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Temperature-dependent quinone cytotoxicity in platelets involves arylation.
Young-Ah Kang1, Ok-Nam Bae, Moo-Yeol Lee
1Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Korea.
Journal of Toxicology and Environmental Health. Part A
|September 14, 2002
Summary
Temperature significantly impacts menadione (MEN) cytotoxicity in platelets. Increased temperatures enhance MEN-induced cell damage and protein thiol depletion, suggesting temperature-dependent arylation is key to MEN toxicity.
Area of Science:
- Biochemistry
- Toxicology
- Cell Biology
Background:
- Menadione (MEN) induces cytotoxicity through protein arylation and oxidative stress.
- Protein arylation is a primary mechanism for MEN toxicity in platelets.
Purpose of the Study:
- To investigate the role of temperature in menadione-induced cytotoxicity in non-cancer cells (platelets).
- To elucidate the mechanism of temperature-dependent MEN cytotoxicity by comparing it with other quinones.
Main Methods:
- Platelets were incubated with menadione at 25°C, 37°C, and 42°C.
- Assessed lactate dehydrogenase (LDH) leakage and protein thiol levels.
- Compared MEN toxicity with benzoquinone (BQ) and dimethoxy-1,4-naphthoquinone (DMNQ).
Main Results:
- Increased temperature significantly enhanced MEN-induced LDH leakage and protein thiol depletion.
- BQ, an arylation agent, showed similar temperature-dependent cytotoxicity to MEN.
- DMNQ, an oxidative stress agent, did not produce cytotoxicity at any temperature.
- MEN uptake was temperature-independent, but extracellular concentration decreased with rising temperature, suggesting increased cellular binding.
Conclusions:
- MEN-induced platelet cytotoxicity is dependent on temperature.
- Arylation, a reaction involving thiol binding, is the primary temperature-related mechanism for MEN toxicity in platelets.