Aflatoxin B1 disrupts transient receptor potential channel activity and increases COX-2 expression in JEG-3 placental cells
Publication in refereed journal


摘要Aflatoxins are fungal metabolites which pose a major threat to food safety. Although these mycotoxins are established hepatocarcinogens, their effect on the reproductive organ is unknown. Transient Receptor Potential Channels (TRPs) are ubiquitously expressed in human tissues, including the placenta. These channels are associated with various functions in the placenta. The fetus and the placenta are especially sensitive to xenobiotic assault; therefore, exposure to the aflatoxins during gestation might lead to the undesirable outcome. Previously we have shown that aflatoxin B1 administered in late gestation may increase cox-2 expression in mouse placentae. In the present study, we examined the effect of aflatoxin B1 on COX-2 by using the placental cell model JEG-3 and the respective signaling pathway. In our result, COX-2 expression was induced by the mycotoxin administration. The intracellular calcium levels were also increased in cells by aflatoxin B1 treatment as little as 1 nM. Immunoblot result showed that some TRP expressions were elevated. As inflated intracellular calcium might activate MAPKs, the underlying signaling pathway was investigated. With the help of TRP-specific inhibitors, the mycotoxin appeared to increase the expression of TRPC-3 and activate PKC beta and ERK. The significance of COX-2 in pregnancy has been well established. Exposure to this mycotoxin may perturb the physiological processes dictated by COX-2 in pregnancy.
著者Zhu Y, Tan YQ, Leung LK
期刊名稱Chemico-Biological Interactions
頁次84 - 90
關鍵詞Aflatoxin B1,TRP,Placental cells
Web of Science 學科類別Biochemistry & Molecular Biology;Pharmacology & Pharmacy;Toxicology;Biochemistry & Molecular Biology;Pharmacology & Pharmacy;Toxicology

上次更新時間 2020-15-09 於 01:16