Balance of Glutathione-Related Processes in Alveolar Macrophages Under Exposure to Suspended Particulate Matter of Atmospheric Air in of Wistar Rats

Abstract

Introduction. Air suspended particulate matter (SPM) directly influence on the human respiratory system. Dispersion is one of the characteristics of SPM determining their pathogenicity. Alveolar macrophages (AMs) produce reactive oxygen species in response to an exposure that may lead to oxidative stress. The aim of the study. To assess the contribution of the glutathione antioxidant system to the protection of AMs from oxidative stress induced by air SPMs in Vladivostok’s districts with various man-made loads. Material and methods. AMs were isolated from bronchoalveolar lavage of 17 Wistar rats. AMs were exposed by model suspensions (MS) for 2 days. MSs were identical air composition of Vladivostok’s districts with insignificant (MS № 1) and high (MS № 2) technogenic load. MS № 1 contained 22% of particles with a diameter of less than 10 µm. MS № 2 contained 70% of particles with a diameter smaller than 10 μm. The levels of malondialdehyde, glutathione and total antioxidant activity in cell culture and culture fluid were determined. Results. The gain in the proportion of fine and ultrafine particles in MS № 2 has been established to lead to an increase in lipid peroxidation in AMs and a compensatory elevation in the antioxidant activity. The elevation of oxidized glutathione concentration in cell culture indicates the intensification of hydroperoxide detoxification by AMs. The reduction of reduced glutathione exocytosis supports intracellular antioxidant processes. Conclusion. An increase in the fraction of fine and ultrafine particles in the air appears to shift AM redox balance towards oxidative stress, contributing to the formation and the progression of pathological disorders.

Effects Of Atmospheric Suspended Particulate Matter On The Immune System

“…We emphasize that activation of the NF-κB pathway is the key process initiating the cascade of reactions [54,67,68]. There is evidence that in patients with COPD, SPM of micro-sized fractions contributes to the modulation of the IL-6 signaling pathway in the direction of conventional signal transduction to T helper blood cells to regulate the inflammatory process and compensate for apoptotic changes [53]. Exposure to air microtoxicants also leads to a significant increase in IL-4 levels [83].…”

“…The thioredoxin system ensures the restoration of disulfide bonds in proteins damaged by oxidation. Another example of redox regulation is the activation of the transcription factor NF-κB by cytosolic thioredoxin, which regulates the immune response, apoptosis and the cell cycle [53][54][55][56][57].…”

“…It is involved in the detoxification of hydrogen peroxide by various glutathione peroxidases, helping to protect cell membranes from oxidative stress. Glutathione activates a number of signaling pathways, including those associated with the transcription factor NF-κB and MAPKs [53][54][55][56].…”

“…Important participants in the cytokine regulation under the influence of SPM are IL-4 and IL-6. It has been shown that both short-term and long-term exposures to SPM lead to a dosedependent increase in IL-6 production [14,53,[80][81][82]. Under the influence of SPM, the increase in IL-6 expression is regulated by the TLR2 and TLR4/NADPH oxidase/ROS/NF-κB signaling pathways.…”

Estimation of the Size Distribution of Suspended Particulate Matters in the Urban Atmospheric Surface Layer and Its Influence on Bronchopulmonary Pathology

“…It has been hypothesized that PMs induce oxidative stress through several different mechanisms. Firstly, the oxidation-reduction cycle of some components absorbed on the particle surface, such as iron or quinones, leads to the generation of ROS, hydrogen peroxide, and a damaging hydroxyl radical in the lungs [32]. Secondly, particle-attached bacterial endotoxins can cause inflammation [33,34].…”