Moor E, Kohen R, Reiter R J, Shohami E
Department of Pharmacology, The Hebrew University of Jerusalem, The School of Pharmacy, Hadassah Ein Kerem, Jerusalem 91120, Israel.
Neurosci Lett. 2001 Dec 28;316(3):169-72. doi: 10.1016/s0304-3940(01)02394-1.
Reactive oxygen species (ROS) are a major cause of secondary brain injury following head trauma. Low molecular weight antioxidants (LMWA) protect the tissue against oxidative damage caused by ROS. In the present study, we measured the extracellular levels of the LMWA ascorbic acid and uric acid in the rat brain before, during and after experimental closed head injury (CHI). A dialysis probe was inserted into the right ventral hippocampus through a chronically implanted guide. CHI was applied to the left hemisphere using a weight-drop device. CHI induced a rapid but transient increase in ascorbic acid levels. Uric acid levels increased to 250% of baseline shortly after CHI and remained elevated at 2 h after CHI. Previous results show that the overall reducing power of brain tissue decreases following CHI. Together with previous results, the current findings suggest that ascorbic acid and uric acid are mobilized from brain cells to the extracellular space.
活性氧（ROS）是头部创伤后继发性脑损伤的主要原因。低分子量抗氧化剂（LMWA）可保护组织免受ROS引起的氧化损伤。在本研究中，我们测量了实验性闭合性颅脑损伤（CHI）前后及期间大鼠脑内LMWA抗坏血酸和尿酸的细胞外水平。通过长期植入的引导管将透析探针插入右腹侧海马体。使用重物下落装置对左半球施加CHI。CHI导致抗坏血酸水平迅速但短暂升高。尿酸水平在CHI后不久升至基线的250%，并在CHI后2小时保持升高。先前的结果表明，CHI后脑组织的总体还原能力下降。结合先前的结果，目前的发现表明抗坏血酸和尿酸从脑细胞中转移到细胞外空间。
