Jump to main content
Jump to site search
PLANNED MAINTENANCE Close the message box

Scheduled maintenance upgrade on Thursday 4th of May 2017 from 8.00am to 9.00am (BST).

During this time our websites will be offline temporarily. If you have any questions please use the feedback button on this page. We apologise for any inconvenience this might cause and thank you for your patience.



Mitochondria and MAPK cascades modulate endosulfan-induced germline apoptosis in Caenorhabditis elegans

Abstract

Endosulfan as a new member of persistent organic pollutants has been shown to induce apoptosis in various animal models. However, the mechanism underlying endosulfan-induced apoptosis have not been well elucidated thus far. Caenorhabditis elegans N2 wild type and mutant strains were used in the present study to clarify the roles of the mitochondria, insulin/insulin-like growth factor-1 (IGF-1) signaling pathway, and mitogen-activated protein kinase (MAPK) cascades in α-endosulfan-induced apoptosis. Our results demonstrated a dose- and time-dependent increase of apoptosis in the meiotic zone of the gonad of C. elegans exposed to graded concentrations of endosulfan. The expression levels of sod-3, localized in the mitochondrial matrix, increased greatly after endosulfan exposure. A significant increase in germ cell apoptosis was observed in abnormal methyl viologen sensitivity-1 (mev-1(kn-1)) mutants (with abnormal mitochondrial respiratory chain complex II and higher ROS levels) compared to that in N2 at equal endosulfan concentrations. We found that the insulin/IGF-1 signaling pathway and its downstream Ras/ERK/MAPK did not participate in the endosulfan-induced apoptosis. However, the apoptosis in the loss-of-function strains of JNK and p38 MAPK signaling pathways were completely or mildly suppressed under endosulfan stress. The apoptotic effects of endosulfan were blocked in mutants of jnk-1/JNK-MAPK, sek-1/MAP2K, and pmk-1/p38-MAPK, suggesting that these downstream genes play an essential role in endosulfan-induced germ cell apoptosis. In contrast, the mkk-4/MAP2K and nsy-1/MAP3K were only partially involved in the apoptosis induction. Our data provide evidence that endosulfan increases germ cell apoptosis, which is regulated by mitochondrial function, JNK and p38 MAPK cascades. These findings contribute to the understanding of the signal transduction pathways involved in endosulfan-induced apoptosis.

Back to tab navigation
Please wait while Download options loads

Supplementary files

Publication details

The article was received on 14 Feb 2017, accepted on 11 Apr 2017 and first published on 17 Apr 2017


Article type: Paper
DOI: 10.1039/C7TX00046D
Citation: Toxicol. Res., 2017, Accepted Manuscript
  •   Request permissions

    Mitochondria and MAPK cascades modulate endosulfan-induced germline apoptosis in Caenorhabditis elegans

    J. Wang, H. Du, Y. Nie, Y. Wang, H. Dai, M. Wang, D. Wang and A. Xu, Toxicol. Res., 2017, Accepted Manuscript , DOI: 10.1039/C7TX00046D

Search articles by author