Developmental Neurotoxicology
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Developmental exposure to PCBs and/or MeHg: effects on a differential reinforcement of low rates (DRL) operant task before and after amphetamine drug challenge.
The current study assessed the effects of developmental PCB and/or MeHg exposure on an operant task of timing and inhibitory control and determined if amphetamine (AMPH) drug challenges differentially affected performance. Long-Evans rats were exposed to corn oil (control), PCBs alone (1 or 3 mg/kg), MeHg alone (1.5 or 4.5 ppm), the low combination (1 mg/kg PCBs+1.5 ppm MeHg), or the high combination (3 mg/kg PCBs+4.5 ppm MeHg) throughout gestation and lactation. An environmentally relevant, formulated PCB mixture was used. Male and female offspring were trained to asymptotic performance on a differential reinforcement of low rates (DRL) operant task as adults. PCB-exposed groups had a lower ratio of reinforced to non-reinforced responses than controls. Groups exposed to MeHg alone were not impaired and the deficits observed in PCB-exposed groups were not seen when PCBs were co-administered with MeHg. AMPH was less disruptive to responding in males receiving PCBs alone, MeHg alone, and 1.0 mg/kg PCB+1.5 ppm MeHg. Paradoxically, the disruption in responding by AMPH in males given 3.0 mg/kg PCB+4.5 ppm MeHg did not differ from controls. Exposed females from all treatment groups did not differ from controls in their AMPH response. Overall, the findings suggest that developmental exposure to PCBs can decrease DRL performance. Co-exposure to MeHg seemed to mitigate the detrimental effects of PCBs on performance. The finding that the disruptive effects of AMPH on DRL performance were lessened in some groups of exposed males suggests that alterations in dopaminergic functioning may have a role in behavioral changes seen after perinatal PCB and MeHg exposure.
- 02
Fenobucarb-induced developmental neurotoxicity and mechanisms in zebrafish.
Fenobucarb (2-sec-butylphenyl methylcarbamate, BPMC) is an extensively used carbamate insecticide. Its developmental neurotoxicity and the underlying mechanisms have not been well investigated. In this study, zebrafish embryos were exposed to various concentrations of BPMC from 6 hpf (hours post fertilization, hpf) to 120 hpf. BPMC induced developmental toxicity with reduced motility in larval zebrafish. The spinal cord neutrophil infiltration, increased ROS production, caspase 3 and 9 activation, central nerve and peripheral motor neuron damage, axon and myelin degeneration were observed in zebrafish treated with BPMC generally in a dose-dependent manner. The expression of eight marker genes for nervous system function or development, namely, a1-tubulin, shha, elavl3, gap43, syn2a, gfap, mbp and manf, was significantly downregulated following BPMC exposure. AChE activity reduction and ache gene expression suppression was also found significantly in BPMC-treated zebrafish. These results indicate that BPMC is highly toxic to zebrafish and that BPMC induces zebrafish developmental neurotoxicity through pathways involved in inflammation, oxidative stress, degeneration and apoptosis.
- 03
Linking particulate matter exposure and neurological disorders: Evidence from epidemiology, biomarkers and mechanistic studies.
Exposure to particulate matter (PM) including fine (PM₂.₅), coarse (PM₁₀), and ultrafine particles (UFPM) has emerged as a critical environmental determinant of neurological disorders, including Alzheimer's and Parkinson's diseases, neurodevelopmental impairments, and cognitive decline. This review integrates evidence from 129 research articles (2002-2025) to elucidate the mechanistic, biomarker-based, and public health dimensions of PM-induced neurotoxicity. Mechanistic pathways include oxidative stress, neuroinflammation, mitochondrial dysfunction, and blood-brain barrier disruption, with documented structural and functional damage in brain regions such as the hippocampus and prefrontal cortex. PM₂.₅ serves as a carrier of neurotoxic metals (e.g., lead, cadmium, vanadium) and understudied organic toxicants (e.g., PAHs, pesticides), amplifying its pathogenic potential. Exposure occurs through the olfactory route, systemic circulation, and gut-brain axis, highlighting multiple entry points into the central nervous system. Biomarkers such as Aβ₄₂, phosphorylated tau (p-tau), and α-synuclein are elevated in experimental models, but require greater validation in human PM-exposed populations. Children and older adults represent the most vulnerable groups due to developmental sensitivity and cumulative neuroinflammatory burden, yet remain underrepresented in cohort studies. Geographic disparities further limit generalizability, with low- and middle-income countries underrepresented despite experiencing the highest PM burdens. Future research must advance longitudinal, cohort and life-course studies, multi-omics biomarker discovery, and real-world mixture toxicology to identify intervention targets. These findings call for urgent integration of air pollution control into public health strategies targeting neurological diseases, emphasizing prevention through regulation, early detection, and equity-focused research frameworks.
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