Wagner D A, Shuker D E, Bilmazes C, Obiedzinski M, Baker I, Young V R, Tannenbaum S R
Cancer Res. 1985 Dec;45(12 Pt 1):6519-22.
The endogenous formation of nitrosoproline (NPRO) following administration of nitrate and proline is reported in ten healthy young adults. There was a relatively constant basal excretion of NPRO, 26 +/- 10 (SD) nmol/day, in excess of amounts found in the diet. This basal synthesis of NPRO was not reduced by ascorbic acid (2 g/day) or alpha-tocopherol (400 mg/day). A significant rise in the excretion of NPRO was observed following the administration of nitrate and proline, ranging from 29 to 318 nmol/24 h with a mean of 100 nmol/24 h. [15N]Nitrate was used as a tracer to study the observed excess excretion of NPRO in urine. The data revealed that urinary NPRO excretion as a result of endogenous synthesis is not totally derived from ingested nitrate as its precursor. The ingestion of ascorbic acid and alpha-tocopherol inhibited the incorporation of [15N]nitrate into NPRO by 81 and 59%, respectively. An additional nitrosamino acid, N-nitrosothiazolidine-4-carboxylic acid, was present in the urine. It was found that N-nitrosothiazolidine-4-carboxylic acid increased 6-fold upon ingestion of nitrate. Ascorbic acid and alpha-tocopherol blocked this nitrate induced synthesis.
据报道，在10名健康年轻成年人中，给予硝酸盐和脯氨酸后会内源性生成亚硝基脯氨酸（NPRO）。NPRO的基础排泄量相对恒定，为26±10（标准差）nmol/天，超过了饮食中发现的量。NPRO的这种基础合成不受抗坏血酸（2克/天）或α-生育酚（400毫克/天）的影响。给予硝酸盐和脯氨酸后，观察到NPRO的排泄量显著增加，范围为29至318 nmol/24小时，平均为100 nmol/24小时。[15N]硝酸盐用作示踪剂，以研究尿液中观察到的NPRO过量排泄情况。数据显示，内源性合成导致的尿液NPRO排泄并非完全源自摄入的硝酸盐作为其前体。摄入抗坏血酸和α-生育酚分别抑制了[15N]硝酸盐掺入NPRO的比例达81%和59%。尿液中还存在另一种亚硝基氨基酸，N-亚硝基噻唑烷-4-羧酸。发现摄入硝酸盐后，N-亚硝基噻唑烷-4-羧酸增加了6倍。抗坏血酸和α-生育酚阻断了这种硝酸盐诱导的合成。
