International Journal of Nutrition and Food Sciences
Volume 9, Issue 3, May 2020, Pages: 78-85
Received: May 14, 2020;
Accepted: May 29, 2020;
Published: Jun. 23, 2020
Views 298 Downloads 92
Xiaoyun Shan, School of Public Health, University of South China, Hengyang, China; Department of Nutrition and Food Hygiene, Nanjing Medical University, Nanjing, China
Pengqi Wang, Lianyungang Health Inspection Bureau, Lianyungang, China
Qing Feng, Department of Nutrition and Food Hygiene, Nanjing Medical University, Nanjing, China
Acrylamide, exists in carbohydrate-rich food heated at high temperatures, is a probable carcinogen to humans. Excessive alcohol intake can also lead to a variety of pathological changes in the body. Acrylamide in the foods and alcohol in the drinks are unavoidable. And studies have demonstrated that combination of the two substances which are taken into the body via diet may cause adverse effects in the cells, even induce impairments on testicular spermatogenesis in male offsprings. Both acrylamide and alcohol are mainly metabolized in the liver, where cytochrome P450 2E1 (CYP2E1) acts as the common metabolic enzyme of the two xenobiotics. This study aimed to explore the effects of acrylamide and alcohol combination on rat hepatoma BRL cells proliferation and the probable mechanisms. MTT, western blotting, EdU fluorescence staining, flow cytometry and PCR were used. Results showed that combination of acrylamide and alcohol at low doses promoted BRL cells proliferation through CYP2E1/Akt/ NF-κB/cyclinB1/cyclinD1 activation and ROS production. The combined effects of acrylamide and alcohol largely depended on ROS level. Furthermore, acrylamide and alcohol could synergistically induce miR-21, which was related to the progress of liver regeneration. These data showed that combination of acrylamide and alcohol at low doses promoted BRL cells proliferation through inducing ROS production, which indicated that intake of fried starch food with small dose of alcohol might have positive effects on liver regeneration.
Rat Hepatoma BRL Cells Proliferation by Acrylamide and Alcohol Combination, International Journal of Nutrition and Food Sciences.
Vol. 9, No. 3,
2020, pp. 78-85.
SMITH, E. A., OEHME, F. W. (1991). Acrylamide and polyacrylamide: a review of production, use, environmental fate and neurotoxicity. Rev Environ Health, 9: 215-228.
IWONA C, CIESLIK, E., TOPOLSKA, K., SURMA, M.. (2019). Dietary acrylamide exposure from traditional food products in lesser poland and associated risk assessment. Annals of Agricultural & Environmental Medicine Aaem.
S RGEL, F., WEISSENBACHER, R., KINZIGSCHIPPERS, M., HOFMANN, A., ILLAUER, M., SKOTT, A., LANDERSDORFER, C. (2002). Acrylamide: increased concentrations in homemade food and first evidence of its variable absorption from food, variable metabolism and placental and breast milk transfer in humans. Chemotherapy, 48: 267.
SCHETTGEN, T., K TTING, B., HORNIG, M., BECKMANN, M. W., WEISS, T., DREXLER, H., ANGERER, J. (2004). Trans-placental exposure of neonates to acrylamide—a pilot study. International Archives of Occupational & Environmental Health, 77: 213-216.
EXON, J. H. (2006). A review of the toxicology of acrylamide. Journal of Toxicology & Environmental Health Part B Critical Reviews, 9: 397-412.
HUANG, Y. F., CHEN, M. L., LIOU, S. H., CHEN, M. F., UANG, S. N., WU, K. Y. (2011). Association of CYP2E1, GST and mEH genetic polymorphisms with urinary acrylamide metabolites in workers exposed to acrylamide. Toxicology Letters, 203: 118.
RONKSLEY, P. E., BRIEN, S. E., TURNER, B. J., MUKAMAL, K. J., GHALI, W. A. (2011). Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis. Bmj, 342: d671.
BRIEN, S. E., RONKSLEY, P. E., TURNER, B. J., MUKAMAL, K. J., GHALI, W. A. (2011). Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies. Bmj, 342: 480-480.
