Assessing the effects of atmospheric pollution on mitochondrial stability in human cells

• Grant number: 24/07910-7
• Support Opportunities: Regular Research Grants
• Start date: October 01, 2024
• End date: September 30, 2026
• Field of knowledge: Biological Sciences - Biochemistry - Metabolism and Bioenergetics
• Principal Investigator: Nadja Cristhina de Souza Pinto
• Grantee: Nadja Cristhina de Souza Pinto
• Host Institution: Instituto de Química (IQ). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated researchers: Guilherme Martins Pereira

Abstract

The human and environmental cost of anthropogenic air pollution is enormous and, likely, still underestimated. Mitigating the environmental and human health effects of air pollution depends, primarily, on actions to reduce exposure, but also on a clear understanding of the biological targets and molecular effects of pollutants that could support strategies for monitoring, prevention, and protection. Several cellular and molecular targets for the citotoxic mechanisms of air pollution components have already been identified, and some are in fact used as exposure biomarkers. However, the complexity of the systemic effects of exposure suggests that other cellular targets may play a relevant role in air pollution toxicity. Mitochondria are essential organelles in eukaryotic cells, and mitochondrial dysfunction is causally associated with numerous human diseases relevant to public health and aging. Despite their central role in cellular homeostasis, little is known about the effects of air pollution components on the structural and functional stability of mitochondria, with controversial results in the literature on these effects. In this context, this project proposes to investigate the effect of air pollution components on mitochondrial genomic stability, bioenergetic, and signaling function, using defined components and environmental samples of air pollution, with the aim of defining molecular targets and key citotoxic agents. The results obtained in this study should significantly expand the understanding of air pollution toxicity and contribute to monitoring and prevention strategies. (AU)