RESUMEN
Introduction: The extensive occurrence of acrylamide in heat processing foods has continuously raised a potential health risk for the public in the recent 20 years. Machine learning emerging as a robust computational tool has been highlighted for predicting the generation and control of processing contaminants. Methods: We used the least squares support vector regression (LS-SVR) as a machine learning approach to investigate the effects of flavone carbon and oxygen glycosides on acrylamide formation under a low moisture condition. Acrylamide was prepared through oven heating via a potato-based model with equimolar doses of asparagine and reducing sugars. Results: Both inhibition and promotion effects were observed when the addition levels of flavonoids ranged 1-10,000 µmol/L. The formation of acrylamide could be effectively mitigated (37.6%-55.7%) when each kind of flavone carbon or oxygen glycoside (100 µmol/L) was added. The correlations between acrylamide content and trolox-equivalent antioxidant capacity (TEAC) within inhibitory range (R 2 = 0.85) had an advantage over that within promotion range (R 2 = 0.87) through multiple linear regression. Discussion: Taking ΔTEAC as a variable, a LS-SVR model was optimized as a predictive tool to estimate acrylamide content (R 2 inhibition = 0.87 and R 2 promotion = 0.91), which is pertinent for predicting the formation and elimination of acrylamide in the presence of exogenous antioxidants including flavonoids.
RESUMEN
Acrylamide (AA) occurs in both various environmental and dietary sources and has raised widespread concern as a probable carcinogen. Glycidamide (GA) is the main genotoxic metabolite through P450 2E1 (CYP2E1). In the present study, we investigated the protective effect of (-)-epigallocatechin gallate (EGCG) and (-)-epicatechin (EC) against AA- and GA-induced hepatotoxicity in HepG2 cells. The results demonstrated that EC and EGCG inhibited AA- and GA-induced cytotoxicity and mitochondria-mediated cellular apoptosis. Moreover, exposure to AA (100 µg/mL) and GA (50 µg/mL) caused cell cycle arrest and DNA damage, while EC and EGCG ranging from 12.5 to 50 µg/mL rescued cell cycle arrest and inhibited DNA damage. Furthermore, EC and EGCG down-regulated pro-apoptotic protein Bax and Caspase 3 after a 24-h treatment in HepG2 cells exposed to AA (100 µg/mL) or GA (50 µg/mL). Also, the intervention with EC or EGCG up-regulated the expression of DNA repair related protein PARP and down-regulated the expression of Cleaved-PARP. Besides, EC exerted better protective effect than EGCG against AA- and GA-induced cytotoxicity in HepG2 cells. Altogether, EC and EGCG were effective in protecting AA- and GA-induced hepatotoxicity via rescuing cellular apoptosis and DNA damage, as well as promoting cell cycle progression in HepG2 cells.