SEN, E., TUNALI, Y., ERKAN, M. (2015). Testicular development of male mice offsprings exposed to acrylamide and alcohol during the gestation and lactation period. Human & Experimental Toxicology, 34: 401-14.
SHAN, X. Y., LI, Y., MENG, X. L., WANG, P. Q., JIANG, P., FENG, Q. (2014). Curcumin and (-)-epigallocatechin-3-gallate attenuate acrylamide-induced proliferation in HepG2 cells. Food & Chemical Toxicology An International Journal Published for the British Industrial Biological Research Association, 66: 194-202.
SUN, H. Z., YANG, T. W., ZANG, W. J., WU, S. F. (2010). Dehydroepiandrosterone-induced proliferation of prostatic epithelial cell is mediated by NFKB via PI3K/AKT signaling pathway. Journal of Endocrinology, 204: 311-318.
CHEN, T., LIU, J., DAI, D. (2014). Oxidative stress and liver regeneration. Chinese Journal of General Surgery.
DIANA B. S., ARRIAGA. C., C., PEDROZA. T., A., I. A. DE L R., V., HERRERA, L., A. (2020). The promising role of mir-21 as a cancer biomarker and its importance in rna-based therapeutics.
MARQUEZ, R. T., WENDLANDT, E., GALLE, C. S., KECK, K., MCCAFFREY, A. P. (2010). MicroRNA-21 is upregulated during the proliferative phase of liver regeneration, targets Pellino-1, and inhibits NF-kappaB signaling. American Journal of Physiology Gastrointestinal & Liver Physiology, 298: 535-41.
NG, R., SONG, G., ROLL, G. R. (2012). A microRNA-21 surge facilitates rapid cyclin D1 translation and cell cycle progression in mouse liver regeneration. Journal of Clinical Investigation, 122: 1097-108.
LI, J. J., CHAN, W. H., LEUNG, W. Y., WANG, Y., XU, C. S. (2015). MicroRNA-21 promotes proliferation of rat hepatocyte BRL-3A by targeting FASLG. Genetics & Molecular Research Gmr, 14: 4150-4160.
WOLFGANG E, T. (2006). Repression of cytochrome P450 activity in human hepatocytes in vitro by a novel hepatotrophic factor, augmenter of liver regeneration. The Journal of pharmacology and experimental therapeutics, 2.
LAMY, E., V LKEL, Y., ROOS, P. H., KASSIE, F., MERSCH-SUNDERMANN, V. (2008). Ethanol enhanced the genotoxicity of acrylamide in human, metabolically competent HepG2 cells by CYP2E1 induction and glutathione depletion. International journal of hygiene and environmental health, 211: 74-81.
SHI, X. M., ZHANG, G. J., CHANG, Z. S., WU, X. L. (2014). Viability Reduction of Melanoma Cells by Plasma Jet via Inducing G1/S and G2/M Cell Cycle Arrest and Cell Apoptosis. Plasma Science IEEE Transactions on, 42: 1640-1647.
DAY, R. M., SUZUKI, Y. J. (2004). Cell proliferation, reactive oxygen and cellular glutathione. Dose Response, 3: 425-442.
CARRERAS, M. C., CONVERSO, D. P., LORENTI, A. S., BARBICH, M., LEVISMAN, D. M., JAITOVICH, A., ANTICO ARCIUCH, V. G., GALLI, S., PODEROSO, J. J. (2004). Mitochondrial nitric oxide synthase drives redox signals for proliferation and quiescence in rat liver development. Hepatology, 40: 157–166.
SAMUNI, Y., GOLDSTEIN, S., DEAN, O. M., BERK, M. (2013). The chemistry and biological activities of N-acetylcysteine. Biochimica et biophysica acta, 1830: 4117.
DIPPOLD, R. P., VADIGEPALLI, R., GONYE, G. E., HOEK, J. B. (2012). Chronic ethanol feeding enhances miR-21 induction during liver regeneration while inhibiting proliferation in rats. American journal of physiology. Gastrointestinal and liver physiology, 303: 733-43.