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[Changes of cdk5, p35 and p53 gene expression levels in arsenic-induced neural cell apoptosis]
Xin Li1, Hong-mei Zhang, Qiao Niu
1Department of Radiation Health, Control of Disease Control of Taiyuan Iron Steel Company, Taiyuan 030003, China.
Objective:
To study the expression levels of cdk5, p35 and p53 genes in arsenic trioxide (As2O3O)-induced neuron apoptosis and to explore the potential mechanism.
Methods:
The cultured primary rats' neurons were divided into 5 groups, which were exposed to 0, 1, 5, 10 micromol/L As2O3 and dimethyl sulfoxide (DMSO) for 8 h, respectively. The cell viability and cell apoptosis were detected by MTT colouration methods and flow cytometry, respectively. The real-time fluorescence quantitative PCR was used to measured the expression levels of cdk5, p35 and p53 genes.
Results:
The cell viability inhibition rates were 16.77%, 19.72% and 27.81% in 1, 5, 10 micromol/L As203 groups, respectively. Compared to the untreated group and DMSO group, the cell apoptosis rates were significantly increased in 5 and 10 micromol/L As2O3 groups (P < 0.05). The expression levels of cdk5, p35 and p53 genes increased with the exposure doses of AsO3. However, there were no significant differences in p35 gene expression between different dose subgroups (P > 0.05). There were significant differences in cdk5 and p53 gene expression between different dose subgroups (P < 0.05). The expression levels of cdk5 gene in 5 and 10 micromol/L As2O3 groups were significantly higher than those in untreated group and DMSO group (P < 0.05). The expression levels of p53 gene in 1, 5 and 10 micromol/L As2O3 groups were significantly higher than that in untreated group (P < 0.05). The expression level of p53 gene in 10 mciromol/L As2O3 group was significantly higher than that in DMSO group (P < 0.05).
Conclusion:
Cdk5, p35 and p53 genes may involve in the process of As2O3-induced neural cell apoptosis.
Insights
Arsenic trioxide (As2O3) exposure increases neuron apoptosis by upregulating cdk5 and p53 gene expression. These findings suggest a role for these genes in As2O3-induced neural cell death.
Area of Science:
- Neuroscience
- Toxicology
- Molecular Biology
Background:
- Arsenic trioxide (As2O3) is a toxicant with known neurotoxic effects.
- Neuron apoptosis is a critical process in neurodegenerative diseases and toxicant-induced neuronal injury.
Purpose of the Study:
- To investigate the expression levels of cyclin-dependent kinase 5 (cdk5), p35, and p53 genes in arsenic trioxide-induced neuron apoptosis.
- To elucidate the potential molecular mechanisms underlying As2O3-induced neurotoxicity.
Main Methods:
- Primary rat neurons were exposed to varying concentrations of As2O3 (0, 1, 5, 10 micromol/L).
- Cell viability was assessed using MTT assays, and apoptosis was quantified by flow cytometry.
- Gene expression levels of cdk5, p35, and p53 were measured using real-time fluorescence quantitative PCR.
Main Results:
- As2O3 exposure significantly increased neuron apoptosis in a dose-dependent manner at concentrations of 5 and 10 micromol/L.
- Expression of cdk5 and p53 genes was significantly upregulated in response to As2O3 exposure.
- While p35 gene expression showed a trend of increase, significant differences were not observed between dose subgroups.
Conclusions:
- The study suggests that cdk5 and p53 genes are involved in the mechanism of arsenic trioxide-induced neural cell apoptosis.
- These findings contribute to understanding the molecular pathways of As2O3 neurotoxicity.
