| Complex I inhibition | Rotenone directly inhibits mitochondrial complex I (NADH dehydrogenase), disrupting ATP production and increasing reactive oxygen species (ROS) generation[@betarbet2000] |
| α-Synuclein aggregation | Studies demonstrate rotenone promotes α-synuclein fibril formation and dopaminergic neuron loss[@sherer2003] |
| Neuroinflammation | Activates microglia and promotes cytokine release |
| Gut-brain axis | Rotenone causes gastrointestinal dysfunction, modeling the prodromal stage of PD[@johnson2012] |
| Redox cycling | Paraquat undergoes cyclic reduction-oxidation, generating superoxide radicals and oxidative stress[@cochem2011] |
| Mitochondrial dysfunction | Some organophosphates inhibit mitochondrial enzymes |
| Dopaminergic specificity | Preferentially accumulates in dopaminergic neurons via the dopamine transporter |
| Protein aggregation | Promotes α-synuclein phosphorylation at Ser129 and aggregation[@liou1997] |
| Acetylcholinesterase inhibition | Leads to cholinergic excess and subsequent neuroinflammation[@slotkin2005] |
| Oxidative stress | Induces ROS generation in neural tissues |
| Neurodevelopment effects | Prenatal exposure may increase lifetime neurodegeneration risk[@kou2019] |
| Sodium channel modulation | Pyrethroids prolong sodium channel opening, causing hyperexcitability |
| Databases | OMIMOrphanetClinicalTrialsPubMed |
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