ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Predictive Toxicology
Phoxim Induces Neurotoxicity and Intestinal Damage in Caenorhabditis elegans
Provisionally accepted
- School of Public Health, Kunming Medical University, Kunming, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
The effects of phoxim exposure (0.5, 1, and 2.5 µg/mL) on survival, neurological function, and intestinal integrity in Caenorhabditis elegans (C.elegans) were investigated. Phoxim at all concentrations significantly increased the mortality rate of C. elegans. Fluorescence microscopy revealed that 2.5 µg/mL phoxim reduced dopaminergic neural processes in the BZ555 transgenic strain of C. elegans from 4 to 2, and 0.5 and 1 µg/mL phoxim accelerated amyloid beta (Aβ)-induced paralysis in the CL4176 strain, with complete paralysis observed at 32 and 36 h, respectively. FD&C Blue #1 staining demonstrated intestinal damage in 46.7% and 68.3% of C. elegans exposed to phoxim at 1 and 2.5 µg/mL, respectively. Exposure to 1 µg/mL phoxim decreased enterocyte numbers and reduced autophagic vesicles in the lgg-1::GFP strain of C. elegans from 1.8 to 1.3. qPCR analysis revealed downregulation of autophagy-related genes (vps-34, atg-13, and unc-51) by 0.53-, 0.43-, and 0.36-fold of the control levels, respectively. RNAi targeting the eat-2 gene further confirmed the impact of phoxim on cell survival through the autophagy pathway. Our results indicate that phoxim exposure reduces dopaminergic neuron integrity, accelerates Aβ-induced paralysis, and damages intestinal cells through inhibition of autophagy in C. elegans.
Keywords: Phoxim, Caenorhabditis elegans, Autophagy, Neurotoxicity, Intestinal damage
Received: 02 Jul 2025; Accepted: 20 Nov 2025.
Copyright: © 2025 ZHANG, Zhao, Bai, Wang and Zou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Qi Wang, 1wangqi@163.com
Wei Zou, zouwei@kmmu.edu.cn
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.