Teerajetgul Yaovalak, Hossain Rayhan Zubair, Yamakawa Kenichi, Morozumi Makoto, Sugaya Kimio, Ogawa Yoshihide
Division of Urology, Department of Organ-oriented Medicine, Faculty of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan.
Urol Res. 2007 Aug;35(4):173-8. doi: 10.1007/s00240-007-0102-8. Epub 2007 Jun 13.
We studied the effects of an intravenous hydroxypyruvate load on endogenous oxalogenesis in rats receiving a standard diet or a vitamin-B6-deficient diet. Twelve male Wistar rats were randomized to two groups and were fed either a standard diet or a vitamin-B6-deficient diet for 3 weeks. Then the animals received an intravenous infusion of 100 mg/ml (960.6 micromol/ml) of hydroxypyruvate slowly over 10 min. Urine samples were collected just before hydroxypyruvate infusion and at hourly intervals until 5 h afterward. Urinary oxalate, glycolate, and citrate levels were measured by capillary electrophoresis. Hourly urinary oxalate excretion peaked within 2 h, while urinary glycolate excretion peaked at 1 h, after the hydroxypyruvate load in both control and vitamin-B6-deficient rats. Both urinary oxalate and glycolate excretion were higher in vitamin-B6-deficient rats than in control rats. Infusion of hydroxypyruvate increased the 5-h urinary oxalate and glycolate excretion to 0.68% (6.56 micromol) and 0.53% (5.10 micromol) of the administered dose (mol/mol), respectively, in the control rats, while oxalate and glycolate excretion, respectively, increased to 2.43% (23.36 micromol) and 0.79% (7.59 micromol) of the dose in the vitamin-B6-deficient rats. Urinary citrate excretion was significantly lower at baseline and all other times in the vitamin-B6-deficient rats than in the control rats. In conclusion, a hydroxypyruvate load increased endogenous oxalate synthesis in control rats, and its synthesis was even greater in vitamin-B6-deficient rats. Vitamin B6 deficiency also resulted in significant hypocitraturia.
我们研究了静脉注射羟基丙酮酸负荷对接受标准饮食或维生素B6缺乏饮食的大鼠内源性草酸生成的影响。将12只雄性Wistar大鼠随机分为两组，分别给予标准饮食或维生素B6缺乏饮食3周。然后，动物在10分钟内缓慢静脉输注100mg/ml（960.6μmol/ml）的羟基丙酮酸。在输注羟基丙酮酸之前以及之后每小时收集尿液样本，直至5小时后。通过毛细管电泳测量尿草酸、乙醇酸和柠檬酸盐水平。在对照组和维生素B6缺乏的大鼠中，羟基丙酮酸负荷后，每小时尿草酸排泄在2小时内达到峰值，而尿乙醇酸排泄在1小时达到峰值。维生素B6缺乏的大鼠尿草酸和乙醇酸排泄均高于对照组大鼠。在对照组大鼠中，输注羟基丙酮酸使5小时尿草酸和乙醇酸排泄分别增加至给药剂量（mol/mol）的0.68%（6.56μmol）和0.53%（5.10μmol），而在维生素B6缺乏的大鼠中，草酸和乙醇酸排泄分别增加至剂量的2.43%（23.36μmol）和0.79%（7.59μmol）。维生素B6缺乏的大鼠在基线及所有其他时间的尿柠檬酸盐排泄均显著低于对照组大鼠。总之，羟基丙酮酸负荷增加了对照组大鼠内源性草酸合成，在维生素B6缺乏的大鼠中其合成甚至更高。维生素B6缺乏还导致显著的低枸橼酸尿症。
