Taylor S W, Hawkins C J, Parry D L, Swinehart J H, Hanson G R
Department of Chemistry, University of Queensland, St. Lucia, Australia.
J Inorg Biochem. 1994 Nov 1;56(2):97-116. doi: 10.1016/0162-0134(94)85041-0.
Changes in vanadium coordination during cell lysis have been followed by EPR spectroscopy of the blood cells of the phleborbranch ascidians Ascidia ceratodes and PHallusia julinea. The spectra obtained for A. ceratodes whole blood samples can be mainly ascribed to aquated oxovanadium(IV) in which the signals are broadened in freshly frozen blood relative to when the cells are lysed by thawing. The sources of this broadening are discussed and it is shown that the oxovanadium(IV) signal has its origin in a small percentage of damaged or lysed cells which release vanadium into a low sulfate, low acid environment in fresh samples. When thawed, the cells lyse releasing acid and sulfate into the environment of the oxovanadium(IV), with consequent narrowing of the EPR spectral linewidth. Freshly frozen P. julinea blood cell samples have EPR spectra with parameters intermediate between aquated oxovanadium(IV) and the "type I" parameters observed in a previous investigation of tissue samples of this species (S. G. Brand, C. J. Hawkins, A. T. Marshall, G. W. Nette, and D. L. Parry, Comp. Biochem. Physiol. 93B, 425 (1989)). A. ceratodes tissue samples also have EPR spectra that differ from that of the blood. It is suggested that EPR studies on tissue samples are more indicative of the resting state of vanadium in the cells as there is more physiological material to provide a pH buffering effect to stabilize the cells. Schemes are presented which incorporate all of the EPR observations in ascidian literature, where cellular lysis is proposed to be accompanied by vanadium undergoing oxidation and a series of chelate exchanges from a "type I" complex to aquated oxovanadium(IV). Protons released during these exchanges are suggested to provide the acidity characteristic of blood cell lysates. The biological implications of the concomitant release of vanadium and tunichrome (S. W. Taylor, D. L. Parry, C. J. Hawkins, and J. H. Swinehart, Comp. Biochem. Physiol. 106A, 531 (1993)) from the blood cells, to the process of wound repair are discussed.
通过对静脉分支海鞘角海鞘和朱利叶斯海鞘血细胞的电子顺磁共振光谱研究，追踪了细胞裂解过程中钒配位的变化。从角海鞘全血样本获得的光谱主要可归因于水合氧钒（IV），其中相对于解冻使细胞裂解时，新鲜冷冻血液中的信号变宽。讨论了这种变宽的来源，并表明氧钒（IV）信号源自一小部分受损或裂解的细胞，这些细胞将钒释放到新鲜样本中低硫酸盐、低酸度的环境中。解冻后，细胞裂解，向氧钒（IV）的环境中释放酸和硫酸盐，从而使电子顺磁共振谱线宽度变窄。新鲜冷冻的朱利叶斯海鞘血细胞样本的电子顺磁共振光谱参数介于水合氧钒（IV）和先前对该物种组织样本研究中观察到的“ I型”参数之间（S.G.布兰德、C.J.霍金斯、A.T.马歇尔、G.W.内特和D.L.帕里，《比较生物化学与生理学》93B，425（1989））。角海鞘组织样本的电子顺磁共振光谱也与血液的不同。有人认为，对组织样本的电子顺磁共振研究更能表明细胞中钒的静止状态，因为有更多的生理物质来提供pH缓冲作用以稳定细胞。文中提出了一些方案，这些方案纳入了海鞘文献中的所有电子顺磁共振观察结果，其中提出细胞裂解伴随着钒经历氧化以及从“ I型”配合物到水合氧钒（IV）的一系列螯合交换。这些交换过程中释放的质子被认为提供了血细胞裂解液的酸度特征。讨论了血细胞中钒和 tunichrome（S.W.泰勒、D.L.帕里、C.J.霍金斯和J.H.斯温哈特，《比较生物化学与生理学》106 A，531（1993））的伴随释放对伤口修复过程的生物学意义。
