Mechanism Investigation of Neurotoxicity of Caenorhabditis elegans Induced by Fumonaxin B1-Mediated Oxidative Stress and Mitochondrial Dysfunction
To study the role of mitochondrial function and oxidative stress in the neurotoxicity induced by fumonisin B1(FB1),the model of Caenorhabditis elegans(C.elegans)was used.The behavioral phenotype of C.elegans treated by FB1,and the changes in indices related to oxidative stress and mitochondrial function were analyzed.The results showed that 20～200 μg/mL FB1 exposure for 24 hours induced abnormal expression of genes(cyp35A2,sod-1,sod-3,ctl-2,and ctl-3)related to cytochrome oxidase,superoxide dismutase(SOD),and catalase(CAT)in a dose-dependent manner.Moreover,100～200 µg/mL FB1 treatment reduced mitochondrial density of C.elegans and significantly decreased the levels of adenosine triphosphate(ATP)and the potential of mitochondrial membrane(P＜0.05).The expression levels of mitochondrial respiratory chain complexes I and V were significantly inhibited by 200 μg/mL FB1 treatment,while the expression level of mitochondrial fission gene drp-1 was increased.Correlation analysis demonstrated a significant correlation between the expression of indices related to oxidative stress and mitochondrial function and the behavioral phenotype of C.elegans.In conclusion,FB1 may induce neurotoxicity by participating oxidative stress,mitochondrial respiratory chain,and mitochondrial dynamics in C.elegans.
NETL
NSTL
万方数据
维普
