info:eu-repo/semantics/article
Effect of melatonin treatment on oxygen consumption by rat liver mitochondria
Fecha
2006-03Registro en:
Reyes Toso, Carlos Felipe; Rebagliati, Ines Rosa; Ricci, C. R.; Linares, L. M.; Albornoz, L. E.; et al.; Effect of melatonin treatment on oxygen consumption by rat liver mitochondria; Springer; Amino Acids; 31; 3; 3-2006; 299-302
0939-4451
CONICET Digital
CONICET
Autor
Reyes Toso, Carlos Felipe
Rebagliati, Ines Rosa
Ricci, C. R.
Linares, L. M.
Albornoz, L. E.
Cardinali, Daniel Pedro
Zaninovich, A.
Resumen
The objective of this study was to examine the in vivo effect of melatonin on rat mitochondrial liver respiration. Two experiments were performed: For experiment 1, adult male rats received melatonin in the drinking water (16 or 50 mg=ml) & vehicle during 45 days. For experiment 2, rats received melatonin in the drinking water (50 mg=ml) for 45 days, or the same amount for 30 days followed by a 15 day-withdrawal period. At sacrifice, a liver mitochondrial fraction was prepared and oxygen consumption was measured polarographically in the presence of excess concentration of DL-3-b-hydroxybutyrate or L-succinate. Melatonin treatment decreased Krebs’ cycle substrate-induced respiration significantly at both examined doses. The stimulation of mitochondrial respiration caused by excess concentration of substrate recovered after melatonin withdrawal. Basal state 4 respiration was not modified by melatonin. Melatonin, by curtailing overstimulation of cellular respiration caused by excess Krebs’ cycle substrates, can protect the mitochondria from oxidative damage.