Incense Aerosol-Induced Neurotoxicity Disrupts α-Synuclein Homeostasis in a Cellular Parkinson's Disease Model, Distinct from Cigarette Aerosols.
In alpha‑synuclein–overexpressing SH‑SY5Y cells, incense aerosol extracts—particularly the organic phase—induce ROS‑linked mitochondrial dysfunction, programmed cell death, and a shift of alpha‑synuclein from oligomers to monomers, with limited rescue by classical antioxidants compared with…
What the AI sees
In alpha‑synuclein–overexpressing SH‑SY5Y cells, incense aerosol extracts—particularly the organic phase—induce ROS‑linked mitochondrial dysfunction, programmed cell death, and a shift of alpha‑synuclein from oligomers to monomers, with limited rescue by classical antioxidants compared with…
Research significance
Points to incense smoke as a distinct environmental driver of alpha‑synuclein mis‑homeostasis and mitochondrial injury, offering mechanistic targets and the rationale that PD interventions may need to address non‑canonical toxicants/mechanisms beyond general antioxidant strategies.
Source abstract
Incense burning is a widespread indoor combustion practice, yet its neurotoxic potential and impact on α-synuclein (α-Syn) proteostasis remain poorly defined. Using SH-SY5Y cells overexpressing α-Syn as a cellular Parkinson's disease model, we exposed cells to size-fractionated incense aerosol extracts (IAE) prepared as organic-phase (OP) or water-soluble phase (WP). α-Syn overexpression augmented vulnerability to IAE, producing greater losses in viability and pronounced increases in intracellular hydrogen peroxide (H2O2), mitochondrial membrane potential depolarization, and engagement of programmed cell-death pathways. Live-cell fluorescence cross-correlation spectroscopy (FCCS) revealed that both OP-IAE and WP-IAE shifted α-Syn from oligomeric to monomeric states in the cytosol, indicating disruption of oligomerization equilibrium. Antioxidant intervention revealed mechanistic differences compared with other indoor air pollutants, cigarette smoke. OP-IAE-induced cytotoxicity cannot be mitigated by N-acetylcysteine (NAC) or rutin, whereas WP-IAE-induced toxicity was partially attenuated, with NAC surpassing rutin. By contrast, for cigarette aerosol extracts (CAE), both OP- and WP-CAEs were robustly rescued by NAC and, to a lesser extent, rutin. Together, these results indicate that incense aerosols, particularly OP-IAE, engage reactive oxygen species (ROS)-linked mitochondrial injury and programmed cell-death pathways while uniquely driving α-Syn monomerization, while exhibiting relative resistance to classical antioxidant intervention compared with cigarette aerosols. This work points out incense smoke as a distinct indoor neurotoxicant with implications for α-Syn homeostasis and Parkinsonian risk in exposed populations.