PUBLICATION
Dibutyl phthalate rapidly alters calcium homeostasis in the gills of Danio rerio
- Authors
- Rodrigues, K., Batista-Silva, H., Sousa de Moura, K.R., Van Der Kraak, G., Mena Barreto Silva, F.R.
- ID
- ZDB-PUB-200813-6
- Date
- 2020
- Source
- Chemosphere 258: 127408 (Journal)
- Registered Authors
- Van Der Kraak, Glen
- Keywords
- Calcium, Fish, Gills, Histology, Phthalate, Transient receptor potential
- MeSH Terms
-
- Animals
- Calcium/metabolism*
- Calcium/toxicity
- Calcium Radioisotopes/metabolism*
- Dibutyl Phthalate/metabolism
- Dibutyl Phthalate/toxicity*
- Endoplasmic Reticulum/metabolism
- Gills/drug effects*
- Gills/metabolism
- Homeostasis/drug effects*
- Sodium-Calcium Exchanger/metabolism
- TRPV Cation Channels/metabolism
- Water Pollutants, Chemical/metabolism
- Water Pollutants, Chemical/toxicity*
- Zebrafish/metabolism*
- PubMed
- 32782161 Full text @ Chemosphere
Citation
Rodrigues, K., Batista-Silva, H., Sousa de Moura, K.R., Van Der Kraak, G., Mena Barreto Silva, F.R. (2020) Dibutyl phthalate rapidly alters calcium homeostasis in the gills of Danio rerio. Chemosphere. 258:127408.
Abstract
This study investigates the impacts of exposure to an environment Ca2+ challenge and the mechanism of action of dibutyl phthalate (DBP) on Ca2+ influx in the gills of Danio rerio. In vitro profile of 45Ca2+ influx in gills was verified through the basal time-course. Fish were exposed to low, normal and high Ca2+ concentrations (0.02, 0.7 and 2 mM) for 12 h. So, gills were morphologically analysed and ex vivo45Ca2+ influx at 30 and 60 min was determined. For the in vitro studies, gills were treated for 60 min with DBP (1 pM, 1 nM and 1 μM) with/without blockers/activators of ionic channels, Ca2+ chelator, inhibitors of ATPases, ionic exchangers and protein kinase C to study the mechanism of DBP-induced 45Ca2+ influx. Exposure to high environmental Ca2+ augmented 45Ca2+ influx when compared to fish exposed to normal and low Ca2+ concentrations. Additionally, histopathological changes were observed in the gills of fish maintained for 12 h in low and high Ca2+. In vitro exposure of gills to DBP (1 pM) disturbed Ca2+ homeostasis. DBP stimulated 45Ca2+ influx in gills through the transitory receptor potential vanilloid 1 (TRPV1), and reverse-mode Na+/Ca2+ exchanger (NCX) activation, protein kinase C and K+ channels and sarco/endoplasmic reticulum Ca2+-ATPase (SERCA). These data suggest that in vivo short-term exposure of gills to low and high Ca2+ leads to 45Ca2+ influx and histopathological changes. Additionally, the DBP-induced rapid 45Ca2+ influx is mediated by TRPV1, NCX activation with the involvement of PKC, K+-channels and SERCA, thereby altering Ca2+ homeostasis.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping