دورية أكاديمية
NAD(P)H-quinone oxidoreductase 1 induces complicated effects on mitochondrial dysfunction and ferroptosis in an expression level-dependent manner.
| العنوان: | NAD(P)H-quinone oxidoreductase 1 induces complicated effects on mitochondrial dysfunction and ferroptosis in an expression level-dependent manner. |
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| المؤلفون: | Lee J; Department of Life Science, Ewha Womans University, Seoul, South Korea., Hyun DH; Department of Life Science, Ewha Womans University, Seoul, South Korea. |
| المصدر: | Bioscience trends [Biosci Trends] 2024 Jun 06; Vol. 18 (2), pp. 153-164. Date of Electronic Publication: 2024 Apr 10. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: International Research and Cooperation Association for Bio & Socio-Sciences Advancement Country of Publication: Japan NLM ID: 101502754 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1881-7823 (Electronic) Linking ISSN: 18817815 NLM ISO Abbreviation: Biosci Trends Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Tokyo : International Research and Cooperation Association for Bio & Socio-Sciences Advancement |
| مواضيع طبية MeSH: | NAD(P)H Dehydrogenase (Quinone)*/metabolism , NAD(P)H Dehydrogenase (Quinone)*/genetics , Ferroptosis*/drug effects , Mitochondria*/metabolism , Mitochondria*/drug effects , Rotenone*/toxicity , Rotenone*/pharmacology, Humans ; Cell Line, Tumor ; Cell Survival/drug effects ; Lipid Peroxidation/drug effects ; Piperazines/pharmacology ; Carbolines |
| مستخلص: | NAD(P)H-quinone oxidoreductase 1 (NQO1) is an essential redox enzyme responsible for redox balance and energy metabolism. Despite of its importance, the brain contains high capacity of polyunsaturated fatty acids and maintains low levels of NQO1 expression. In this study, we examined how levels of NQO1 expression affects cell survival in response to toxic insults causing mitochondrial dysfunction and ferroptosis, and whether NQO1 has a potential as a biomarker in different stressed conditions. Following treatment with rotenone, overexpressed NQO1 in SH-SY5Y cells improved cell survival by reducing mitochondrial reductive stress via increased NAD + supply without mitochondrial biogenesis. However, NQO1 overexpression boosted lipid peroxidation following treatment with RSL3 and erastin. A lipid droplet staining assay showed increased lipid droplets in cells overexpressing NQO1. In contrast, NQO1 knockdown protected cells against ferroptosis by increasing GPX4, xCT, and the GSH/GSSG system. Also, NQO1 knockdown showed lower iron contents and lipid droplets than non-transfectants and cells overexpressing NQO1, even though it could not attenuate cell death when exposed to rotenone. In summary, our study suggests that different NQO1 levels may have advantages and disadvantages depending on the surrounding environments. Thus, regulating NQO1 expression could be a potential supplementary tool when treating neuronal diseases. |
| فهرسة مساهمة: | Keywords: NAD+; NQO1; ferroptosis; lipid peroxidation; mitochondrial biogenesis; reductive stress |
| المشرفين على المادة: | EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)) EC 1.6.5.2 (NQO1 protein, human) 03L9OT429T (Rotenone) 0 (RSL3 compound) 0 (erastin) 0 (Piperazines) 0 (Carbolines) |
| تواريخ الأحداث: | Date Created: 20240410 Date Completed: 20240605 Latest Revision: 20240613 |
| رمز التحديث: | 20240613 |
| DOI: | 10.5582/bst.2024.01020 |
| PMID: | 38599881 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1881-7823 |
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| DOI: | 10.5582/bst.2024.01020 |