Oxygen metabolism and mitochondrial function in the lung and heart after exposure to residual oil fly ash

EVELSON, PABLO; MAGNANI, NATALIA; MARCHINI, TIMOTEO; ALVAREZ, SILVIA

Fly Ash: Chemical Composition, Sources and Potential Environmental Impacts

Nova Science Publishers Inc

Lugar: New York; Año: 2013; p. 363 - 377

There is strong evidence that ambient air particulate matter (PM) currently present a serious risk to human health. Epidemiological studies have established a direct correlation between the levels of these particles and acute morbidity and mortality from cardiopulmonary diseases. Human and animal models have shown a pulmonary and systemic inflammatory response and oxidative stress associated with the exposure to environmental particles which could, in turn, alter heart oxygen metabolism and cardiovascular function. Increased production of reactive oxygen species leading to oxidative damage have been suggested to significantly contribute to the cardiopulmonary toxicity of PM inhalation. Because of the unique composition of Residual Oil Fly Ashes (ROFA), especially rich in metals, it is the most frequently PM surrogate to evaluate their role in many biological studies. Tissue injury after ROFA inhalation has been suggested to be triggered by local reactive oxygen species production which, in turn, could be generated not only from the particles themselves, but from chemicals coated on their surface as well. Moreover, oxygen-derived free radicals may also be generated by the interaction of particulate pollutants and their components, with cellular enzymes and organelles. It is well established that mitochondria represent an important modulator of the cellular response to a wide variety of metabolic and environmental stressors. Moreover, superoxide anion is produced by this organelle under normal physiological conditions as a by-product of redox reactions during electron transport in the respiratory chain. Therefore, in addition to serving as an oxidant production source, mitochondria are highly susceptible to reactive oxygen species, which could also indirectly perturb the organelle function. Considering that tissue injury mediated by reactive oxygen species appears to be a key mechanism in the observed damage triggered by exposure to ROFA, oxygen metabolism and mitochondrial function are important areas of study for clarifying the molecular mechanisms involved in this process.