Protective effect of boldine on dopamine-induced membrane permeability transition in brain mitochondria and viability loss in PC12 cells
- Authors
- Youn, Young Chul; Kwon, Oh Sang; Han, Eun Sook; Song, Jin Ho; Shin, Yong Kyoo; Lee, Chung Soo
- Issue Date
- Feb-2002
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Keywords
- boldine; catecholamines; brain mitochondria; PC12 cells; protection
- Citation
- BIOCHEMICAL PHARMACOLOGY, v.63, no.3, pp 495 - 505
- Pages
- 11
- Journal Title
- BIOCHEMICAL PHARMACOLOGY
- Volume
- 63
- Number
- 3
- Start Page
- 495
- End Page
- 505
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/25143
- DOI
- 10.1016/S0006-2952(01)00852-8
- ISSN
- 0006-2952
1873-2968
- Abstract
- Boldine ([S]-2,9-dihydroxy-1,10-dimethoxyaporphine) has been shown to exert antioxidant and anti-inflammatory effects. The present study elucidated the protective effect of boldine on catecholamine-induced membrane permeability transition in brain mitochondria and viability loss in PC12 cells. Dopamine (200 muM) and 6-hydroxydopamine (6-OHDA, 100 muM) attenuated Ca2+ and succinate-induced mitochondrial swelling and membrane potential formation. Boldine (10-100 muM) and 10 mug/mL of superoxide dismutase (SOD) or catalase reduced the effect of catecholamine oxidation on brain mitochondria. Boldine, SOD, and catalase decreased catecholamine-induced mitochondrial cytochrome c release. Antioxidant enzymes attenuated the depressant effect of catecholamines on mitochondrial electron flow, whereas boldine did not reduce it. Boldine inhibited the catecholamine-induced decrease in thioredoxin reductase activity and the increase in thiol oxidation in mitochondria. It also showed a scavenging action on hydrogen peroxide and hydroxyl radicals and decreased the formation of melanin from dopamine. Boldine and antioxidant enzymes decreased the dopamine-induced cell death, including apoptosis, in PC12 cells. The results suggest that boldine may attenuate the catecholamine oxidation-induced brain mitochondrial dysfunction and decrease the dopamine-induced death of PC12 cells through a scavenging action on reactive oxygen species and inhibition of melanin formation and thiol oxidation. (C) 2002 Elsevier Science Inc. All rights reserved.
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