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Vitamin E retards the lipoperoxidation resulting from anticancer drug administration
Anticancer Research
|January 1, 1983
Summary
Cytotoxic drugs increase lipoperoxide levels in rats, but vitamin E supplementation with 5-fluorouracil reduces these levels. Glutathione peroxidase activity was affected in erythrocytes but not liver or brain tissue.
Area of Science:
- Biochemistry
- Pharmacology
- Toxicology
Background:
- Cytotoxic drugs are widely used in cancer chemotherapy.
- These drugs can cause oxidative stress, leading to increased lipoperoxide levels.
- The role of glutathione peroxidase in mitigating this toxicity is not fully understood.
Purpose of the Study:
- To investigate the effects of common cytotoxic drugs on lipoperoxide levels and glutathione peroxidase activity in rats.
- To evaluate the potential protective effect of vitamin E supplementation against drug-induced oxidative stress.
Main Methods:
- Rats were treated with 5-fluorouracil, methotrexate, cyclophosphamide, or vincristine.
- Lipoperoxide levels were measured in liver, plasma, and brain tissue.
- Glutathione peroxidase activity was assessed in liver, brain, and erythrocytes.
- A separate group received vitamin E concurrently with 5-fluorouracil.
Main Results:
- Cytotoxic drugs increased lipoperoxide levels in liver and plasma, but not brain.
- Glutathione peroxidase activity was unchanged in liver and brain but decreased in erythrocytes for 5-fluorouracil and methotrexate treatments.
- Vitamin E supplementation significantly reduced lipoperoxide levels in rats treated with 5-fluorouracil.
Conclusions:
- Cytotoxic chemotherapy agents can induce oxidative stress, evidenced by increased lipoperoxides.
- Vitamin E may offer a protective effect against chemotherapy-induced oxidative damage.
- Erythrocyte glutathione peroxidase activity is sensitive to certain cytotoxic drugs, suggesting potential therapeutic monitoring or intervention strategies.