Developmental heptachlor exposure increases susceptibility of dopamine neurons to N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)in a gender-specific manner.

摘要: Abstract Parkinson's disease (PD) is primarily thought of as a aging. However, recent evidence points to the potential for exposure xenobiotics during development increase risk PD. Here, we report that developmental organochlorine pesticide heptachlor alters dopamine system and increases neurotoxicity in an animal model Exposure pregnant mice led increased levels transporter (DAT) vesicular monoamine 2 (VMAT2) at both protein mRNA level their offspring. Increased DAT VMAT2 were accompanied by alterations nuclear transcription factors control neuron regulate adulthood. At 12 weeks age, heptachlor-exposed offspring administered moderate dose (2× 10 mg/kg) parkinsonism-inducing agent MPTP. Greater evidenced greater loss striatal potentiation glial fibrillary acidic α-synuclein was observed The male than female offspring, suggesting males are more susceptible long-term effects exposure. These data suggest causes thereby rendering it dopaminergic damage