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Multicenter Study
. 2008 May 18;263(2):212-22.
doi: 10.1016/j.canlet.2008.01.006. Epub 2008 Feb 15.

Hepatitis B virus infection contributes to oxidative stress in a population exposed to aflatoxin B1 and high-risk for hepatocellular carcinoma

Affiliations
Multicenter Study

Hepatitis B virus infection contributes to oxidative stress in a population exposed to aflatoxin B1 and high-risk for hepatocellular carcinoma

Zhi-Ming Liu et al. Cancer Lett. .

Abstract

Biomarkers of hepatitis B virus (HBV) infection, aflatoxin B1 (AFB1) exposure and oxidative stress were detected in 71 hepatocellular carcinoma (HCC) patients and 694 controls from southern China. Plasma level of AFB1-albumin-adducts (AAA) and protein carbonyl content (PCC) were significantly higher in the 71 HCC cases than in any age/gender matched HBV sero-status groups (p<0.001). HCC patients positive for the p53-249 G-T mutation had a marginally higher level of PCC than those negative for the mutation (p=0.077). HBV infection had a prominent influence on the association between AFB1 exposure and oxidative stress biomarkers in the controls. Our study indicates a significant contribution from HBV infection to oxidative stress in a population with AFB1 exposure which might substantially increase risk for HCC in this region.

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Figures

Figure 1
Figure 1. Comparison of Protein Concentration among age and gender matched HCC and HBV sero-status groups (n=71 per group)
** Levels of TP, ALB and GLO in HCC patients were significantly lower than any HBV sero-status group (P<0.01). Only p values less than 0.1 are indicated. Null (null for all HBV markers), sAg(+) (HBsAg(+) regardless of sAb or cAb status), sAb(+) (sAg(-)sAb(+)cAb(-)), and cAb(+) (sAg(-)cAb(+)).
Figure 2
Figure 2. Comparison of Protein Adducts Levels among age and gender matched HCC and HBV sero-status groups (n=71 per group)
★ HCC patients had significantly higher levels of AAA and PCC than any HBV group of controls (P<0.001). Only p values less than 0.1 are indicated. Null (null for all HBV markers), sAg(+) (HBsAg(+) regardless of sAb or cAb status), sAb(+) (sAg(-)sAb(+)cAb(-)), and cAb(+) (sAg(-)cAb(+)).
Figure 3
Figure 3
Associations between plasma AAA and PCC (A), plasma AAA and urinary AFB1 (B), urinary AFB1 and 8-OHdG (C), urinary AFB1 and plasma PCC (D).
Figure 4
Figure 4. Comparison of Urinary AFB1 and 8-OHdG levels among HBV Sero-status groups in 290 adults from Nanning, China
Only p values less than 0.1 are indicated. Null (null for all HBV markers), sAg(+) (HBsAg(+) regardless of sAb or cAb status), sAb(+) (sAg(-)sAb(+)cAb(-)), and cAb(+) (sAg(-)cAb(+)).
Figure 5
Figure 5
Diagram of the association profile among biomarkers for oxidative stress, HBV infection and AFB1 exposure. Only significant associations are indicated. HBV status is specified when the associations are significant in sub-set(s) of HBV serology. Null (null for all HBV markers), sAg(+) (HBsAg(+) regardless of sAb or cAb status), sAb(+) (sAg(-)sAb(+)cAb(-)), and cAb(+) (sAg(-)cAb(+)). * Also significant between eAb(+) and eAb(-) among 87 sAg(-)cAb(+) subjects. ** Also significant between non-active HBV infection and HBV-free subjects.

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