Carbon monoxide exposure in rat heart: glutathione depletion is prevented by antioxidants.
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.
Patel
Ashvin P
AP
School of Biological Sciences, University of Plymouth, Devon, UK.
John Moody
A
A
Handy
Richard D
RD
Robert Sneyd
J
J
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002248:Carbon Monoxide / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism*; D006321:Heart / Q000187:drug effects*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D000975:Antioxidants; D002248:Carbon Monoxide; D005978:Glutathione