PUBLICATION
Sulfonamides (SAs) exposure causes neurobehavioral toxicity at environmentally relevant concentrations (ERCs) in early development of zebrafish
- Authors
- Huo, W.B., Jia, P.P., Li, W.G., Xie, X.Y., Yang, G., Pei, D.S.
- ID
- ZDB-PUB-230702-26
- Date
- 2023
- Source
- Aquatic toxicology (Amsterdam, Netherlands) 261: 106614106614 (Journal)
- Registered Authors
- Jia, Panpan, Pei, Desheng
- Keywords
- Carbonic anhydrase metabolism, Developmental toxicity, Folic acid metabolism, Neurobehavior, Sulfonamides, Zebrafish
- MeSH Terms
-
- Animals
- Anti-Bacterial Agents/pharmacology
- Carbonic Anhydrases*
- Ecosystem
- Folic Acid/pharmacology
- Larva
- Sulfanilamide/pharmacology
- Sulfonamides/toxicity
- Tryptophan Hydroxylase/pharmacology
- Water Pollutants, Chemical*/toxicity
- Zebrafish
- PubMed
- 37390778 Full text @ Aquat. Toxicol.
Citation
Huo, W.B., Jia, P.P., Li, W.G., Xie, X.Y., Yang, G., Pei, D.S. (2023) Sulfonamides (SAs) exposure causes neurobehavioral toxicity at environmentally relevant concentrations (ERCs) in early development of zebrafish. Aquatic toxicology (Amsterdam, Netherlands). 261:106614106614.
Abstract
Antibiotics, due to their stability and persistence in the environment, can have chronic impacts on various ecosystems and organisms. However, the molecular mechanisms underlying antibiotic toxicity at environmental concentrations, particularly the neurotoxic effects of sulfonamides (SAs), remain poorly understood. In this study, we assessed the neurotoxicity of six SAs including the sulfadiazine (SD), sulfathiazole (ST), sulfamethoxazole (SMX), sulfisoxazole (SIZ), sulfapyridine (SPD), and sulfadimethoxine (SDM) by exposing zebrafish to environmentally relevant concentrations (ERCs). The SAs exhibited concentration-dependent effects on zebrafish behavior, including spontaneous movement, heartbeat, survival rate, and body metrics, ultimately leading to depressive-like symptoms and sublethal toxicity during early life stages. Notably, even the lowest SA concentration (0.05 μg/L) induced neurotoxicity and behavioral impairment in zebrafish. We observed a dose-dependent increase in melancholy behavior as indicated by increased resting time and decreased motor activity in zebrafish larvae. Following exposure to SAs from 4 to 120 h post-fertilization (hpf), key genes involved in folate synthesis [sepiapterin reductase a (spra), phenylalanine hydroxylase (pah), tyrosine hydroxylase (th), and tryptophan hydroxylase 1 (tryptophan 5-monooxygenase) a tryptophan hydroxylase (tph1a)] and carbonic anhydrase (CA) metabolism [carbonic anhydrase II (ca2), carbonic anhydrase IV a (ca4a), carbonic anhydrase VII (ca7), and carbonic anhydrase XIV (ca14)] were significantly downregulated or inhibited at different concentrations. Our findings demonstrate that acute exposure to six SAs at environmentally relevant concentrations induces developmental and neurotoxic effects in zebrafish, impacting folate synthesis pathways and CA metabolism. These results provide valuable insights into the potential role of antibiotics in depressive disorders and neuroregulatory pathways.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping