Aluminum maltolate induced cellular stress is associated with ER stress related responses and alterations in NMDAR2B levels: Modulatory effects of coenzyme Q10.

Chronic aluminum (Al) exposure has been implicated as a significant environmental risk factor in the development and progression of neurodegenerative diseases. This study aimed to investigate the Al maltolate (Al-Malt) induced cellular stress responses in SH-SY5Y cells in vitro by evaluating the changes in endoplasmic reticulum (ER) stress related markers and NMDAR2B levels, and to assess the modulatory effects of coenzyme Q10 (CoQ10). Cellular viability and metabolic activity following exposure to Al-Malt were assessed using the MTT assay. NMDAR2B levels were measured by the ELISA, while GRP78 and CHOP mRNA expression levels, which are ER stress biomarkers, were analyzed by the RT-PCR. 250 and 500 μ Al-Malt exposure resulted in reduced cellular viability and metabolic activity by approximately ∼18% and ∼ 30% respectively. GRP78 mRNA expression increased ∼2.2 and ∼ 2.6 fold, while CHOP mRNA expression increased by ∼1.86 and ∼ 2.31 fold at 250 and 500 μ Al-Malt, respectively. NMDAR2B levels decreased by approximately ∼26% and ∼ 40% compared to control. CoQ10 pretreatment attenuated these cellular responses. These findings suggest an association between Al exposure, ER stress related responses, and alterations in NMDAR2B levels in an in vitro neuronal model, and indicate that CoQ10 may modulate Al-induced cellular stress. However, further studies using primary neuronal cultures and in vivo models are warranted to validate and extend these results.