Objective: To explore the relationship between pyrethroid bifenthrin and Parkinson’s disease on mouse model.

Background: Pyrethroid is now widely used on account of its high efficiency and low toxicity compared to other pesticides. Bifenthrin, one pyrethroid used extensively, was previously demonstrated to cause developmental toxicity. Considering that some pyrethroid was demonstrated to induce dopaminergic degeneration, while the evidence for bifenthrin is still limited.

Methods: Mice were randomly divided into five groups (n=9, per group): vehicle group, 5 mg/kg bifenthrin group, 10 mg/kg bifenthrin group, 20 mg/kg bifenthrin group and 40 mg/kg bifenthrin group. Behavior assessment including pole test and rotarod test were conducted. Detection of dopamine, dopac, homovanilic acid and 5-HT by high performance liquid choromatography were performed. Besides, measurement of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) were also done. Pathologically, protein level of tyrosine hydroxylase (TH), α-synuclein and vasicular monoamine transporter 2 (VMAT2) were evaluated by western blotting and immunofluorescence or immunohistochemistry.

Results: In this study, we first demonstrated that high dose of bifenthrin was able to cause decreased body weight in mice and bradykinesia indicated by pole test and rotarod test. Pathologically, bifenthrin caused loss of TH and accumulation of α-synuclein. Furthermore, bifenthrin induced decreased expression of VMAT2. Additionally, bifenthrin caused increased oxidative index such as SOD and glutathione which might contribute to the pathological changes.

Conclusions: Our data showed that bifenthrin could induce pathological change resembling PD in mice, providing strong evidence that bifenthrin exposure could contribute to the pathogenesis of PD.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/exposure-to-bifenthrin-contributes-to-parkinsons-disease-in-mouse-model/