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石化工人基因多形性與DNA損傷相關之研究(2/2)
Date Issued
2002-07-31
Date
2002-07-31
Author(s)
DOI
902320B002125
Abstract
Vinyl chloride monomer (VCM) has
been recognized as a human carcinogen.
A large number of epidemiology studies
have suggested an association between
VCM exposure and liver cancer. DNA
damage is a critical step in the
carcinogenesis. DNA adducts and
cytogenetic methods including
chromosome aberrations, sister chromatid
exchange frequency and micronuclei have
been used to assess DNA damage in VCM
exposure workers. However, the
dose-response relationship between the
low dose exposure to VCM and DNA
damage remains unclear. In this study, we
used sister chromatid exchange (SCE )
Comet assay and urinary 8-OHdG to
assess the VCM-induced DNA damage,
and to evaluate the association between
gene polymorphism and VCM-related
damage.
Analysis showed that SCE was
higher in high exposure group than in
control group ( 8.0 vs 7.2, p<0.05). Low
exposure group also had higher SCE than
control, but this did not reach a
significance. SCE also increased with age
and smoking. Further, XRCC1 Gln-Gln,
CYP2E1 C2C2 and ALDH2 1-2/2-2 had
higher SCE than their counterpart. When
susceptible genotypes were considered
together, those with at least 2 susceptible
genotypes had higher SCE in low
exposure group. Similar trend was also
observed in high exposure group,
although not significant. There is no
association between genotypes and SCE
in controls.
Urinary 8-OHdG was not associated
with VCM exposure, age and smoking.
However, 8-OHdG was significantly
associated with Hepatitis B and C
injection, and alcohol drinking. Interesting,
plasma vitamin A levels were inversely
associated with urinary 8-OHdg. Urinary
TdGA was found to be associated with air
VCM levels. However, there was no
relationship between the urinary TdGA
levels and DNA SSB.
Our results indicated that SCE is
more sensitive than urinary 8-OHdG and
comet assay in detecting VCM-induced
genotoxicity.Furthermore, metabolic and
DNA repair genotypes may modify DNA
damage caused by VCM.
been recognized as a human carcinogen.
A large number of epidemiology studies
have suggested an association between
VCM exposure and liver cancer. DNA
damage is a critical step in the
carcinogenesis. DNA adducts and
cytogenetic methods including
chromosome aberrations, sister chromatid
exchange frequency and micronuclei have
been used to assess DNA damage in VCM
exposure workers. However, the
dose-response relationship between the
low dose exposure to VCM and DNA
damage remains unclear. In this study, we
used sister chromatid exchange (SCE )
Comet assay and urinary 8-OHdG to
assess the VCM-induced DNA damage,
and to evaluate the association between
gene polymorphism and VCM-related
damage.
Analysis showed that SCE was
higher in high exposure group than in
control group ( 8.0 vs 7.2, p<0.05). Low
exposure group also had higher SCE than
control, but this did not reach a
significance. SCE also increased with age
and smoking. Further, XRCC1 Gln-Gln,
CYP2E1 C2C2 and ALDH2 1-2/2-2 had
higher SCE than their counterpart. When
susceptible genotypes were considered
together, those with at least 2 susceptible
genotypes had higher SCE in low
exposure group. Similar trend was also
observed in high exposure group,
although not significant. There is no
association between genotypes and SCE
in controls.
Urinary 8-OHdG was not associated
with VCM exposure, age and smoking.
However, 8-OHdG was significantly
associated with Hepatitis B and C
injection, and alcohol drinking. Interesting,
plasma vitamin A levels were inversely
associated with urinary 8-OHdg. Urinary
TdGA was found to be associated with air
VCM levels. However, there was no
relationship between the urinary TdGA
levels and DNA SSB.
Our results indicated that SCE is
more sensitive than urinary 8-OHdG and
comet assay in detecting VCM-induced
genotoxicity.Furthermore, metabolic and
DNA repair genotypes may modify DNA
damage caused by VCM.
Subjects
Polyvinyl chloride
comet assay
DNA single-strand breaks
thiodiglycolic acid (TdGA)
SDGs
Publisher
臺北市:國立臺灣大學公共衛生學院職業醫學與工業衛生研究所
Coverage
計畫年度:90;起迄日期:2001-08-01/2002-07-31
Type
report
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