Hansen T V, Aaseth J, Alexander J
Arch Toxicol. 1982 Sep;50(3-4):195-202. doi: 10.1007/BF00310851.
Pentavalent vanadium (V5) as Na48VO3 was given i.p. to male Wistar rats at a dose of 5 mumol/kg in order to study its organ distribution pattern. Two days after injection, kidneys reached a V level of about 28 nmol/g wet weight, followed in decreasing order by spleen, liver, bone, blood plasma, testis, lung, erythrocytes and brain in control rats. A similar distribution pattern was seen after injection of tetravalent vanadium (V4) given as 48VOSO4. Two chelators, desferrioxamine B (Desferal) or Ca-Na3-diethylene triamine pentaacetic acid (DTPA), were given i.p. 24 h after the vanadium injections to different groups of rats at two dosage levels, 30 and 100 mumol/kg. Desferal (30 mumol/kg) reduced the vanadium content of the kidney by 17%, of the liver by 0%, and of the lung by 7%. The corresponding figures for the effect of DTPA (30 mumol/kg) were 7%, plus 15%, and 0%, respectively. At 100 mumol/kg, Desferal reduced the same organ levels by 20%, 26%, and 25%, respectively, and DTPA by 9%, 18%, and 25%, respectively. Both chelators raised faecal excretion at the low level, and both urinary and faecal excretion at the high level. Spleen and bone seemed to bind vanadium to a higher degree than the other organs under examination. Human erythrocytes, when incubated with 48VOSO4 (V4) or Na48VO3 (V5), were found to accumulate nearly the double amount of V5 as compared to V4. Glutathione (GSH) which is the main reducing substance within the erythrocytes, reduced the uptake of V5 to the V4 level when incubated together with GSH before addition to the cell suspension. Pretreating the erythrocytes with diethyl-maleate (DEM) which blocks the reducing SH groups of intracellular GSH, also reduced the uptake of V5. This may indicate a GSH dependent reduction of V5 to V4 within the erythrocytes. Four chelators, among them Desferal and DTPA, were found to reduce the cellbound amount of vanadium, either by extracting vanadium as V4, or by inhibiting uptake by the red blood cells.
为了研究五价钒（V5）以偏钒酸钠（Na48VO3）形式腹腔注射给雄性Wistar大鼠（剂量为5 μmol/kg）后的器官分布模式。注射两天后，对照组大鼠肾脏中的钒含量达到约28 nmol/g湿重，其次依次为脾脏、肝脏、骨骼、血浆、睾丸、肺、红细胞和脑。注射四价钒（V4）以硫酸氧钒（48VOSO4）形式给药后也观察到类似的分布模式。在钒注射24小时后，给不同组的大鼠腹腔注射两种螯合剂，去铁胺B（去铁敏）或钙三钠二乙烯三胺五乙酸（DTPA），剂量分别为30和100 μmol/kg。去铁敏（30 μmol/kg）使肾脏中的钒含量降低了17%，肝脏中的钒含量降低了0%，肺中的钒含量降低了7%。DTPA（30 μmol/kg）的相应降低率分别为7%、增加15%和0%。在100 μmol/kg时，去铁敏使相同器官中的钒含量分别降低了20%、26%和25%，DTPA则分别降低了9%、18%和25%。两种螯合剂在低剂量时均增加了粪便排泄，在高剂量时增加了尿液和粪便排泄。脾脏和骨骼似乎比其他受检器官对钒的结合程度更高。当人红细胞与硫酸氧钒（V4）或偏钒酸钠（V5）一起孵育时发现，与V4相比，红细胞积累的V5量几乎是其两倍。谷胱甘肽（GSH）是红细胞内主要的还原物质，在加入细胞悬液前与GSH一起孵育时，可将V5的摄取量降低至V4水平。用马来酸二乙酯（DEM）预处理红细胞，它会阻断细胞内GSH的还原性巯基，这也降低了V5的摄取。这可能表明红细胞内V5向V4的还原依赖于GSH。发现四种螯合剂，其中包括去铁敏和DTPA，可通过以V4形式提取钒或抑制红细胞摄取来降低细胞结合的钒量。
