These author contributed equally to this work.
Molecular mechanisms of silk gland damage caused by phoxim exposure and protection of phoxim-induced damage by cerium chloride in Bombyx mori
Version of Record online: 11 MAR 2014
© 2014 Wiley Periodicals, Inc.
Volume 30, Issue 9, pages 1102–1111, September 2015
How to Cite
Li, B., Sun, Q., Yu, X., Xie, Y., Hong, J., Zhao, X., Sang, X., Shen, W. and Hong, F. (2015), Molecular mechanisms of silk gland damage caused by phoxim exposure and protection of phoxim-induced damage by cerium chloride in Bombyx mori. Environ. Toxicol., 30: 1102–1111. doi: 10.1002/tox.21983
- Issue online: 12 AUG 2015
- Version of Record online: 11 MAR 2014
- Manuscript Accepted: 2 MAR 2014
- Manuscript Revised: 24 FEB 2014
- Manuscript Received: 29 DEC 2013
- The program of Science and Technology supporting of Suzhou City. Grant Number: SYN201352
- The National High Technology Research and Development Program of China (863 Program). Grant Number: 2013AA102507
- The Priority Academic Program Development of Jiangsu Higher Education Institutions, the National Natural Science Foundation of China. Grant Number: 31072086
- China Agriculture Research System. Grant Number: CARS-22-ZJ0305
- Bombyx mori;
- silk gland;
- phoxim insecticide;
- cerium chloride;
- gene expression profile
It is known that exposure to organophosphorus pesticides (OP) including phoxim can produce oxidative stress, neurotoxicity, and greatly attenuate cocooning rate in the silkworm, Bombyx mori. Cerium treatment has been demonstrated to relieve phoxim-induced toxicity in B. mori; however, very little is known about the molecular mechanisms of silk gland injury due to OP exposure and protection of gland damage due to cerium pretreatment. The aim of this study was to evaluate silk gland damage and its molecular mechanisms in phoxim-induced silkworm toxicity and the protective mechanisms of cerium following exposure to phoxim. The results showed that phoxim exposure resulted in severe gland damage, reductions in protein synthesis and the cocooning rate of silkworms. Cerium (Ce) attenuated gland damage caused by phoxim, promoted protein synthesis, increased the antioxidant capacity of the gland and increased the cocooning rate of B. mori. Furthermore, digital gene expression data suggested that phoxim exposure led to significant up-regulation of 714 genes and down-regulation of 120 genes. Of these genes, 122 were related to protein metabolism, specifically, the down-regulated Ser2, Ser3, Fib-L, P25, and CYP450. Ce pretreatment resulted in up-regulation of 162 genes, and down-regulation of 141 genes, importantly, Ser2, Ser3, Fib-L, P25, and CYP333B8 were up-regulated. Treatment with CeCl3 + phoxim resulted in higher levels of Fib-L, P25, Ser2, Ser3, CAT, TPx, and CYP333B8 expression in the silk gland of silkworms. These findings indicated that Ce increased cocooning rate via the promotion of silk protein synthesis-related gene expression in the gland under phoxim-induced toxicity. These findings may expand the application of rare earths in sericulture. © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 1102–1111, 2015.