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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 한국응용약물학회 The journal of applied pharmacology : the official journal of the Korean Society of Applied Pharmacology The journal of applied pharmacology : the official journal of the Korean Society of Applied Pharmacology 제10권 제3호
- 발행연도
- 2002.1
- 수록면
- 152 - 158 (7page)
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The present study elucidated the effect of $\beta$-carbolines (harmaline and harmalol) on brain mitochondlial dysfunction caused by the tyrosinase-induced oxidation of dopamine. Harmaline, harmalol and antioxidant enzymes (SOD and catalase) attenuated the dopamine-induced alteration of membrane potential, cytochrome c release and thiol oxidation in mitochondria. In contrast, antioxidant enzymes failed to reverse mitochondrial dysfunction induced by dopmnine plus tyrosinase. $\beta$-Carbolines decreased the damaging effect of dopamine plus tyrosinase against mitochondria, except no effect of harmalol on thiol oxidation. Antioxidant enzymes decreased the melanin formation from dopamine in the reaction mixture containing mitochondria but did not reduce the formation of dopamine quinone caused by tyrosinase. Both harmalol and harmaline inhibited the formation of reactive quinone and melanin. Harmalol being more effective for quinone formation and vise versa. The results indicate that compared to MAO-induced dopamine oxidation, the toxic effect of dopamine in the presence of tyrosinase against mitochondria may be accomplished by the dopamine quinone and toxic substances other than reactive oxygen species. $\beta$-Carbolines may decrease the dopamine plus tyrosinase-induced brain mitochondrial dysfunction by inhibition of the formation of reactive quinone and the change in membrane permeability.
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