Program

PO3-13-25

Nickel chloride suppresses cell proliferation and induces G2/M cell-cycle arrest in cultured human astrocytes

[Speaker] Ruedeemars Yubolphan:1
[Co-author] Pornpun Vivithanaporn:1
1:Department of Pharmacology, Faculty of Science, Mahidol University, Bangkok, Thailand

Background: Nickel, an environmental pollutant, can be deposited in the human body through occupational exposure and dietary. Welders exposed to nickel fume showed cognitive impairment and children drinking nickel-contaminated water displayed learning disability. Astrocytes, the most abundant glial cells in the brain, play a prominent role in the protection of other brain cells from toxins and oxidants. Astrocyte proliferation is important in the detoxification and repairment processes. Heavy metals, including cadmium, manganese, mercury, and arsenic, are toxic to astrocytes and impair astrocyte functions. Nickel is toxic to neurons, while nickel toxicity in astrocytes has not been reported. The present study aims to determine the effect of nickel in cell proliferation and cell cycle of human astrocytes.
Method: U-87 MG human astrocytoma cells were exposed to 50, 100, and 500 µM nickel chloride (NiCl2). Cell proliferation was determined by monitoring CFSE fluorescent intensity. Cell cycle was examined by measuring DNA content in the cells using propidium iodide staining. A minimum of 10,000 events/sample was analyzed using a BD Accuri C6 flow cytometer (BD Bioscience).
Results: At 96 hours post-exposure, NiCl2 increased the mean CFSE fluorescent intensity in a dose-dependent manner, indicating that nickel suppressed cell proliferation of cultured astrocytes. 100 and 500 µM NiCl2 increased percentage of cells in G2/M phase and decrease percentage of cells at G0/G1 phase at 48 hours post-exposure.
Conclusion: Our finding indicated that nickel suppresses cell proliferation of astrocytes through inducing G2/M phase arrest.

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