Oxidative stress and mitochondrial damage induced by a novel pesticide fluopimomide in Caenorhabditis elegans

被引:2
作者
Liu, Huimin [1 ]
Fu, Guanghan [1 ]
Li, Wenjing [1 ]
Liu, Bingjie [1 ]
Ji, Xiaoxue [1 ]
Zhang, Shouan [2 ]
Qiao, Kang [1 ,3 ]
机构
[1] Shandong Agr Univ, Coll Plant Protect, Key Lab Pesticide Toxicol & Applicat Tech, Tai An 271018, Shandong, Peoples R China
[2] Univ Florida, Trop Res & Educ Ctr, Dept Plant Pathol, IFAS, Gainesville, FL 33031 USA
[3] Shandong Huayang Technol Co Ltd, Tai An 271411, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
Fluopimomide; Caenorhabditis elegans; Toxicity; Oxidative stress; Mitochondrial damage; COMPLEX-II; DYSFUNCTION; BEHAVIOR; MODEL; MECHANISMS; RESISTANCE; EXPOSURE;
D O I
10.1007/s11356-023-28893-z
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Fluopimomide is a novel pesticide intensively used in agricultural pest control; however, its excessive use may have toxicological effects on non-target organisms. In this study, Caenorhabditis elegans was used to evaluate the toxic effects of fluopimomide and its possible mechanisms. The effects of fluopimomide on the growth, pharyngeal pumping, and antioxidant systems of C. elegans were determined. Furthermore, the gene expression levels associated with mitochondria in the nematodes were also investigated. Results indicated that fluopimomide at 0.2, 1.0, and 5.0 mg/L notably (p < 0.001) decreased body length, pharyngeal pumping, and body bends in the nematodes compared to the untreated control. Additionally, fluopimomide at 0.2, 1.0, and 5.0 mg/L notably (p < 0.05) increased the content of malondialdehyde by 3.30-, 21.24-, and 33.57-fold, respectively, while fluopimomide at 1.0 and 5.0 mg/L significantly (p < 0.001) increased the levels of reactive oxygen species (ROS) by 49.14% and 77.06% compared to the untreated control. In contrast, fluopimomide at 1.0 and 5.0 mg/L notably reduced the activities of target enzyme succinate dehydrogenase and at 5.0 mg/L reduced the activities of antioxidant enzyme superoxide dismutase. Further evidence revealed that fluopimomide at 1.0 and 5.0 mg/L significantly inhibited oxygen consumption and at 0.2, 1.0, and 5.0 mg/L significantly inhibited ATP level in comparison to the untreated control. The expression of genes related to the mitochondrial electron transport chain mev-1 and isp-1 was significantly downregulated. ROS levels in the mev-1 and isp-1 mutants after fluopimomide treatments did not change significantly compared with the untreated mutants, suggesting that mev-1 and isp-1 may play critical roles in the toxicity induced by fluopimomide. Overall, the results demonstrate that oxidative stress and mitochondrial damage may be involved in toxicity of fluopimomide in C. elegans.
引用
收藏
页码:91794 / 91802
页数:9
相关论文
共 53 条
[1]   Slm35 links mitochondrial stress response and longevity through TOR signaling pathway [J].
Aguilar-Lopez, Jose L. ;
Laboy, Raymond ;
Jaimes-Miranda, Fabiola ;
Garay, Erika ;
DeLuna, Alexander ;
Funes, Soledad .
AGING-US, 2016, 8 (12) :3255-+
[2]   RETRACTED: Pesticide pollutants in the environment-A critical review on remediation techniques, mechanism and toxicological impact (Retracted Article) [J].
Akash, S. ;
Sivaprakash, Baskaran ;
Rajamohan, Natarajan ;
Pandiyan, C. Muruga ;
Vo, Dai-Viet N. .
CHEMOSPHERE, 2022, 301
[3]   Progress in understanding molecular mechanisms and evolution of resistance to succinate dehydrogenase inhibiting (SDHI) fungicides in phytopathogenic fungi [J].
Avenot, Herve F. ;
Michailides, Themis J. .
CROP PROTECTION, 2010, 29 (07) :643-651
[4]   Chronic exposure to a glyphosate-containing pesticide leads to mitochondrial dysfunction and increased reactive oxygen species production in Caenorhabditis elegans [J].
Bailey, Denise C. ;
Todt, Callie E. ;
Burchfield, Shelbie L. ;
Pressley, Aireal S. ;
Denney, Rachel D. ;
Snapp, Isaac B. ;
Negga, Rekek ;
Traynor, Wendy L. ;
Fitsanakis, Vanessa A. .
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, 2018, 57 :46-52
[5]   Toxic effect of the novel chiral insecticide IPP and its biodegradation intermediate in nematode Caenorhabditis elegans [J].
Bian, Tingting ;
Zhu, Xiaolin ;
Guo, Jing ;
Zhuang, Ziheng ;
Cai, Zhiqiang ;
Zhao, Xiubo .
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY, 2018, 164 :604-610
[6]   Paraquat exposure over generation affects lifespan and reproduction through mitochondrial disruption in C. elegans [J].
Bora, Snigdha ;
Vardhan, Gadi Sri Harsha ;
Deka, Nikhita ;
Khataniar, Lipika ;
Gogoi, Debajani ;
Baruah, Aiswarya .
TOXICOLOGY, 2021, 447
[7]  
BRENNER S, 1974, GENETICS, V77, P71
[8]   Impact of drug solvents on C. elegans pharyngeal pumping [J].
Calahorro, Fernando ;
Holden-Dye, Lindy ;
O'Connor, Vincent .
TOXICOLOGY REPORTS, 2021, 8 :1240-1247
[9]  
Collins James J, 2008, WormBook, P1, DOI 10.1895/wormbook.1.137.1
[10]   Intergenerational reproductive toxicity of chlordecone in male Caenorhabditis elegans [J].
Dai, Shuhao ;
Zhang, Ying ;
Miao, Yan ;
Liu, Ran ;
Pu, Yuepu ;
Yin, Lihong .
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH, 2019, 26 (11) :11279-11287