Abstract

Introduction. Currently, there is evidence of a triggering role of environmental factors in developing rheumatoid arthritis (RA). The purpose of this work was to investigate the role of oxidative stress in provoking the preclinical stage of RAf in susceptible individuals and its possible relationship with the effects of ecotoxicants. Materials and methods. Examination of cases collecting biosamples was carried out during rheumatologic examination of the persons in the regional hospitals of 45 administrative districts of the Republic of Tatarstan (RT), Russia. Serum markers of oxidative stress were measured, namely levels of oxidized proteins, oxidized lipids, oxyguanine, and antibodies to oxidized LDL. The environmental parameters of residences of the persons included in the project were measured. Information was collected on the parameters of the environmental situation in the administrative districts of the Republic of Tatarstan in 2008-2018 (from publicly available reports of the Ministry of Ecology of the Republic of Tatarstan). Results. There was performed a comparison of the levels of oxidative markers in samples from individuals living in regions with the highest and lowest concentrations of certain atmosphere ecotoxicants, including carbon monoxide, hydrocarbons (volatile organic compounds (VOCs) free), particulate matter, VOCs, sulfur dioxide, and nitrogen oxide. The levels of oxidized proteins and oxidized LDL were significantly higher in residents of areas with the highest carbon monoxide and VOCs compared to residents of areas with the lowest content of these substances. The contribution of environmental indicators to the provocation of the anti-LDG antibody production in groups with genetic and preclinical RA stages was revealed to account for 40%. According to the results of multiple regression analysis, in individuals from the above groups and individuals at early RA stage, the levels of oxidized LDL and oxidized proteins depended on the effect of a combination of certain environmental factors. Limitations. In this article, we limited ourselves to the analysis of the RA association with air pollution indices. The study of other environmental factors (soil, water pollution, radiation levels) is ongoing. This will allow clarifying the specific mechanisms of the influence of the exposome on the development of the disease in total. In addition, the conclusions presented are speculative since the identified patterns were obtained by analyzing data in the limited data samples. Conclusion. Since environmental factors can be considered modifiable to a certain extent, the study of their role in the RA development and specific mechanisms of the disease triggered by these factors on persons at risk are of fundamental and applied importance.

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