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Value of the 8-oxodG/dG ratio in chronic liver inflammation of patients with hepatocellular carcinoma

The aim of this study was to examine the role of oxidative DNA damage in chronic liver inflammation in the evolution of hepatocellular carcinoma. The accumulated data demonstrated that oxidative DNA damage and chronic liver inflammation are involved in the transformation of normal hepatocytes and th...

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Autores principales: Li, Pengcheng, Ramm, Grant A, Macdonald, Graeme A
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4761657/
https://www.ncbi.nlm.nih.gov/pubmed/26890046
http://dx.doi.org/10.1016/j.redox.2016.02.003
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author Li, Pengcheng
Ramm, Grant A
Macdonald, Graeme A
author_facet Li, Pengcheng
Ramm, Grant A
Macdonald, Graeme A
author_sort Li, Pengcheng
collection PubMed
description The aim of this study was to examine the role of oxidative DNA damage in chronic liver inflammation in the evolution of hepatocellular carcinoma. The accumulated data demonstrated that oxidative DNA damage and chronic liver inflammation are involved in the transformation of normal hepatocytes and their evolution towards hepatocellular carcinoma. However, the levels of 8-oxy-2′-deoxy-guanosine (8-oxodG), a biomarker of oxidative DNA damage, were overestimated and underestimated in previous reports due to various technical limitations. The current techniques are not suitable to analyze the 8-oxodG levels in the non-malignant liver tissues and tumors of hepatocellular carcinoma patients unless they are modified. Therefore, in this study, the protocols for extraction and hydrolysis of DNA were optimized using 54 samples from hepatocellular carcinoma patients with various risk factors, and the 8-oxodG and 2′-deoxyguanosine (dG) levels were measured. The patients enrolled in the study include 23 from The Princess Alexandra Hospital and The Royal Brisbane and Women's Hospitals, Brisbane, Australia, and 31 from South Africa. This study revealed that the 8-oxodG/dG ratios tended to be higher in most non-malignant liver tissues compared to hepatocellular carcinoma tissue (p=0.2887). It also appeared that the ratio was higher in non-malignant liver tissue from Southern African patients (p=0.0479), but there was no difference in the 8-oxodG/dG ratios between non-malignant liver tissues and tumors of Australian hepatocellular carcinoma patients (p=0.7722). Additionally, this study also revealed a trend for a higher 8-oxodG/dG ratio in non-malignant liver tissues compared to tumoural tissues of patients with HBV. Significant differences were not observed in the 8-oxodG/dG ratios between non-cirrhotic and cirrhotic non-malignant liver tissues.
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spelling pubmed-47616572016-03-07 Value of the 8-oxodG/dG ratio in chronic liver inflammation of patients with hepatocellular carcinoma Li, Pengcheng Ramm, Grant A Macdonald, Graeme A Redox Biol Research Paper The aim of this study was to examine the role of oxidative DNA damage in chronic liver inflammation in the evolution of hepatocellular carcinoma. The accumulated data demonstrated that oxidative DNA damage and chronic liver inflammation are involved in the transformation of normal hepatocytes and their evolution towards hepatocellular carcinoma. However, the levels of 8-oxy-2′-deoxy-guanosine (8-oxodG), a biomarker of oxidative DNA damage, were overestimated and underestimated in previous reports due to various technical limitations. The current techniques are not suitable to analyze the 8-oxodG levels in the non-malignant liver tissues and tumors of hepatocellular carcinoma patients unless they are modified. Therefore, in this study, the protocols for extraction and hydrolysis of DNA were optimized using 54 samples from hepatocellular carcinoma patients with various risk factors, and the 8-oxodG and 2′-deoxyguanosine (dG) levels were measured. The patients enrolled in the study include 23 from The Princess Alexandra Hospital and The Royal Brisbane and Women's Hospitals, Brisbane, Australia, and 31 from South Africa. This study revealed that the 8-oxodG/dG ratios tended to be higher in most non-malignant liver tissues compared to hepatocellular carcinoma tissue (p=0.2887). It also appeared that the ratio was higher in non-malignant liver tissue from Southern African patients (p=0.0479), but there was no difference in the 8-oxodG/dG ratios between non-malignant liver tissues and tumors of Australian hepatocellular carcinoma patients (p=0.7722). Additionally, this study also revealed a trend for a higher 8-oxodG/dG ratio in non-malignant liver tissues compared to tumoural tissues of patients with HBV. Significant differences were not observed in the 8-oxodG/dG ratios between non-cirrhotic and cirrhotic non-malignant liver tissues. Elsevier 2016-02-09 /pmc/articles/PMC4761657/ /pubmed/26890046 http://dx.doi.org/10.1016/j.redox.2016.02.003 Text en © 2016 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Research Paper
Li, Pengcheng
Ramm, Grant A
Macdonald, Graeme A
Value of the 8-oxodG/dG ratio in chronic liver inflammation of patients with hepatocellular carcinoma
title Value of the 8-oxodG/dG ratio in chronic liver inflammation of patients with hepatocellular carcinoma
title_full Value of the 8-oxodG/dG ratio in chronic liver inflammation of patients with hepatocellular carcinoma
title_fullStr Value of the 8-oxodG/dG ratio in chronic liver inflammation of patients with hepatocellular carcinoma
title_full_unstemmed Value of the 8-oxodG/dG ratio in chronic liver inflammation of patients with hepatocellular carcinoma
title_short Value of the 8-oxodG/dG ratio in chronic liver inflammation of patients with hepatocellular carcinoma
title_sort value of the 8-oxodg/dg ratio in chronic liver inflammation of patients with hepatocellular carcinoma
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4761657/
https://www.ncbi.nlm.nih.gov/pubmed/26890046
http://dx.doi.org/10.1016/j.redox.2016.02.003
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