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目的：研究半胱氨酸（Ｃｙｓ）和高半胱氨酸（ＨｏＣｙｓ）对一氧化氮（ＮＯ）诱导的动脉舒张的抑制作用的机制．方法：用Ｃｙｓ或ＨｏＣｙｓ对去内皮细胞血管环预处理，观察张力变化．结果：Ｃｙｓ或ＨｏＣｙｓ抑制ＮＯ诱导的ｃＧＭＰ增加．加入Ｃｙｓ或ＨｏＣｙｓ，再加入ＮＯ７５ｎｍｏｌ·Ｌ－１，抑制血管舒张的效应随时间逐渐消失，与此二化合物在Ｋｒｅｂｓ液中巯基的丢失一致．超氧化物歧化酶（ＳＯＤ）３５ｋＵ·Ｌ－１抑制但不完全阻断Ｃｙｓ和ＨｏＣｙｓ对ＮＯ诱导的血管舒张的抑制作用．相反，加热失活的ＳＯＤ和过氧化氢酶（１００ｋＵ·Ｌ－１）均不拮抗Ｃｙｓ的抑制作用．在Ｋｒｅｂｓ液中预先加入ＳＯＤ３５ｋＵ·Ｌ－１显著抑制Ｃｙｓ诱导的细胞色素Ｃ的还原．ＳＯＤ浓度增至３５０ｋＵ·Ｌ－１，效应虽增强，但不能完全抑制细胞色素Ｃ的还原．直接将黄嘌呤３００μｍｏｌ·Ｌ－１和黄嘌呤氧化酶１Ｕ·Ｌ－１加入细胞色素Ｃ６０μｍｏｌ·Ｌ－１和Ｃｙｓ１００μｍｏｌ·Ｌ－１的混和物仍可见ＳＯＤ对细胞色素Ｃ还原的抑制作用，提示Ｃｙｓ降低细胞色素Ｃ能力有限，且部分由于产生超氧化物所致．ＨｏＣｙｓ１００μｍｏｌ·Ｌ－１诱导的细胞色素Ｃ的还原速率比Ｃｙｓ慢．在主动脉?
AIM: To investigate the mechanism of cys and cysteine (Ho cys) inhibition of nitric oxide (NO) -induced arterial vasodilation. Methods: The vascular endothelial cells were pretreated with Cys or HoCys to observe the changes of tension. Results: Cys or HoCys inhibited NO-induced increase in cGMP. Adding Cys or HoCys, then adding NO75nmol·L-1, the effect of inhibiting vasodilation gradually disappeared with time, consistent with the loss of sulfhydryl group of these two compounds in Krebs solution. Superoxide dismutase (SOD) 35kU · L-1 inhibits but does not completely block the inhibitory effect of Cys and HoCys on NO-induced vasodilatation. In contrast, neither heat-inactivated SOD nor catalase (100 kU · L-1) antagonized the inhibitory effect of Cys. Pre-addition of SOD35kU · L-1 in Krebs solution significantly inhibited Cys-induced reduction of cytochrome C. SOD concentration increased to 350kU · L-1, although the effect is enhanced, but can not completely inhibit cytochrome C reduction. The inhibitory effect of SOD on the reduction of cytochrome C was observed by directly adding xanthine 300 μmol·L-1 and xanthine oxidase 1 U · L-1 to the mixture of cytochromes C 60 μmol·L-1 and Cys 100 μmol·L-1, suggesting that Cys The ability to reduce cytochrome C is limited, and partly due to superoxide production. The reduction rate of cytochrome C induced by HoCys100μmol·L-1 was slower than that of Cys. In the aorta?