The effect of ruthenium red during Ca2+ depletion and repletion in the isolated perfused rat liver.
Perfusion of rat liver with Ca(2+)-depleted buffer induces oxidative stress and liver damage, which can be prevented by Ca2+ repletion (Okuda et al. J Lab Clin Med). In the present study, we investigated the action of ruthenium red on acute Ca2+ loading after Ca2+ depletion in the isolated perfused rat liver. The major findings of this study are that 1) Ca2+ depletion-induced liver damage was related to mitochondrial disfunction; 2) ruthenium red inhibited the oxidative stress and liver damage normally seen during Ca2+ depletion; 3) ruthenium red inhibited the Ca2+ depletion-induced mitochondrial disfunction. These observations suggest that mitochondrial Ca2+ cycling is responsible for Ca2+ depletion-induced oxidative stress and liver damage.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008930:Mitochondria, Liver / Q000187:drug effects; D010101:Oxygen Consumption; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control; D012430:Ruthenium Red / Q000494:pharmacology*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D017392:Thiobarbituric Acid Reactive Substances; D012430:Ruthenium Red; D007770:L-Lactate Dehydrogenase; D002118:Calcium