Effect of caffeine on acrylamide-induced cellular hepatotoxicity

Abstract Objectives This study aims to determine the effects of caffeine on protein oxidation and endoplasmic reticulum (ER) stress in acrylamide (AA)-induced cellular hepatotoxicity. Methods First, HepG2 cells were incubated with 10 1 , 10 3 , and 10 4 µM AA. MTT assay was used to evaluate the cell viability. The western blot method was used to measure protein carbonyl (PC) levels to evaluate protein oxidation, and glucose-regulated protein 78 (GRP78), activating transcription factor 4 (ATF4), and C/EBP homologous (CHOP) levels to evaluate ER stress. Then, according to our results, cells were incubated with 10, 50, and 200 µM caffeine simultaneously with 10 4 µM AA and cell viability, PC, GRP78, ATF4 and CHOP levels were measured with the same methods. Results 10 3 and 10 4 µM AA caused a significant decrease in cell viability (p<0.05 and p<0.001, respectively). 10 4 μM AA caused a significant increase in PC (p<0.05), GRP78 (p<0.01), ATF4 (p<0.001), and CHOP (p<0.001) levels. 50 and 200 μM caffeine significantly reduced PC levels in AA-incubated cells (p<0.05 and p<0.01, respectively). Caffeine concentrations did not significantly change in cell viability, GRP78, ATF4, and CHOP levels (p>0.05 for all). Conclusions Our study showed that AA, especially at higher concentrations, caused an increase in cytotoxicity, protein oxidation, and ER stress, and caffeine decreases protein oxidation without changing AA-induced cytotoxicity and ER stress.