EN
INTRODUCTION: A number of literature reports pointed out a connection between neurodegenerative disorders morbidity and air pollution with particulate matter (PM) containing transition metals. PM exerts their effect by activation of immune system and oxidative stress induction. AIM(S): The aim of this study was to assess whether exposure to PM is associated with proinflammatory activation of macrophagal cells and negative neuronal cells condition including reactive oxygen species (ROS) generation. METHOD(S): Particulate matter NIST1648A (standard material) and LAp120 (NIST1648A devoid of organic components) were investigated for their biological potency in mouse macrophagal cell line RAW 264.7 and in human neuronal cell line SH-SY5Y. It was assessed using metabolic activity assay (resazurin reduction (RES) test), ROS generation assay (DCFH-DA test), nitric oxide (NO) synthesis and superoxide anion (O2-) release (NBT reduction test). RESULTS: At highest concentration (100 μg/ml) and longest incubation time (48 h), NIST1648A slightly increased metabolic activity, NO synthesis and O2-release in macrophagal cells. In these conditions LAp120 decreased metabolic activity and O2‑release without influence of NO synthesis. Both forms of PM shortly increased the ROS generation. In neuronal cells both forms of the PM resulted in increase of ROS generation and decreased metabolic activity. CONCLUSIONS: The PM tested in this study possess a potential to direct activation of innate immunity and to direct damage of neuronal cells probably by oxidative stress induction. FINANCIAL SUPPORT: The study was supported by APARIC project – NCN grant No. 2015/16/W/ST5/00005, and statutory funds of Institute of Pharmacology Polish Academy of Sciences.