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Cytotoxic effects of autoxidative glycation
R Carubelli1, J E Schneider, Q N Pye
1Oklahoma Medical Research Foundation, Dean A McGee Eye Institute, Oklahoma City, USA.
Free Radical Biology & Medicine
|February 1, 1995
Summary
Ribose and copper ions together kill Q beta phage by generating damaging free radicals. Chelators protect the phage, indicating a role for metal ions in this cytotoxic effect.
Area of Science:
- Biochemistry
- Molecular Biology
- Free Radical Chemistry
Background:
- The Q beta phage is a single-stranded RNA virus.
- Ribose and copper sulfate (CuSO4) are common laboratory reagents.
- Free radicals can damage biological molecules.
Purpose of the Study:
- To investigate the cytotoxic effect of ribose and CuSO4 on Q beta phage.
- To elucidate the mechanism of phage inactivation.
Main Methods:
- Incubation of Q beta phage with ribose and CuSO4 at 37°C.
- Assessing phage viability over time.
- Using diethylenetriaminepentaacetic acid (a chelator) to test its effect.
- Isolating RNA to test its infectivity.
Main Results:
- Complete loss of viable phage after 20 minutes of incubation.
- Cytotoxicity required both ribose and cupric ions.
- Phage survival correlated with incubation time and concentrations of ribose and CuSO4.
- Chelator addition abolished the cytotoxic effect.
- Isolated RNA remained infective.
Conclusions:
- Ribose and copper ions generate cytotoxic free radicals, likely superoxide and hydroxyl radicals.
- These radicals attack protein components of the phage.
- The mechanism involves transition metal-catalyzed autoxidation and Fenton reaction.
- The phage's RNA is protected, suggesting protein damage is the primary cause of inactivation.