Neuroprotection against oxidative stress by serum from heat acclimated rats

Elie Beit-Yannai; Victoria Trembovler; Michal Horowitz; Philip Lazarovici; Ron Kohen; Esther Shohami

doi:10.1016/S0304-3940(98)00670-3

Neuroprotection against oxidative stress by serum from heat acclimated rats

Elie Beit-Yannai, Victoria Trembovler, Michal Horowitz, Philip Lazarovici, Ron Kohen, Esther Shohami^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

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 free 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.

Original language	English
Pages (from-to)	89-92
Number of pages	4
Journal	Neuroscience Letters
Volume	254
Issue number	2
DOIs	https://doi.org/10.1016/S0304-3940(98)00670-3
State	Published - 2 Sep 1998

Bibliographical note

Funding Information:
R.K., P.L. and E.S. are affiliated to the David R. Bloom Center for Pharmacy. V.T. was supported in part by the Israel Ministry of Absorption.

Keywords

Cell viability
Heat-acclimation
PC12
Uric acid
Xanthine-oxidase

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10.1016/S0304-3940(98)00670-3

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title = "Neuroprotection against oxidative stress by serum from heat acclimated rats",

abstract = "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 free 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.",

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note = "Funding Information: R.K., P.L. and E.S. are affiliated to the David R. Bloom Center for Pharmacy. V.T. was supported in part by the Israel Ministry of Absorption. ",

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AU - Lazarovici, Philip

AU - Kohen, Ron

AU - Shohami, Esther

N1 - Funding Information: R.K., P.L. and E.S. are affiliated to the David R. Bloom Center for Pharmacy. V.T. was supported in part by the Israel Ministry of Absorption.

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N2 - 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 free 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.

AB - 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 free 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.

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KW - Xanthine-oxidase

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Neuroprotection against oxidative stress by serum from heat acclimated rats

Abstract

Bibliographical note

Keywords

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