Neuroprotection against oxidative stress by serum from heat acclimated rats

被引:6
作者
Beit-Yannai, E
Trembovler, V
Horowitz, M
Lazarovici, P
Kohen, R
Shohami, E [1 ]
机构
[1] Hebrew Univ Jerusalem, Dept Pharmacol & Expt Therapeut, IL-91120 Jerusalem, Israel
[2] Hebrew Univ Jerusalem, Pharm Sch Pharm, IL-91120 Jerusalem, Israel
[3] Hebrew Univ Jerusalem, Fac Med Dent, Dept Physiol, IL-91120 Jerusalem, Israel
关键词
heat-acclimation; uric acid; xanthine-oxidase; cell viability; PC12;
D O I
10.1016/S0304-3940(98)00670-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Exposure of PC12 cells, to 1% serum derived from normothermic (CON) rats resulted in 79% cell death. Sister cultures treated with 1% serum derived from heat acclimated (ACC) rats, were neuroprotected and expressed a significant reduction in cell death. In PC12 cells exposed to a tree radical generator causing an oxidative stress, 90% cell death was measured in CON serum treated cultures, while ACC serum treated cultures were neuroprotected. Xanthine oxidase activity and uric acid (UA) levels were lower in ACC serum compared to CON. Addition of UA to both sera abolished the difference in cell viability, and toxicity of ACC serum reached that of CON. These findings suggest a causal relationship between the lower levels of UA in ACC and the neuroprotective effect observed. The present study proposes heat acclimation as an experimental and/or clinical tool for the achievement of neuroprotection. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:89 / 92
页数:4
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