Background: Acrylamide (AA), a known neurotoxin, has been considered to be a probable human carcinogen.
The discovery of AA in many common foods in 2002 has caused worldwide attention and led to numerous
research efforts on the metabolism of AA.
Methods: By collecting research literatures related to metabolism of AA, the present review not only summarized
the major metabolic pathways and enzymes of AA, but also compared the interindividual and the interspecies differences
of AA metabolism among humans, rats and mice. Moreover, the application of the metabolites as biomarkers
for the AA exposure assessment in human population was also discussed.
Results: The interindividual differences of AA metabolism may be attributed to the activity and/or genetic polymorphisms of metabolic
enzymes in individuals with different gender, age, smoking and alcohol status. Moreover, the metabolism of AA in humans may be more
prone to the phase II conjugation with glutathione (GSH) than the phase I conversion of AA to glycidamide (GA) when compared with
rats and mice. Both the hemoglobin (Hb) adducts and urinary mercapturic acid (MA) metabolites have been successfully used as biomarkers
for the risk assessment of AA and new metabolic biomarkers are being developed.
Conclusion: The genotoxic risk from AA may be determined by the balance between the phase I P450 2E1 (CYP2E1)-dependent toxification
pathway to form genotoxic GA and the phase II GSH-conjugated detoxification pathway to form MA metabolite. Understanding
the metabolism of AA in the body is helpful for developing effective intervention strategies to mitigate its toxicity.