Permethrin, a member of the family of synthetic pyrethroids, can inducespecific conditions typical in neurons affected by Parkinson Disease (PD). Among these, an impairment in expression of Nurr1, a transcription factor essential for the maintenance of dopaminergic neuronshas been observed. Considering that the primary source of exposure to permethrin is diet, we are interested in evaluating if other components of diet,in particular tocotrienols, could be able to exert a protective effect towards this neurological damage. Tocotrienols, members of the vitamin E family, are natural compounds (found in a number of vegetable oils, wheat germ, barley, and certain types of nuts and grains) that has been shown to exhibit important biological activities such as neuroprotective, anti-cancerand anti-inflammatory. Given that, we evaluatedin vitro effects of tocotrienols (extracted fromElaesisguineensison oil)on PC12 cells culture treated with permethrin. PC12 cells were seeded and treated for 72h with permethrin 1uM,alone or combined with 1uM of tocotrienols. Then, RT-PCR was performed to evaluate Nurr1 gene expression. In cells cultures under stress condition, such as those induced by permethrin, Nurr1 gene expression increases, maybe as a compensatory effect to damage. In contrast, when cells are co-treated with tocotrienols, this increase does not occur. We hypothesized that tocotrienolscan prevent cells over reaction to oxidative stress and downregulate the expression of Nurr1 gene. Pesticides, mainly assumed with diet, can modulate gene expression leading to the onset and progression of age-related diseases and permethrin, in particular, can induce stress in neuronal dopaminergic cells mimicking PD condition. Hence, the present study shows that tocotrienolscouldcounterbalance in vitrocellular damage induced by permethrin, indicating tocotrienols supplementation or food enrichment as possible waysto remediate or to reduce oxidative damages induced by food contaminants.

Tocotrienol protective effect on neuronal damage induced by permethrin in PC12 cells

BORDONI, LAURA;NASUTI, Cinzia Carla;GABBIANELLI, Rosita
2016-01-01

Abstract

Permethrin, a member of the family of synthetic pyrethroids, can inducespecific conditions typical in neurons affected by Parkinson Disease (PD). Among these, an impairment in expression of Nurr1, a transcription factor essential for the maintenance of dopaminergic neuronshas been observed. Considering that the primary source of exposure to permethrin is diet, we are interested in evaluating if other components of diet,in particular tocotrienols, could be able to exert a protective effect towards this neurological damage. Tocotrienols, members of the vitamin E family, are natural compounds (found in a number of vegetable oils, wheat germ, barley, and certain types of nuts and grains) that has been shown to exhibit important biological activities such as neuroprotective, anti-cancerand anti-inflammatory. Given that, we evaluatedin vitro effects of tocotrienols (extracted fromElaesisguineensison oil)on PC12 cells culture treated with permethrin. PC12 cells were seeded and treated for 72h with permethrin 1uM,alone or combined with 1uM of tocotrienols. Then, RT-PCR was performed to evaluate Nurr1 gene expression. In cells cultures under stress condition, such as those induced by permethrin, Nurr1 gene expression increases, maybe as a compensatory effect to damage. In contrast, when cells are co-treated with tocotrienols, this increase does not occur. We hypothesized that tocotrienolscan prevent cells over reaction to oxidative stress and downregulate the expression of Nurr1 gene. Pesticides, mainly assumed with diet, can modulate gene expression leading to the onset and progression of age-related diseases and permethrin, in particular, can induce stress in neuronal dopaminergic cells mimicking PD condition. Hence, the present study shows that tocotrienolscouldcounterbalance in vitrocellular damage induced by permethrin, indicating tocotrienols supplementation or food enrichment as possible waysto remediate or to reduce oxidative damages induced by food contaminants.
2016
23412240
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11581/399103
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