Abstract

The occurrence of micro(nano)plastics into various environmental and biological settings influences their physicochemical and toxic behavior. Simulated body fluids are appropriate media for understanding the degradation, stability, and interaction with other substances of any material in the human body. When the particles enter the human body via inhalation, which is one of the avenues for micro(nano)plastics, they first come into contact with the lung lining fluid under neutral conditions and then are phagocytosed under acidic conditions to be removed. Therefore, it is important to examine the physicochemical transformation and toxicity characteristics after interaction with phagolysosomal simulant fluid (PSF). Here, we focused on exploring how the physicochemical differences (e.g. surface chemistry, elemental distribution, and surface charge) of micro(nano)plastics under pH 4.5 phagolysosome conditions impact cytotoxicity and the oxidative characteristics of lung epithelia cells. The cytotoxicity of lung epithelia cells to those treated with PSF and non-treated micro(nano)plastics was tested by various viability indicators including cell counting kit-8 (CCK-8), MTT, and LDH. Furthermore, the cytotoxicity background was examined through the oxidative processes (e.g. reactive oxygen species, antioxidant, superoxide dismutase (SOD), catalase, and reduced glutathione). The results showed that all tested surface physicochemical characteristics were significantly influenced by the phagolysosome conditions. The staged responses were observed with the treatment duration, and significant changes were calculated in carbonyl, carbon-nitrogen, and sulfonyl groups. Moreover, the negativity of the zeta potentials declined between exposure of 2–40 h and then increased at 80 h compared to control owing to the chemical functional groups and elemental distribution of the plastic particles. The tested viability indicators showed that the micro(nano)plastics treated with PSF were cytotoxic to the lung epithelia cells compared to non-treated micro(nano)plastics, and SOD was the dominant enzyme triggering cytotoxicity due to the particle degradation and instability.

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