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- 저자 : Markewitz, (검색결과 1 건)
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백서 폐동맥 내피세포에서 cytokine 및 내독소에 의한 nitric oxide 생성과 미토콘드리아 aconitase 활성도의 관계
김세규(Se Kyu Kim),장준(Joon Chang),이원영(Won Young Lee),장상호(Sang Ho Jang),박전한(Jeon Han Park),김세종(Se Jong Kim),김성규(Sung Kyu Kim),(Boaz A . Markewitz),(John R . Michael) 대한내과학회 1999 대한내과학회지 Vol.56 No.2
N/A Objective : Both constitutive and inducible forms of nitric oxide synthase exist in endothelial cells. Disorders that produce acute lung injury frequently release endotoxin and cytoknes, such as interferon(IFNγ) and tumor necrosis factor (TNFα). Endotoxin and these cytokines likely act as important mediators of cell injury. Because nitric oxide (NO) avidly reacts with iron, it may affect the activity of key enzymes, such as mitochondrial aconitase, which contain an iron-sulfur structure as a prosthetic group. Method : We studied the effect of IFNγ, TNFα and E. coli lipopolysaccharide(LPS) on NO production and mitochondrial aconitase activity in cultured rat lung microvascular endothelial cells(RLMVC). Result : Exposing RLMVC for 24 hours to IFNγ(500 U/mL), TNFα(300 U/mL) and LPS(5 ㎍/mL) significantly increases nitrite production to 20±1 μM compared to 0.07 μM in control cells(P<0.05, n=4). Cytokine treatment also reduced mitochondrial aconitase activity from 196±8 to 102±34 nmole/min/mg of cell protein(P<0.05, n=4). Treatment with the inhibitor of nitric oxide synthase N-monomethyl-L-arginine(NMMA) (0.5 mM) not only significantly blunted the cytokine- mediated increase in nitrite formation (3±0.5 μM vs 20±1 μM with cytokines, P<0.05, n=4), but also prevented the cytokine-mediated drop in aconitase activity (161± 24 vs. 196±8 nmole/min/mg of cell protein, NS). Conclusion : Exposing RLMVC to IFNγ, TNFα and E. coli LPS substantially decreases mitochondrial aconitase activity. Nitric oxide appears to mediate this effect. Our results suggest that the excessive production of NO by endothelial cells, in response to cytokines and endotoxin, may inhibit the function of the endothelial cell itself.
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