Abstract
The possible role of lipid peroxidation in the nephrotoxicity of the antitumour drug cisplatin was studied in vitro. In contrast to Adriamycin, cisplatin did not induce lipid peroxidation in rat kidney microsomes containing a NADPH-generating system. Pretreatment of rat kidney microsomes with cisplatin did not reduce the activity of a microsomal glutathione (GSH)-dependent protective factor against lipid peroxidation induced by Fe(2+)-ascorbate. However, pretreatment of rat kidney microsomes with 0.1 mM N-ethyl maleimide (NEM) did reduce this GSH-dependent protection. Cisplatin also did not reduce the activity of a cytosolic GSH-dependent protective factor against Fe(2+)-ascorbate-induced lipid peroxidation. The results of our experiments indicate that, in contrast to Adriamycin, cisplatin does not induce lipid peroxidation in vitro in various test systems. It also does not destroy microsomal and cytosolic GSH-dependent protective factors against lipid peroxidation.
| Original language | English |
|---|---|
| Pages (from-to) | 1193-9 |
| Number of pages | 7 |
| Journal | Biochemical Pharmacology |
| Volume | 44 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 25 Sept 1992 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Animals
- Ascorbic Acid
- Cisplatin
- Cytosol
- Doxorubicin
- Ferric Compounds
- Hot Temperature
- Kidney
- Lipid Peroxidation
- Male
- Microsomes
- NADP
- Rats
- Rats, Wistar
- Thiobarbiturates
- Comparative Study
- Journal Article
- Research Support, Non-U.S. Gov't
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