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Pyridine nucleotide changes in hepatocytes exposed to quinones
1Department of Pharmacology, School of Pharmacy, University of London, UK.
Free Radical Research Communications
|January 1, 1990
Summary
Quinones cause cell damage through arylation and redox cycling. This study shows redox cycling quinones alter cellular pyridine nucleotides (NAD+, NADP+) to combat oxidative stress, impacting cell viability.
Area of Science:
- Biochemistry
- Cell Biology
- Toxicology
Background:
- Quinone toxicity arises from mechanisms like arylation and redox cycling.
- Cellular pyridine nucleotides (NAD+, NADP+) are crucial for cellular redox balance.
Purpose of the Study:
- To investigate the cytotoxicity of four quinones with varying arylation and redox cycling abilities.
- To examine the effects of these quinones on cellular pyridine nucleotide levels in isolated hepatocytes.
Main Methods:
- Hepatocytes were exposed to menadione, 2-hydroxy-1,4-naphthoquinone, 2,3-dimethoxy-1,4-naphthoquinone, and p-benzoquinone.
- Cytotoxicity, NAD+, NADP+, and NADPH levels were measured.
- The role of poly(ADP-ribose)polymerase was assessed using 3-aminobenzamide.
Main Results:
- High concentrations of all tested quinones decreased NAD+ and cell viability.
- 3-aminobenzamide did not protect against quinone-induced toxicity, unlike dimethyl sulfate.
- Non-toxic concentrations of redox-cycling quinones induced similar pyridine nucleotide interconversions (NAD+ decrease, NADP+/NADPH increase).
Conclusions:
- Redox cycling quinones trigger pyridine nucleotide interconversion in cells.
- This interconversion is likely a cellular response to mitigate oxidative stress.
- Poly(ADP-ribose)polymerase is not implicated in the toxicity of these specific quinones.