Neuroprotection against oxidative stress by serum from heat acclimated rats.
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.
Department of Pharmacology and Experimental Therapeutics, The Hebrew University of Jerusalem, Israel.
E
E
Beit-Yannai
V
V
Trembovler
M
M
Horowitz
P
P
Lazarovici
R
R
Kohen
E
E
Shohami
D000064:Acclimatization / Q000502:physiology*; D000818:Animals; D001790:Blood Physiological Phenomena; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D006358:Hot Temperature; D008297:Male; D018696:Neuroprotective Agents; D018384:Oxidative Stress / Q000502:physiology*; D016716:PC12 Cells / Q000502:physiology; D051381:Rats / Q000097:blood; D011919:Rats, Inbred Strains; D012016:Reference Values; D014527:Uric Acid / Q000097:blood / Q000494:pharmacology; D014969:Xanthine Oxidase / Q000097:blood
D018696:Neuroprotective Agents; D014527:Uric Acid; D014969:Xanthine Oxidase