Cellular Apoptosis Induced by Deoxynivalenol

细胞凋亡 赫拉 体内 丙二醛 谷胱甘肽 氧化应激 免疫印迹 生物 毒性 分子生物学 流式细胞术 体外 男科 化学 生物化学 医学 生物技术 基因 有机化学
作者
Qing’ai Chen,Ying Cui,Jiaru Zhao,Wanlin Zeng,Ning Jin,Lan Yang,Junhua Yuan
出处
期刊:Indian Journal of Microbiology [Springer Nature]
卷期号:62 (1): 61-69 被引量:4
标识
DOI:10.1007/s12088-021-00965-z
摘要

Deoxynivalenol (DON) is synthesized by Fusarium species that frequently infect crops during storage, and it's harm risk to human is reflected in the consumption of infected food crops or indirectly through foods of animal origin. In this study, Hela and Chang liver cells were used to research the cellular apoptosis induced by deoxynivalenol. Cells were treated by DON toxin with a series of concentration and incubated for different time. MTT, fluorescence microscope, flow cytometer and Western blot methods were used to analyze the effect of DON on the cell apoptosis in vitro and in vivo systematically. The results showed that DON was toxic to the cells tested. After being treated by DON, the morphology of Chang livers and Hela cells changed significantly. The DON promoted apoptosis in a dose- and time-dependent manner. The activity of Caspase 3 was significantly increased in DON-induced apoptosis. Moreover, endogenous Glutathione (GSH) level in these cell lines was gradually decreased. In the early apoptosis progress, oxidative stress was induced by DON. When DON reached 10 µg/mL, a markedly increased content of Malondialdehyde (MDA) was detected in both Hela and Chang liver cells. Furthermore, an in vivo test indicated that DON had toxicity to mice by causing weight loss and swollen spleen, and significantly increased expression of AST and ALT. In conclusion, the DON was toxic to mice and could induce the apoptosis of tested cells undergoing a Caspase-3 related pathway.
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