GIST Scholar
College of Life Sciences and Medical Engineering
Department of Biomedical Science and Engineering
1. Journal Articles
Catalase deficiency induces reactive oxygen species mediated pexophagy and cell death in the liver during prolonged fasting
- Type
- Article
- Citation
- BIOFACTORS, v.47, no.1, pp.112 - 125
- Issued Date
- 2021-01
- Abstract
- Peroxisomes are dynamic organelles that participate in a diverse array of cellular processes, including beta-oxidation, which produces a considerable amount of reactive oxygen species (ROS). Although we showed that catalase depletion induces ROS-mediated pexophagy in cells, the effect of catalase deficiency during conditions that favor ROS generation remains elusive in mice. In this study, we reported that prolonged fasting in catalase-knockout (KO) mice drastically increased ROS production, which induced liver-specific pexophagy, an autophagic degradation of peroxisomes. In addition, increased ROS generation induced the production of pro-inflammatory cytokines in the liver tissues of catalase-KO mice. Furthermore, there was a significant increase in the levels of aspartate transaminase and alanine transaminase as well as apparent cell death in the liver of catalase-KO mice during prolonged fasting. However, an intra-peritoneal injection of the antioxidant N-acetyl-l-cysteine (NAC) and autophagy inhibitor chloroquine inhibited the inflammatory response, liver damage, and pexophagy in the liver of catalase-KO mice during prolonged fasting. Consistently, genetic ablation of autophagy, Atg5 led to suppression of pexophagy during catalase inhibition by 3-aminotriazole (3AT). Moreover, treatment with chloroquine also ameliorated the inflammatory response and cell death in embryonic fibroblast cells from catalase-KO mice. Taken together, our data suggest that ROS-mediated liver-specific pexophagy observed during prolonged fasting in catalase-KO mice may be responsible for the process associated with hepatic cell death.
- Publisher
- WILEY
- ISSN
- 0951-6433
- Appears in Collections:
- Department of Biomedical Science and Engineering > 1. Journal Articles
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