Abstract
Rat hearts were perfused for 15min with buffer equilibrated with 0.01% or 0.05% CO. The buffer was equilibrated with 21% O(2) throughout. The ventricular glutathione content decreased by 76% and 84%, 90min post-exposure to 0.01% and 0.05% CO, respectively, compared with 0% CO controls (0.45+/-0.01 micromol/g wet tissue; +/-SEM, n=3). Both reduced and oxidised glutathione contributed to this decline. When ascorbate and Trolox C were included during exposure to 0.05% CO the glutathione pool was partly protected; here the glutathione decrease was 46%. In most hearts additional creatine kinase activity in the perfusate indicated minor tissue injury occurring immediately after the start and/or about 10min after the end of exposure to 0.01% CO or 0.05% CO. Ventricle lactate levels were unaffected by exposure to 0.01% CO. This evidence supports a role for oxidative stress in CO cardiotoxicity.
| Original language | English |
|---|---|
| Pages (from-to) | 392-396 |
| Number of pages | 5 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 302 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 10 Jan 2003 |
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology
Keywords
- Animals
- Antioxidants
- Carbon Monoxide
- Glutathione
- Heart
- Male
- Myocardium
- Rats
- Sprague-Dawley