No abstract

Acrylamide is widely found in various types of fried foods and cigarettes, and is not only neurotoxic and carcinogenic, but also has many potential toxic effects. The current assessment of acrylamide intake through dietary questionnaires is confounded by a variety of factors, which poses limitations to safety assessment. In this review, we focus on the levels of AAMA, the urinary metabolite of acrylamide in humans, and its association with other diseases, and discuss the current research gaps in AAMA and the future needs. We reviewed a total of 25 studies from eight countries. In the general population, urinary AAMA levels were higher in smokers than in nonsmokers, and higher in children than in adults; the highest levels of AAMA were found in the population from Spain compared with the general population from other countries. In addition, AAMA is associated with several diseases, especially cardiovascular system diseases. Therefore, AAMA, as a biomarker of internal human exposure, can re ect acrylamide intake in the short term, which is of great signi cance for tracing acrylamide-containing foods and setting the allowable intake of acrylamide in foods.

Recent studies have shown that phosphoglycerate kinase 1 (PGK1) may improve neurodegeneration. However, the role of PGK1 in acrylamide(ACR)-induced neuronal damage is not yet clear. In this study, SD rats were treated with 6 mg/kg and 18 mg/kg of ACR, and PC12 cells were treated with 1.25 mM and 2.5 mM of ACR, and PC12 cells were transfected with PGK1 siRNA. Behavioral responses and histopathological changes in the rats were monitored, and transmission electron microscopy was used to observe changes in neurons and internal organelles in the hippocampal tissues of the various groups. Western blot and RT-qPCR were used to detect changes in the expression of neuronal-related proteins BDNF, Syn1, Nrf2 signaling pathway-related proteins and PGK1 in the hippocampal tissues of the rats and PC12 cells. Immunohistochemistry and immunofluorescence were used to analyze PGK1 expression in the hippocampal tissues of the rats. The results showed that after ACR treatment, obvious hindlimb clasping effect was observed in rats, hippocampal tissue pathology occurred, neuronal boundaries became blurred, mitochondria swelled, and organelles became sparse. BDNF and Syn1 mRNA expression and protein levels decreased both in vivo and in vitro, while Nrf2 and PGK1 mRNA expression and protein levels increased both in vivo and in vitro. In PC12 cells, inhibition of PGK1 can alleviate cell damage, and increase the expression of BDNF and Syn1 while Nrf2 expression is suppressed. These results suggest that inhibiting the expression of PGK1 can protect nerve cell damage induced by ACR.

Acrylamide is widely found in various types of fried foods and cigarettes, and is not only neurotoxic and carcinogenic, but also has many potential toxic effects. The current assessment of acrylamide intake through dietary questionnaires is confounded by a variety of factors, which poses limitations to safety assessment. In this review, we focus on the levels of AAMA, the urinary metabolite of acrylamide in humans, and its association with other diseases, and discuss the current research gaps in AAMA and the future needs. We reviewed a total of 25 studies from eight countries. In the general population, urinary AAMA levels were higher in smokers than in nonsmokers, and higher in children than in adults; the highest levels of AAMA were found in the population from Spain compared with the general population from other countries. In addition, AAMA is associated with several diseases, especially cardiovascular system diseases. Therefore, AAMA, as a biomarker of internal human exposure, can reflect acrylamide intake in the short term, which is of great significance for tracing acrylamide-containing foods and setting the allowable intake of acrylamide in foods.