한빛사논문
- 조회369
Soyeon Jeon, Sung-Hyun Kim, Jiyoung Jeong, Dong-Keun Lee, Sinuk Lee, Songyeon Kim, Gyuri Kim, Muchuchamy Maruthupandy, Wan-Seob Cho*
Lab of Toxicology, Department of Health Sciences, The Graduate School of Dong-A University, 37, Nakdong-daero 550 beon-gil Saha-gu, Busan 49315, Republic of Korea
*Corresponding author.
Abstract
Pulmonary alveolar proteinosis (PAP) has been reported in rodents treated with nanoparticles (NPs). However, little is known about the type of NPs producing PAP and their toxicity mechanisms. Here, we assembled seven PAP-inducing NPs and TiO2 NPs as a negative control. At 1 and 6 months after a single intratracheal instillation in rats, pulmonary inflammation and the gene expression of ATP-binding cassette (ABC) transporters and related genes were evaluated in separated alveolar macrophages (AMs). One month after intratracheal instillation, seven NPs (Eu2O3, In2O3, Pr6O11, Sm2O3, Tb4O7, and NiO) caused PAP, but only In2O3 NPs caused persistent PAP at 6 months after treatment. The levels of phospholipids, indicators of PAP, showed good correlations with the gene expression profile of five transporters (ABCA1, ABCB4, ABCB8, ABCG1, and ABCG4), which effluxing phospholipids in AMs. Among them, ABCG1 and ABCG4 might be key transporters involved in PAP development because both showed a negative correlation with the magnitude of PAP, while others might be compensatory transporters for PAP recovery, as they showed a positive correlation. In conclusion, the identification of seven PAP-producing NPs implies that PAP may be an emerging occupational disease and that ABCG1 and ABCG4 may be therapeutic targets for PAP.
논문정보
- Research article
- 2021년 07월 (BRIC 등록일 2021-08-19)
- 국내 연구진
- 의약학 > 응용의학
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