Morita T, Mikami F, Kanagawa A, Sera M, Ueki H
Department of Biochemistry, Faculty of Pharmacy and Pharmaceutical Sciences, Fukuyama University, Japan.
Chem Pharm Bull (Tokyo). 1991 Dec;39(12):3287-9. doi: 10.1248/cpb.39.3287.
Vanadate stimulated the release of rat hepatic lipase activity from liver slices into an incubation medium in a time- and dose-dependent manner. Insulin, however, failed to have this stimulatory action, and the release by heparin was recognized, but was not additive to that by vanadate. Amiloride, an inhibitor of tyrosine kinase in some receptors and of the Na+/H+ exchange system suppressed the vanadate-stimulated release. Biochanin A, a different type of tyrosine kinase inhibitor than amiloride, also suppressed the effect of vanadate. The stimulation by vanadate was clearly preserved in Na(+)-, K(+)-, or Ca(2+)-free medium, suggesting that neither the Na+/H+ exchange system, Na+, K(+)-adenosine triphosphatase, nor Ca(2+)-influx into cells is involved in the action of this substance. These results suggest that vanadate-stimulated release of the enzyme activity is associated with the activation of the tyrosine kinase activity.
钒酸盐以时间和剂量依赖的方式刺激大鼠肝切片中的肝脂肪酶活性释放到孵育培养基中。然而,胰岛素未能产生这种刺激作用,肝素能促进酶释放,但与钒酸盐的作用并非相加效应。阿米洛利是某些受体中酪氨酸激酶和Na⁺/H⁺交换系统的抑制剂,它能抑制钒酸盐刺激的释放。生物chanin A是一种与阿米洛利不同类型的酪氨酸激酶抑制剂,也能抑制钒酸盐的作用。在无Na⁺、K⁺或Ca²⁺的培养基中,钒酸盐的刺激作用仍然明显,这表明Na⁺/H⁺交换系统、Na⁺, K⁺-腺苷三磷酸酶以及Ca²⁺内流进入细胞均不参与该物质的作用。这些结果表明,钒酸盐刺激的酶活性释放与酪氨酸激酶活性的激活有关。