Posted on Jun 13, 2018, 7 p.m.
Pesticides have been shown to prevent mitochondria from functioning correctly, leading to cell death in human neurones with increased susceptibility to Parkinson’s Disease, as published in the FASEB Journal.
It has been found that even low levels of pesticide can lead to the development of Parkinson’s disease in those at risk for the development of the condition. Maneb, rotenone, paraquat, and other pesticides have been shown to have an effect on Parkinson’s disease, latest research shows they have an effect carried out under conditions that more closely mimic human physiology. Researchers explain this study is applicable to human cases saying it is the first to investigate what happens inside human cells.
Human stem cells were used with a mutation in the a-synuclein gene associated with increased risk for the condition, and transformed them into dopamine producing neurones. Exposed to pesticides dopamine producing neurons will produce nitric oxide that prevents movement of mitochondria at areas of the nerve cell where needed most. Nitric oxide is involved in modification of microtube structures that normally transport mitochondria around the cell. Mitochondrial lack of transportation can lead to not enough energy being produced to maintain the cell.
Exact causes of Parkinson’s disease is still unclear, it is known that it can develop due to death of dopamine producing neurones in certain areas of the brain and lack of dopamine to the areas, resulting lack of mitochondrial energy causes neurones to die leading to Parkinson’s disease.
Dose of pesticide exposure effect level is lower than previously thought. Results show that with some current laws people with a predisposition to the condition can still be very likely to develop Parkinson’s disease after exposure to the agrochemicals, even at low levels. Production of nitric oxide can be slowed or stopped with use of NOS inhibitors. Nos inhibitor Nw-nitro-L-arginine methyl ester was used during this study to stop the effects of pesticides.
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