Acute exposure to diesel-biodiesel particulate matter promotes murine lung oxidative stress by Nrf2/HO-1 and inflammation through the NF-κB/TNF-α pathways

Abstract

Air pollution caused by diesel burning contributes to respiratory impairments that may lead to death. In Brazil, biodiesel has been added to regular diesel. This mixture of diesel-biodiesel (DB) fuel has been used in buses and trucks to reduce air pollution. However, no study has demonstrated whether DB reduces the burden of diesel burning on pulmonary parenchyma. Therefore, we aimed to investigate the outcomes of the exposure of murine lungs to DB particulate matter from fuel burning by public transport in Rio de Janeiro City. DB particulate matter was collected from the exhaust pipes of a bus engine. Female C57BL/6 mice were treated with 250 μg or 1000 μg of DB particulate matter by intranasal instillation over five consecutive days. We demonstrated that DB particulate matter penetrated the lung in the 250 μg and 1000 μg groups. In addition, the DB particulate matter number in pulmonary parenchyma was 175-fold higher in the 250 μg group and 300-fold higher in the 1,000 μg group compared to control mice. The instillation of DB particulate matter increased the macrophage number and protein levels of tumor necrosis factor-α in murine lungs. DB particulate matter enhanced reactive oxygen species production in both exposed groups and the malondialdehyde levels compared to the control group. Expression of the glutamate cysteine ligase modifier subunit was lower in the 250 μg group than in the control group and was reduced in the 1000 μg group compared to the control and 250 μg groups. The protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2), nuclear factor κappa B (NF-κB) and heme oxygenase-1 (HO-1) were higher in the 250 μg group and lower in the 1,000 μg group than in control mice and the 250 μg group. In conclusion, DB particulate matter instillation promotes oxidative stress by activating the Nrf2/HO-1 and inflammation by NF-κB/TNF-α pathways.