Heat shock preconditioning induces protein carbonylation and alters antioxidant protection in superficially injured guinea pig gastric mucosa in vitro

According to our previous studies, heat shock preconditioning of gastric mucosa requires modulation of protein synthesis and eicosanoid pathways to induce protection against superficial injury. This may be caused by heat shock-induced oxidative stress. We studied the effect of heat shock preconditio...

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Bibliographic Details
Published in:Digestive diseases and sciences 2007-08, Vol.52 (8), p.1897-1905
Main Authors: OKSALA, Niku K. J, PAIMELA, Hannu, ALHAVA, Esko, ATALAY, Mustafa
Format: Article
Language:English
Subjects:
Animals
Arachidonic Acid - pharmacology
Biological and medical sciences
Bones, joints and connective tissue. Antiinflammatory agents
Cytoprotection - physiology
Gastric Mucosa - pathology
Gastric Mucosa - physiology
Guinea Pigs
Hot Temperature
HSP72 Heat-Shock Proteins - analysis
In Vitro Techniques
Indomethacin - pharmacology
Lipid Peroxidation
Lipids
Medical sciences
Oxidation
Oxidation-Reduction
Oxidative Stress
Pharmacology. Drug treatments
Protein Carbonylation - physiology
Proteins
Reactive Oxygen Species - analysis
Superoxide Dismutase - analysis
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Summary:According to our previous studies, heat shock preconditioning of gastric mucosa requires modulation of protein synthesis and eicosanoid pathways to induce protection against superficial injury. This may be caused by heat shock-induced oxidative stress. We studied the effect of heat shock preconditioning with normothermic recovery on redox status in superficially injured (1.25 mmol NaCl for 5 min) Ussing chamber perfused guinea pig gastric mucosa allowed to recover for 3 hr after injury. Protein oxidation, lipid peroxidation, level of superoxide dismutase, level of heat shock protein 72 (HSP72), and level of oxygen radical absorbance capacity were measured. Superficial injury increased lipid peroxidation. Heat shock preconditioning decreased oxygen radical absorbance capacity and increased protein carbonyl and HSP72 levels, but inhibited electrophysiologic recovery. Exposure to indomethacin and arachidonic acid (AA) partially abolished this pro-oxidative and inhibitory effect on recovery, but maintained HSP72 levels and decreased protein carbonyls, lipid peroxidation, and oxygen radical absorbance capacity. In conclusion, superficial injury increased lipid peroxidation. Heat shock preconditioning alone induced oxidative stress via indomethacin- and AA-sensitive mechanisms. The development of optimal cytoprotective strategy may therefore require control of oxidative stress and modulation of the eicosanoid pathways.
ISSN:0163-2116
1573-2568
DOI:10.1007/s10620-006-9214-1