Prominent contribution of hydrogen peroxide to intracellular reactive oxygen species (ROS) generated upon exposure to naphthalene secondary organic aerosols (SOA)
Saavedra, Gabriela G.
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Multiple studies have found an association between exposure to particulate matter (PM) and adverse health endpoints. One of the suggested mechanisms in which inhalable particles exert damage is by inducing the overproduction of reactive oxygen and nitrogen species (ROS/RNS). Hydrogen peroxide is one type of ROS that has been implicated in pathological disorders induced by PM exposure. It has also received increasing attention owing to its dominant role in cellular signaling, metabolic processes, and oxidative stress. However, its biological role upon exposure to PM remains unclear. Secondary organic aerosols (SOA) make up a substantial fraction of ambient fine PM and play a role in the proinflammatory effects of the particles. In this study, the contribution of hydrogen peroxide to intracellular ROS/RNS production upon exposure to water-soluble components of SOA generated from the photooxidation of naphthalene in the presence of NOx (PM samples) was investigated using the general oxidative stress indicator carboxy-H2DCF and catalase as a hydrogen peroxyde scavenger. The intracellular ROS/RNS response with and without the addition of catalase to the PM samples was measured, where the presence of catalase substantially suppressed ROS/RNS response. The hydrogen peroxide produced by water-soluble components in the naphthalene SOA extracted in phosphate buffer solution (PBS) was quantified and ranged from 9.04 ± 0.16 to 11.32 ± 0.27 μM, corresponding to a hydrogen peroxide yield of 3.1 to 3.8 ng/µg. The measured hydrogen peroxide was product of interactions between quinone compounds and peroxide compounds in naphthalene SOA and PBS. Additionally, cells exposed to PM samples released hydrogen peroxide at a rate of 0.21 ± 0.01 to 0.26 ± 0.03 pmol/min/104 cells, which was associated with the mediation of immune responses and/or oxidative stress induced by naphthalene SOA exposure. These findings confirmed that hydrogen peroxide was the main ROS produced by cells exposed to naphthalene SOA and that it was the driver of the PM-induced ROS/RNS response, although this contribution can vary depending on the specific SOA precursors and formation conditions. Findings in this study also showed that, in addition to the hydrogen peroxide produced by cells upon exposure to PM samples, the hydrogen peroxide produced by the PM samples upon interaction with the extracting solution could have diffused into the cell and contribute to the intracellular ROS/RNS response. Although future studies are needed to estimate the contribution of both sources of hydrogen peroxide to the intracellular ROS/RNS response, this study highlights that the diffusion of extracellular ROS/RNS into the cells could represent one of the pathways in which exposure to PM leads to oxidative stress.