ABSTRACT Objective: Epidemiological studies have found that lead exposure increases the risk for Park-inson’s disease and patients with Parkinson’s disease have lower odds of developing non-smoking-related cancer (1). It would be inter-esting therefore to find the molecular links be-tween Parkinson’s disease and cancer. To do this, we studied mRNA expression of alpha-synuclein gene, a promising genetic marker for Parkinson’s disease, and expression of the tu-mor suppressor gene p53 after oxidative stress induced by lead. Methods: We used ATDC5 cell line as a model of tumor and treated by lead nitrate for 0, 2, 4, 16, 24 and 48 hours. The mRNAs of alpha-synuclein and p53 were quan-tified by reverse transcriptase polymerase chain reaction and expressed as mean (&#177;SD) for 3 samples at each time point. Results: Ex-pression of both of alpha-synuclein and p53 mRNA increased with increasing exposure of lead treatment. The levels of alpha-synuclein and p53 mRNA were correlated with each other (r=0.9830; P&lt;0.001). Conclusion: We propose that lead’s neurotoxicity in PD is caused by al-pha-synuclein expression and aggregation, which releases the inhibitory influence of al-pha-synuclein on p53 expression, thereby al-lowing p53 to act as the cell’s guardian of the genome and reduce tumorigenic potential. Treatments that reduce alpha-synuclein aggre-gation may need to account for a concomitant reduction in p53’s protective effect.
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nullZuo, P. and Rabie, A. (2009) Effects of lead exposure on alpha-synuclein and p53 transcription. Journal of Biomedical Science and Engineering, 2, 86-89. doi: 10.4236/jbise.2009.22016.
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