Bishayee A, Chatterjee M
Department of Pharmaceutical Technology, Jadavpur University, Calcutta, India.
Biol Trace Elem Res. 1995 Jun;48(3):275-85. doi: 10.1007/BF02789409.
The influence of vanadium, an important dietary micronutrient, was evaluated on the cytosolic reduced glutathione (GSH) content and glutathione S-transferase (GST) activity in several rat target tissues. Supplementation of drinking water with vanadium at the level of 0.2 or 0.5 ppm for 4, 8, or 12 wk was found to increase the GSH level with a concomitant elevation in GST activity in the liver followed by small intestine mucosa, large intestine mucosa, and kidney. The results were almost dose-dependent and mostly pronounced with 0.5 ppm vanadium after 12 wk of its continuous supplementation. Neither the GSH level nor GST activity was significantly altered in forestomach and lung following vanadium supplementation throughout the study. The levels of vanadium that were found to increase the content of GSH and activity of GST in the liver, intestine, and kidney did not exert any toxic manifestation as evidenced from water and food consumption as well as the growth responses of the experimental animals. Moreover, these doses of vanadium did not impair either hepatic or renal functions as they did not alter the serum activities of glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), sorbitol dehydrogenase (SDH), as well as serum urea and creatinine level. All these results clearly indicate that vanadium under the doses employed in our study has a significant inducing role on GSH content with a concurrent elevation in GST activity in the liver and specific extrahepatic tissues without any apparent sign of cytotoxicity. This attribute of vanadium may have a greater importance in terms of biotransformation and detoxification of xenobiotics, including carcinogens. In addition, since the ability to afford an increment in the endogenous GSH-GST pool by anticarcinogenic natural substances has been found to correlate with their activity to inhibit neoplastic transformation, the trace element vanadium may be considered as a novel anticancer agent.
评估了重要膳食微量营养素钒对几只大鼠靶组织中胞质还原型谷胱甘肽(GSH)含量和谷胱甘肽S-转移酶(GST)活性的影响。发现以0.2或0.5 ppm的水平在饮用水中添加钒4、8或12周,可使肝脏中的GSH水平升高,同时GST活性也随之升高,其次是小肠黏膜、大肠黏膜和肾脏。结果几乎呈剂量依赖性,在连续补充12周后,0.5 ppm钒的作用最为明显。在整个研究过程中,补充钒后,前胃和肺中的GSH水平和GST活性均未发生显著变化。从实验动物的水和食物消耗以及生长反应可以看出,在肝脏、肠道和肾脏中发现的能增加GSH含量和GST活性的钒水平未产生任何毒性表现。此外,这些剂量的钒并未损害肝脏或肾脏功能,因为它们未改变血清谷氨酸草酰乙酸转氨酶(GOT)、谷氨酸丙酮酸转氨酶(GPT)、山梨醇脱氢酶(SDH)的活性以及血清尿素和肌酐水平。所有这些结果清楚地表明,在我们研究中使用的剂量下,钒对肝脏和特定肝外组织中的GSH含量具有显著的诱导作用,同时GST活性也会升高,且没有任何明显的细胞毒性迹象。钒的这一特性在包括致癌物在内的外源性物质的生物转化和解毒方面可能具有更重要的意义。此外,由于发现抗癌天然物质增加内源性GSH-GST库的能力与其抑制肿瘤转化的活性相关,微量元素钒可被视为一种新型抗癌剂。