Herrero M C, Alvarez C, Cartañà J, Bladé C, Arola L
Departament d'Enginyeria Química i Bioquímica, Universitat de Barcelona, Tarrogona, Spain.
Res Commun Chem Pathol Pharmacol. 1993 Feb;79(2):243-8.
Female Wistar rats were treated with nickel (single i.p. injection of 6 mg Ni(II)/kg body weight) and twenty amino acids and glutathione (GSH) concentrations were determined in liver 90 minutes later. Hepatic GSH content dramatically diminished after nickel injection. Glycine and glutamate levels, precursor amino acids of GSH, were not affected by nickel treatment, whereas cysteine level, the third precursor, was drastically increased in comparison with control rats. These findings showed that hepatic GSH depletion, caused by acute nickel exposure, was not due to a reduction in the availability of precursor amino acids. Nickel treatment also induced a 2-fold increase in phenylalanine and a decrease in taurine to one fifth. Therefore, the role of taurine in protecting membranes was clearly jeopardized in liver after nickel exposure, which could account for some of the toxicologic actions of this metal. However, further research is needed to explore such suggestion.
对雌性Wistar大鼠进行镍处理(腹腔注射一次,剂量为6毫克镍(II)/千克体重),90分钟后测定肝脏中20种氨基酸和谷胱甘肽(GSH)的浓度。注射镍后,肝脏中的谷胱甘肽含量显著降低。谷胱甘肽的前体氨基酸甘氨酸和谷氨酸水平不受镍处理的影响,而第三种前体半胱氨酸水平与对照大鼠相比大幅增加。这些发现表明,急性镍暴露导致的肝脏谷胱甘肽耗竭并非由于前体氨基酸可用性的降低。镍处理还使苯丙氨酸增加了2倍,牛磺酸减少至五分之一。因此,镍暴露后肝脏中牛磺酸保护细胞膜的作用显然受到损害,这可能解释了这种金属的一些毒理学作用。然而,需要进一步的研究来探索这一观点。