PUBLICATION
Carbendazim has the potential to induce oxidative stress, apoptosis, immunotoxicity and endocrine disruption during zebrafish larvae development
- Authors
- Jiang, J., Wu, S., Wang, Y., An, X., Cai, L., Zhao, X., Wu, C.
- ID
- ZDB-PUB-150610-7
- Date
- 2015
- Source
- Toxicology in vitro : an international journal published in association with BIBRA 29(7): 1473-81 (Journal)
- Registered Authors
- Keywords
- Apoptosis, Carbendazim, Endocrine disruption, Immunotoxicity, Oxidative stress, Zebrafish larvae
- MeSH Terms
-
- Animals
- Benzimidazoles/toxicity*
- Carbamates/toxicity*
- Cytokines/metabolism
- Endocrine Disruptors/toxicity*
- Fungicides, Industrial/toxicity*
- Gene Expression Regulation, Developmental/drug effects
- Immunity, Innate/drug effects
- Immunity, Innate/genetics
- Iodide Peroxidase/genetics
- Larva/drug effects
- Larva/growth & development
- Larva/metabolism
- Oxidative Stress/drug effects
- RNA, Messenger/metabolism
- Receptors, Estrogen/genetics
- Receptors, Steroid/genetics
- Zebrafish
- PubMed
- 26055223 Full text @ Toxicol. In Vitro
- CTD
- 26055223
Citation
Jiang, J., Wu, S., Wang, Y., An, X., Cai, L., Zhao, X., Wu, C. (2015) Carbendazim has the potential to induce oxidative stress, apoptosis, immunotoxicity and endocrine disruption during zebrafish larvae development. Toxicology in vitro : an international journal published in association with BIBRA. 29(7):1473-81.
Abstract
Increasing evidence have suggested deleterious effects of carbendazim on reproduction, apoptosis, immunotoxicity and endocrine disruption in mice and rats, however, the developmental toxicity of carbendazim to aquatic organisms remains obscure. In the present study, we utilized zebrafish as an environmental monitoring model to characterize the effects of carbendazim on expression of genes related to oxidative stress, apoptosis, immunotoxicity and endocrine disruption during larval development. Different trends in gene expression were observed upon exposing the larvae to 4, 20, 100, and 500μg/L carbendazim for 4 and 8d. The mRNA levels of catalase, glutathione peroxidase and manganese superoxide dismutase (CAT, GPX, and Mn/SOD) were up-regulated after exposure to different concentrations of carbendazim for 4 or 8d. The up-regulation of p53, Apaf1, Cas8 and the down-regulation of Bcl2, Mdm2, Cas3 in the apoptosis pathway, as well as the increased expression of cytokines and chemokines, including CXCL-C1C, CCL1, IL-1b, IFN, IL-8, and TNFα, suggested carbendazim might trigger apoptosis and immune response during zebrafish larval development. In addition, the alteration of mRNA expression of VTG, ERα, ERβ1, ERβ2, TRα, TRβ, Dio1, and Dio2 indicated the potential of carbendazim to induce endocrine disruption in zebrafish larvae. These data suggested that carbendazim could simultaneously induce multiple responses during zebrafish larval development, and bidirectional interactions among oxidative stress, apoptosis pathway, immune and endocrine systems might be present.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping