In vitro effects induced by diesel exhaust at an air-liquid interface in a human lung alveolar carcinoma cell line A549.

Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie

PubMedID: 25983017

Okubo T, Hosaka M, Nakae D. In vitro effects induced by diesel exhaust at an air-liquid interface in a human lung alveolar carcinoma cell line A549. Exp Toxicol Pathol. 2015;.
The present study examined the effects induced in vitro in human adenocarcinoma-derived alveolar basal epithelial A549 cells by diesel particulate matter (DPM) administered into the culture medium or by diesel exhaust administered at an air-liquid interface. When A549 cells were exposed to DPM in the culture medium, cell proliferation was inhibited at doses of 10-100µg/mL; generation of interleukin (IL)-8 and the antioxidant enzyme, heme oxygenase-1 (HO-1), were inhibited at a dose of 100µg/mL, and hydroxyl radicals were produced, but could be inhibited by catalase or superoxide dismutase. In contrast, when A549 cells were exposed to diesel exhaust, cell proliferation was inhibited in the absence, but not in the presence, of a diesel particulate filter (DPF); in the absence of a DPF IL-8 was produced in the same amount as in the control cells but was suppressed in the presence of a DPF; HO-1 mRNA was transiently over-expressed in the presence of a DPF, and it was also increased slightly produced in the absence of a DPF but statistically not significant in the presence of a DPF, and it was also increased slightly produced in the absence of a DPF but statistically not significant; HO-1 was transiently produced independent of the absence or the presence of a DPF; and hydroxyl radicals were weakly produced, even in the presence of a DPF but could be inhibited by catalase or superoxide dismutase. It is thus suggested that oxidative stress may be induced by exposure to DPM or diesel exhaust and thereby exerts cytotoxic effect. The introduction of a DPF is effective to protect cells from the toxicity of diesel exhaust presumably by suppression of an oxidative stress.