Free radical overproduction contributes to tissue damage induced by acute hyperglycemia. Dehydroepiandrosterone, which has recently been found to have antioxidant properties, was administered i.p. to rats at different doses (10, 50 or 100 mg/kg body weight) 3 h before treatment with dextrose (5 g/kg). Lipid peroxidation was evaluated on liver, brain and kidney homogenates, measuring both steady-state concentrations of thiobarbituric acid reactive substances, and fluorescent chromolipids, evaluated as hydroxynonenal adducts. Formation of thiobarbituric acid reactive substances was significantly higher in hyperglycemic than in normoglycemic animals. Three hours (but not 1 h) dehydroepiandrosterone-pretreatment protected tissues against lipid peroxidation induced by dextrose; both thiobarbituric acid reactive substances and hydroxynonenal adducts in liver, kidney and brain homogenates were significantly lower in dehydroepiandrosterone-pretreated animals. Dehydroepiandrosterone did not modify the cytosolic level of antioxidants, such as alpha-tocopherol or glutathione, nor the activities of glutathione peroxidase, reductase or transferase. The results of this study indicate that the 'in vivo' administration of dehydroepiandrosterone increases tissue resistance to lipid peroxidation triggered by acute hyperglycemia.

Dehydroepiandrosterone administration prevents the oxidative damage induced by acute hyperglycemia in rats.

ARAGNO, Manuela;TAMAGNO, Elena;DANNI, Oliviero;BOCCUZZI, Giuseppe
1997

Abstract

Free radical overproduction contributes to tissue damage induced by acute hyperglycemia. Dehydroepiandrosterone, which has recently been found to have antioxidant properties, was administered i.p. to rats at different doses (10, 50 or 100 mg/kg body weight) 3 h before treatment with dextrose (5 g/kg). Lipid peroxidation was evaluated on liver, brain and kidney homogenates, measuring both steady-state concentrations of thiobarbituric acid reactive substances, and fluorescent chromolipids, evaluated as hydroxynonenal adducts. Formation of thiobarbituric acid reactive substances was significantly higher in hyperglycemic than in normoglycemic animals. Three hours (but not 1 h) dehydroepiandrosterone-pretreatment protected tissues against lipid peroxidation induced by dextrose; both thiobarbituric acid reactive substances and hydroxynonenal adducts in liver, kidney and brain homogenates were significantly lower in dehydroepiandrosterone-pretreated animals. Dehydroepiandrosterone did not modify the cytosolic level of antioxidants, such as alpha-tocopherol or glutathione, nor the activities of glutathione peroxidase, reductase or transferase. The results of this study indicate that the 'in vivo' administration of dehydroepiandrosterone increases tissue resistance to lipid peroxidation triggered by acute hyperglycemia.
155(2)
233
240
M. ARAGNO; E. BRIGNARDELLO; E. TAMAGNO; V. GATTO; O. DANNI; G. BOCCUZZI
File in questo prodotto:
Non ci sono file associati a questo prodotto.

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: http://hdl.handle.net/2318/39764
Citazioni
  • ???jsp.display-item.citation.pmc??? 18
  • Scopus 128
  • ???jsp.display-item.citation.isi??? 116
social impact