Research reportAlpha synuclein protein is involved in Aluminum-induced cell death and oxidative stress in PC12 cells

- Aluminum maltolate induced apoptosis in PC12 cells.
- Aluminum maltolate increased oxidative stress in PC12 cells.
- Aluminum maltolate did not affect basal expression of α-syn protein.
- Knockdown of α-syn expression inhibited Almal-induced apoptosis in PC12 cells.
- Knockdown of α-syn expression inhibited Almal-induced oxidative stress in PC12 cells.

Increased expression and aggregation of α-synuclein (α-syn) protein plays a critical role in mediating the toxic effects of a number of neurodegenerative substances including metals. Thus, knockdown expression of α-syn is proposed as a possible modality for treatment of Parkinson disease (PD). Aluminum (Al) is a neurotoxic metal that contributes to pathogenesis of PD. The aim of this study was to investigate the role of α-syn protein in mediating Al-induced toxicity in PC12 cells. Specific α-syn small interference RNA (siRNA) was applied to knockdown the expression of α-syn protein in PC12 cells. The effects of different concentrations of Al-maltolate (Almal) were then evaluated on cell viability and oxidative stress in the α-syn downregulated cells. The results showed that Almal dose dependently induced apoptosis and increased malondialdehyde (MDA) and catalase activity in PC12 cells. Downregulation of α-syn protein significantly increased cell viability and decreased oxidative markers in Almal-treated cells. These findings suggest that α-syn protein may mediate Al-induced apoptosis and oxidative stress in PC12 cells.