants were proven to be associated with susceptibility to hepatological pathology, and correlations with the natural course of the diseases were subsequently postulated. Baishideng Publishing Group Inc 2021-06-27 2021-06-27 /pmc/articles/PMC8239493/ /pubmed/34239698 http://dx.doi.org/10.4254/wjh.v13.i6.620 Text en ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved. https://creativecommons.org/licenses/by-nc/4.0/This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.
spellingShingle Review
Prysyazhnyuk, Vasyl
Sydorchuk, Larysa
Sydorchuk, Ruslan
Prysiazhniuk, Iryna
Bobkovych, Kateryna
Buzdugan, Inna
Dzuryak, Valentina
Prysyazhnyuk, Petro
Glutathione-S-transferases genes-promising predictors of hepatic dysfunction
title Glutathione-S-transferases genes-promising predictors of hepatic dysfunction
title_full Glutathione-S-transferases genes-promising predictors of hepatic dysfunction
title_fullStr Glutathione-S-transferases genes-promising predictors of hepatic dysfunction
title_full_unstemmed Glutathione-S-transferases genes-promising predictors of hepatic dysfunction
title_short Glutathione-S-transferases genes-promising predictors of hepatic dysfunction
title_sort glutathione-s-transferases genes-promising predictors of hepatic dysfunction
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8239493/
https://www.ncbi.nlm.nih.gov/pubmed/34239698
http://dx.doi.org/10.4254/wjh.v13.i6.620
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