Oxidative stress due to free radical formation and initiation of abnormal oxidative reactions is involved in several diseases of newborns, such as hypoxic-ischemic encephalopathy. Melatonin, an endogenously produced indoleamine primarily formed in the pineal gland, is a potent free radical scavenger as well as an indirect antioxidant. The present study was conducted to evaluate the formation of oxidative damage mediators and the possible effect of melatonin treatment in a model of hypoxic-ischemic encephalopathy in 7-day-old rats. Pups were subjected to permanent ligation of the right common carotid artery and exposed for 2.5 hr to a nitrogen-oxygen mixture (92% and 8%, respectively) (hypoxia-ischemia, HI). Melatonin was injected intraperitoneally to a group of rats at the dose of 15 mg/kg 30 min before starting the ischemic procedure (HI-Melatonin). After 24 hr of treatment, in homogenized cerebral cortex, desferoxamine (DFO)-chelatable free iron, total F2-isoprostanes and total F4-neuroprostanes, originating from the free radical-catalyzed peroxidation of arachidonic and docosahexaenoic acids, respectively, were determined. HI induced a significant increase in DFO-chelatable iron, total F2-isoprostanes and F4-neuroprostanes in both right and left side of the cerebral cortex. In HI-Melatonin-treated animals the levels of free iron, F2-isoprostanes, and F4-neuroprostanes were significantly lower than that in HI rats and the values were similar to controls. These data show the important neuroprotective role of melatonin in reducing oxidative damage resulting from HI. Melatonin could represent a potential safe approach to perinatal brain damage in humans. © 2008 The Authors.

Signorini, C., Ciccoli, L., Leoncini, S., Carloni, S., Perrone, S., Comporti, M., et al. (2009). Free iron, total F2-isoprostanes and total F4-neuroprostanes in a model of neonatal hypoxic-ischemic encephalopathy: neuroprotective effect of melatonin. JOURNAL OF PINEAL RESEARCH, 46(2), 148-154 [10.1111/j.1600-079X.2008.00639.x].

Free iron, total F2-isoprostanes and total F4-neuroprostanes in a model of neonatal hypoxic-ischemic encephalopathy: neuroprotective effect of melatonin

SIGNORINI, C.;CICCOLI, L.;LEONCINI, S.;COMPORTI, M.;BUONOCORE, G.
2009-01-01

Abstract

Oxidative stress due to free radical formation and initiation of abnormal oxidative reactions is involved in several diseases of newborns, such as hypoxic-ischemic encephalopathy. Melatonin, an endogenously produced indoleamine primarily formed in the pineal gland, is a potent free radical scavenger as well as an indirect antioxidant. The present study was conducted to evaluate the formation of oxidative damage mediators and the possible effect of melatonin treatment in a model of hypoxic-ischemic encephalopathy in 7-day-old rats. Pups were subjected to permanent ligation of the right common carotid artery and exposed for 2.5 hr to a nitrogen-oxygen mixture (92% and 8%, respectively) (hypoxia-ischemia, HI). Melatonin was injected intraperitoneally to a group of rats at the dose of 15 mg/kg 30 min before starting the ischemic procedure (HI-Melatonin). After 24 hr of treatment, in homogenized cerebral cortex, desferoxamine (DFO)-chelatable free iron, total F2-isoprostanes and total F4-neuroprostanes, originating from the free radical-catalyzed peroxidation of arachidonic and docosahexaenoic acids, respectively, were determined. HI induced a significant increase in DFO-chelatable iron, total F2-isoprostanes and F4-neuroprostanes in both right and left side of the cerebral cortex. In HI-Melatonin-treated animals the levels of free iron, F2-isoprostanes, and F4-neuroprostanes were significantly lower than that in HI rats and the values were similar to controls. These data show the important neuroprotective role of melatonin in reducing oxidative damage resulting from HI. Melatonin could represent a potential safe approach to perinatal brain damage in humans. © 2008 The Authors.
Signorini, C., Ciccoli, L., Leoncini, S., Carloni, S., Perrone, S., Comporti, M., et al. (2009). Free iron, total F2-isoprostanes and total F4-neuroprostanes in a model of neonatal hypoxic-ischemic encephalopathy: neuroprotective effect of melatonin. JOURNAL OF PINEAL RESEARCH, 46(2), 148-154 [10.1111/j.1600-079X.2008.00639.x].
File in questo prodotto:
File Dimensione Formato  
Pineal pdf 2009.pdf

non disponibili

Tipologia: Post-print
Licenza: NON PUBBLICO - Accesso privato/ristretto
Dimensione 290.44 kB
Formato Adobe PDF
290.44 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/20249
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo