PUBLICATION
Parental exposure to cadmium chloride causes developmental toxicity and thyroid endocrine disruption in zebrafish offspring
- Authors
- Tian, J., Hu, J., He, W., Zhou, L., Huang, Y.
- ID
- ZDB-PUB-200428-7
- Date
- 2020
- Source
- Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 234: 108782 (Journal)
- Registered Authors
- He, Wei, Hu, Jia, Tian, Jingjing
- Keywords
- Cadmium chloride, Developmental toxicity, Thyroid endocrine disorder, Zebrafish
- MeSH Terms
-
- Thyroid Gland/drug effects*
- Thyroid Gland/pathology
- Survival Rate
- Pregnancy
- Water Pollutants, Chemical/toxicity
- Paternal Exposure/adverse effects*
- Female
- Maternal Exposure/adverse effects*
- Prenatal Exposure Delayed Effects/chemically induced*
- Prenatal Exposure Delayed Effects/pathology
- Fertility/drug effects
- Larva/drug effects
- Larva/growth & development
- Larva/metabolism
- Animals, Newborn
- Animals
- Zebrafish/embryology
- Zebrafish/growth & development*
- Zebrafish/metabolism
- Thyroid Hormones/metabolism
- Endocrine Disruptors/toxicity*
- Male
- Cadmium Chloride/toxicity*
- PubMed
- 32339758 Full text @ Comp. Biochem. Physiol. C Toxicol. Pharmacol.
Citation
Tian, J., Hu, J., He, W., Zhou, L., Huang, Y. (2020) Parental exposure to cadmium chloride causes developmental toxicity and thyroid endocrine disruption in zebrafish offspring. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP. 234:108782.
Abstract
Cadmium is a common heavy metal pollutant. Previous studies have found that long-term cadmium exposure can cause damage to multiple organs/systems in humans and experimental animals; however, there are few studies that elucidate its effects on offspring development, discuss whether it can be transmitted to offspring from the parent, and debate whether it affects the functional development of the thyroid hormone system in offsprings. In this study, sexually mature zebrafish were exposed to different concentrations of cadmium chloride (0.01 μmol/L, 0.1 μmol/L, and 1 μmol/L) to study reproductive toxicity. It was found that parental zebrafish exposed to 1 μmol/L of cadmium chloride produced offsprings with different degrees of malformation. At 5 days post-fertilization (dpf), the levels of 3,5,3'-triiododenosine (T3) and thyroxine (T4) in the zebrafish were decreased. At 10 dpf, the T4 and T3 levels in the zebrafish of the offspring were significantly reduced. At the same time, the expression of thyroid receptor (trα and trβ) genes in five dpf larvae was significantly up-regulated in the 1 μmol/L treatment group relative to the control group. The mRNAs of thyroid hormone synthesis and metabolism-related genes (tshβ, dio1, dio2, ugt1ab, and ttr) were significantly up-regulated in the 0.1 μmol/L and 1 μmol/L treatment groups. This study demonstrates that parental cadmium chloride exposure produces reproductive toxicity in zebrafish and that the effects can be transferred from the parent to the offspring, resulting in developmental toxicity in the thyroid endocrine system.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping