Brief Article
Copyright ©2012 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Sep 28, 2012; 18(36): 5084-5089
Published online Sep 28, 2012. doi: 10.3748/wjg.v18.i36.5084
Decreased mitochondrial deoxyribonucleic acid and increased oxidative damage in chronic hepatitis C
Hsu-Heng Yen, Kai-Lun Shih, Ta-Tsung Lin, Wei-Wen Su, Maw-Soan Soon, Chin-San Liu
Hsu-Heng Yen, Kai-Lun Shih, Wei-Wen Su, Maw-Soan Soon, Department of Gastroenterology and Hepatology, Changhua Christian Hospital, Changhua 500, Taiwan, China
Ta-Tsung Lin, Chin-San Liu, Vascular and Genomic Research Center, Changhua Christian Hospital, Changhua 500, Taiwan, China
Author contributions: Yen HH and Liu CS contributed equally to this manuscript; Yen HH and Liu CS designed the study and are equally responsible for the drafting, reading and final approval of the manuscript; Shih KL, Su WW and Soon MS participated in the study design, drafting, reading and final approval of the manuscript; Lin TT and Liu CS performed the laboratory study and participated in the data analysis and final approval of the manuscript.
Supported by Changhua Christian Hospital, 99-CCH-IPR-12
Correspondence to: Hsu-Heng Yen, MD, Department of Gastroenterology and Hepatology, Changhua Christian Hospital, 135 Nanhsiao Street, Changhua 500, Taiwan, China. 91646@cch.org.tw
Telephone: +886-4-7238595 Fax: +886-4-7228289
Received: March 10, 2012
Revised: May 9, 2012
Accepted: May 13, 2012
Published online: September 28, 2012
Abstract

AIM: To determine whether alteration of the mitochondria DNA (mtDNA) copy number and its oxidative damage index (mtDNA∆CT) can be detected by analysis of peripheral blood cells in hepatitis C virus (HCV)-infected patients.

METHODS: This study enrolled two groups of patients aged 40-60 years: a control group and an HCV-infected group in Department of Gastroenterology and Hepatology in Changhua Christian Hospital. Patients with co-infection with hepatitis B virus or human immunodeficiency virus, autoimmune disease, malignant neoplasia, pregnancy, thyroid disease, or alcohol consumption > 40 g/d were excluded. HCV-infected patients who met the following criteria were included: (1) positive HCV antibodies for > 6 mo; (2) alanine aminotransferase (ALT) levels more than twice the upper limit of normal on at least two occasions during the past 6 mo; and (3) histological fibrosis stage higher than F1. The mtDNA copy number and oxidative damage index of HCV mtDNA (mtDNA∆CT) were measured in peripheral blood leukocytes. The association between mtDNA copy number and mtDNA∆CT was further analyzed using clinical data.

RESULTS: Forty-seven normal controls (male/female: 26/21, mean age 50.51 ± 6.15 years) and 132 HCV-infected patients (male/female: 76/61, mean age 51.65 ± 5.50 years) were included in the study. The genotypes of HCV-infected patients include type 1a (n = 3), type 1b (n = 83), type 2a (n = 32), and type 2b (n = 14). Liver fibrosis stages were distributed as follows: F1/F2/F3/F4 = 1/61/45/25 and activity scores were A0/A1/A2/A3 = 7/45/55/25. There were no age or gender differences between the two groups. HCV-infected patients had higher hepatitis activity (aspartate transaminase levels 108.77 ± 60.73 vs 23.19 ± 5.47, P < 0.01; ALT levels 168.69 ± 93.12 vs 23.15 ± 9.45, P < 0.01) and lower platelet count (170.40 ± 58.00 vs 251.24 ± 63.42, P < 0.01) than controls. The mtDNA copy number was lower in HCV-infected patients than in controls (173.49 vs 247.93, P < 0.05). The mtDNA∆CT was higher in HCV-infected patients than in controls (2.92 vs 0.64, P < 0.05). To clarify the clinical significance of these results in HCV-infected patients, their association with different clinical parameters among HCV-infected patients was analyzed. A negative association was found between mtDNA copy number and elevated aspartate transaminase levels (r = -0.17, P < 0.05). Changes in mtDNA copy number were not associated with HCV RNA levels, HCV genotypes, liver fibrosis severity, or inflammatory activity in the liver biopsy specimen. However, a correlation was observed between mtDNA∆CT and platelet count (r = -0.22, P < 0.01), HCV RNA level (r = 0.36, P < 0.01), and hepatitis activity (r = 0.20, P = 0.02). However, no difference in the change in mtDNA∆CT was observed between different fibrosis stages or HCV genotypes.

CONCLUSION: Oxidative stress and mtDNA damage are detectable in patient’s peripheral leukocytes. Increased leukocyte mtDNA∆CT correlates with higher HCV viremia, increased hepatitis activity, and lower platelet count.

Keywords: Hepatitis C; Mitochondria; Oxidative stress; Mitochondrial DNA; Biomarker