Neurodevelopmental and behavioural effects of arsenic in zebrafish (Danio rerio)
Bibliographic record
Abstract
The current study was designed to investigate the molecular mechanisms by which arsenic causes neurobehavioural impairments in larval zebrafish following early developmental exposure to environmentally relevant concentrations. Zebrafish embryos were exposed to arsenic [0 (control), 5, 10, 50, and 100 µg/L as arsenite] from 1-120 hpf (hours-post-fertilization) and raised in clean water until 30-dpf (days-post-fertilization) to assess long-term effects. Arsenic-induced ROS, apoptosis, and lipid peroxidation were measured at 5-dpf. In addition, gene expression analysis and immunostaining (24-hpf and 5-dpf) were performed to examine how embryonic arsenic exposure affects neurogenesis and development of neural signalling pathways, including dopaminergic, serotonergic, and cholinergic pathways. Furthermore, arsenic-induced behavioural alterations in zebrafish larvae were evaluated by assessing photomotor response (5-dpf), thigmotaxis (15-dpf), social preference (21-dpf), and novel object recognition capacity (30-dpf). Embryonic arsenic exposure resulted in a dose-dependent increase in ROS production, abundance of apoptotic cells, and lipid peroxidation. Moreover, arsenic exposure significantly reduced hypothalamic neurogenesis and the expression of diencephalic dopaminergic neurons and peripheral motor neurons. Arsenic exposure also caused dysregulation of genes associated with neurogenesis, and dopaminergic, serotonergic and cholinergic signalling, and antioxidant response. Behavioural analysis revealed arsenic exposure impaired photomotor reflexes and locomotion at 5-dpf, heightened anxiety response at 15-dpf, and compromised cognitive function at 30-dpf. Interestingly, pretreatment with an antioxidant, N-acetyl-l-cysteine (NAC), ameliorated arsenic-induced ROS production and behavioural impairments (photomotor response and thigmotaxis). Overall, our study demonstrated that embryonic arsenic exposure causes behavioural deficits in larval zebrafish by inducing oxidative stress, leading to the disruption of neurogenesis and neural signalling pathways.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.001 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".