<a><b>OBJECTIVE:
</b></a>Acrylamide
exposure from daily-consumed food has raised global concern.<b> </b>We aimed to assess the exposure-response
relationships of internal acrylamide exposure with oxidative DNA damage, lipid peroxidation
and fasting plasma glucose (FPG) alteration, and investigate the mediating role
of oxidative DNA damage and lipid peroxidation in the association of internal acrylamide
exposure with FPG.
<p><b>RESEARCH
DESIGN AND METHODS:</b>
FPG and urinary biomarkers of oxidative DNA damage (8-hydroxy-deoxy-guanosine, 8-OHdG),
lipid peroxidation (8-iso-prostaglandin-F2α, 8-iso-PGF2α) and acrylamide
exposure (N-acetyl-S-(2-carbamoylethyl)-L-cysteine, AAMA; N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine,
GAMA) were measured for 3,270 general adults from the Wuhan-Zhuhai cohort. The
associations of urinary acrylamide metabolites with 8-OHdG, 8-iso-PGF2α and FPG
were assessed by linear mixed models. The mediating roles of 8-OHdG and 8-iso-PGF2α
were evaluated by mediation analysis.</p>
<p><b>RESULTS:</b> We found
significant linear positive dose-response relationships of urinary acrylamide metabolites
with 8-OHdG, 8-iso-PGF2α and FPG (except GAMA with FPG), and 8-iso-PGF2α with
FPG. Each 1-unit increase in log-transformed level of AAMA, ΣUAAM (AAMA+GAMA)
or 8-iso-PGF2α was associated with a 0.17-, 0.15- or 0.23-mmol/L increase in
FPG, respectively (<i>P </i>or/and<i> P trend</i><0.05). Each 1% increase in AAMA,
GAMA or ΣUAAM was associated with a 0.19%, 0.27% or 0.22% increase in 8-OHdG,
respectively, and a 0.40%, 0.48% or 0.44% increase in 8-iso-PGF2α, respectively
(<i>P </i>and<i> P trend</i><0.05). Increased 8-iso-PGF2α rather than 8-OHdG
significantly mediated 64.29% and 76.92% of the AAMA and ΣUAAM associated-FPG
increases, respectively.</p>
<p><b>CONCLUSIONS:</b> Exposure of
general adult population to acrylamide was associated with FPG elevation, oxidative
DNA damage and lipid peroxidation, which in turn partly mediated
acrylamide-associated FPG elevation.<b></b></p>
Ameliorative effect of supplementation with l-glutamine on oxidative stress, DNA damage, cell viability and hepatotoxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat hepatocyte cultures