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Developmental neurotoxicity of maneb: Notochord defects, mitochondrial dysfunction and hypoactivity in zebrafish
Fangjie Cao1, Christopher L Souders2, Pengfei Li3
1Department of Applied Chemistry, College of Science, China Agricultural University, Beijing 100193, China; Department of Physiological Sciences and Center for Environmental and Human Toxicology, University of Florida Genetics Institute, Interdisciplinary Program in Biomedical Sciences Neuroscience, College of Veterinary Medicine, University of Florida, Gainesville, FL 32611, USA.
Abstract:
Broad applications and exposure to the fungicide maneb can lead to toxicity in non-target organisms. Maneb is also associated with neurogenerative diseases such as Parkinson's disease (PD). The objectives of this study were to determine the acute toxicity of maneb to zebrafish by measuring mitochondrial bioenergetics, locomotor activity, and the expression of genes related to the oxidative damage response, as well as those related to dopamine signaling due to its association with PD. Zebrafish embryos at 6 h post-fertilization (hpf) were exposed to either solvent control (0.1% DMSO, v/v), or one dose of 0.1, 0.5, 1.0 and 10.0 µM maneb for 96 h. Maneb was moderately toxic to zebrafish embryos, and had a 96-h LC50 value of 4.29 μM (~ 1.14 mg/L). Maneb induced a dose-dependent increase in mortality, decreased hatching rate, and increased notochord deformity rate at both 1.0 and 10.0 µM after 72 and 96 h. Total body length was also significantly reduced with 1.0 µM maneb. A 50-60% decrease in mean basal oxygen consumption rate was also observed in embryos following a 24 hpf exposure to 10.0 µM maneb but oligomycin-induced ATP production and FCCP-induced maximum respiration remained unaffected. No change was detected in the expression levels of genes associated with oxidative stress (sod1 and sod2), nor those related to dopamine synthesis (th1), dopamine transporter (dat), dopamine receptors (drd1, drd2a, drd3, and drd4b). Thus, modifying the expression of these transcripts may not be a mechanism for maneb-induced developmental toxicity in zebrafish. To assess the potential for neurotoxicity, a dark photokinesis assay was conducted in larvae following 7 d exposure to 0.1, 0.5 and 1.0 μM maneb. Larvae exposed to 0.5 and 1.0 μM maneb showed signs related to hypoactivity, and this reduced activity is hypothesized to be associated with notochord defects as this deformity was prevalent at higher concentrations of maneb. Overall, these data demonstrate that maneb negatively affects embryonic development (i.e. notochord development), affects basal oxygen consumption rates of embryos, and induces hypoactivity in larval fish. This study improves understanding regarding the developmental neurotoxicity of the fungicide maneb to zebrafish.
Insights
The fungicide maneb is toxic to zebrafish embryos, causing developmental issues and reduced activity. This study investigated maneb
Area of Science:
- Environmental Toxicology
- Developmental Neurotoxicity
- Zebrafish Model Organism
Background:
- Broad use of maneb fungicide raises concerns for non-target organism toxicity.
- Maneb exposure is linked to neurodegenerative diseases, including Parkinson's disease (PD).
- Understanding maneb's developmental toxicity and neurotoxic potential is crucial.
Purpose of the Study:
- To determine the acute toxicity of maneb in zebrafish embryos.
- To assess maneb's impact on mitochondrial bioenergetics and locomotor activity.
- To investigate gene expression related to oxidative stress and dopamine signaling.
Main Methods:
- Zebrafish embryos were exposed to varying maneb concentrations (0.1–10.0 µM) for 96 hours.
- Assessed mortality, hatching rates, notochord development, and body length.
- Measured oxygen consumption, and conducted dark photokinesis assays in larvae.
Main Results:
- Maneb exhibited moderate toxicity with a 96-h LC50 of 4.29 µM.
- Increased mortality, reduced hatching, and notochord deformities observed at higher doses.
- Maneb exposure decreased basal oxygen consumption and induced larval hypoactivity.
Conclusions:
- Maneb negatively impacts zebrafish embryonic development and basal oxygen consumption.
- Maneb exposure leads to developmental neurotoxicity, evidenced by larval hypoactivity.
- Gene expression changes in oxidative stress and dopamine pathways were not significant.
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