Abstract
Acrolein (Acr) is a reactive aldehyde in the environment. Acr causes oxidative stress and a cascade of catalytic events and has, thereby, been associated with increased risk of pulmonary diseases. Whether apiaceous vegetables (API) consumption can prevent Acr-induced pulmonary toxicity has not yet been explored hence, we investigated the effects of API on Acr-induced pulmonary damages in C57BL/6J mice. The mice were assigned into either negative control [NEG group; American Institute of Nutrition (AIN)-93G diet only], positive control (POS group; AIN-93G+Acr) or API intervention group (API group; AIN-93G+21% API+Acr). After 1 week of dietary intervention, the POS and API mice were exposed to Acr (10 µmol/kg body weight/day) for 5 days. During the exposure period, assigned diets remained the same. Prominent indicators lung of toxicity of POS mice were found, including mucus accumulation, macrophage infiltration, and hemorrhage, all of which were ameliorated by the API. Serum and lung inflammation markers, such as a tumor necrosis factor alpha were also increased by Acr while reduced by API. In the liver, API upregulated expression of glutathione S-transferases, which enhanced the metabolism of Acr into water-soluble 3-hydroxypropyl mercapturic acid for excretion. This is consistent with observed reductions in serum Acr-protein adducts. Taken together, our results suggest that API may provide protection against Acr-induced pulmonary damages and inflammation via enhancement of the hepatic detoxification of Acr.