Endogenous tumor necrosis factor functions as a resistant factor against hyperthermic cytotoxicity
Y Tsuji1, N Watanabe, T Okamoto
1Department of Internal Medicine (Section 4), Sapporo Medical College, Japan.
Cancer Research
|November 15, 1992
Summary
Endogenous tumor necrosis factor (enTNF) protects cells from heat-induced damage by scavenging reactive oxygen species. This protective effect involves increased manganous superoxide dismutase, similar to exogenous TNF treatments.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Tumor necrosis factor (TNF) induces cytotoxicity via reactive oxygen molecules.
- Endogenous TNF (enTNF) confers resistance to exogenous TNF by scavenging reactive oxygen.
- Intracellular hydroxyl radical production contributes to heat-induced cytotoxicity.
Purpose of the Study:
- To investigate if enTNF protects against heat-induced cytotoxicity.
- To elucidate the mechanism of enTNF-mediated protection against heat stress.
Main Methods:
- Transfection of L-M cells with human TNF expression vector to produce enTNF.
- Transfection of HeLa cells with antisense TNF mRNA to inhibit enTNF synthesis.
- Assessing heat resistance and intracellular manganous superoxide dismutase levels.
Main Results:
- L-M cells producing enTNF showed resistance to heat treatment.
- HeLa cells with inhibited enTNF synthesis became more heat-sensitive.
- Heat resistance correlated with enTNF expression and manganous superoxide dismutase levels.
Conclusions:
- Endogenous TNF provides intracellular protection against heat-induced cytotoxicity.
- This protection is mediated by scavenging reactive oxygen species through induced manganous superoxide dismutase.
- The protective mechanism of enTNF mirrors that of exogenous TNF treatment.
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