Ammonia exposure induces oxidative stress and inflammation by destroying the microtubule structures and the balance of solute carriers in the trachea of pigs.

Ammonia (NH3) is the most alkaline gaseous compound in the atmosphere and the primary gas pollutant in the piggery. It can cause irritation and damage to the airway after inhalation. However, the effects and toxicity mechanism of NH3 on the trachea are still unclear. In order to evaluate the toxic effects of NH3 inhalation on pig trachea, the changes of oxidative stress parameters (SOD, GSH, GSH-Px, and MDA), tissue structure and transcriptome in the trachea of pigs were examined after 30 days of exposure to NH3. Our results showed SOD, GSH-Px and GSH in the trachea in the NH3-treatment group were significantly decreased (P < 0.05) compared with the control group, on the contrary, MDA content was significantly higher (P < 0.05). The analysis of differentially expressed genes (DEGs) showed that 2542 DEGs (1109 up-regulated DEGs and 1433 down-regulated DEGs) were significantly changed under NH3 exposure, including many DEGs associated with inflammation, oxidative stress, microtubule activity and SLC family, and the qRT-PCR verification results of these DEGs were consistent with the transcriptome results. The results indicated that NH3 exposure could break down the mucosal barrier of the respiratory tract, induce oxidative stress and inflammation, reduce the activity of microtubules and disrupt the balance of SLC transporters. In this study, transcriptome analysis was used for the first time to explore the toxic mechanism of NH3 on pig trachea, providing new insights for better assessing the toxicity mechanism of NH3, as well as references for comparative medicine.