title: Evolution of liver antioxidant status and iron implication during the development of deoxycorticosterone-saline hypertension in rats.
abstract: Hypertension is known to be associated with an oxidative stress resulting from an imbalance of antioxidant defense mechanisms in various tissues. The purpose of this study was to investigate the relationship between the increase of arterial blood pressure, measured during the gradual development of experimental hypertension in deoxycorticosterone (DOCA)-salt-treated rats, and an early imbalance of liver antioxidant status. The levels of liver oxidant/antioxidant markers and iron were studied during the induction of hypertension in 3-, 6-, and 8-wk DOCA-salt-treated Sprague-Dawley rats. Hepatic antioxidant defenses were decreased as early as 3 wk of hypertensive treatment: the decrease of peroxidase-reductase-transferase and catalase activities was associated with a significant increase of thiobarbituric acid reactive substances (TBARS) levels. Liver oxidative stress increased until 6 wk and remained stable at 8 wk of DOCA-salt treatment. Concurrently, liver iron levels were increased at 6 wk and returned to normal values after 8 wk of hypertensive treatment. Iron seems to be an inductor of liver oxidative stress and responsible for the persistent oxidative stress, most likely through secondary free-radical release. Thus, our data (1) confirm that hypertension in DOCA-salt-treated rats might be a free-radical-dependent disease where hepatic oxidant/antioxidant imbalance is obviously involved from the beginning of blood pressure elevation and (2) suggest that the use of suitable iron chelators might reverse liver oxidative stress associated with the increase of blood pressure.
authors.affiliation: Laboratoire de Physiologie-Pharmacologie-Nutrition Préventive Expérimentale, UFR des Sciences Médicales et Pharmaceutiques, 25030 Besançon Cedex, France.
authors.forename: Fatiha
authors.initials: F
authors.lastname: Elhaïmeur
authors.forename: Laurence
authors.initials: L
authors.lastname: Nicod
authors.forename: Carol
authors.initials: C
authors.lastname: Courderot-Masuyer
authors.forename: Sophie
authors.initials: S
authors.lastname: Robin
authors.forename: Catherine
authors.initials: C
authors.lastname: Guyon
authors.forename: Malika
authors.initials: M
authors.lastname: Bouhaddi
authors.forename: Jacques
authors.initials: J
authors.lastname: Regnard
authors.forename: Lysiane
authors.initials: L
authors.lastname: Richert
authors.forename: Alain
authors.initials: A
authors.lastname: Berthelot
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001794:Blood Pressure; D003600:Cytosol / Q000378:metabolism; D003900:Desoxycorticosterone / Q000737:chemistry* / Q000494:pharmacology; D005978:Glutathione / Q000378:metabolism; D006973:Hypertension / Q000378:metabolism*; D007501:Iron / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D016877:Oxidants / Q000378:metabolism; D018384:Oxidative Stress; D010100:Oxygen / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012965:Sodium Chloride / Q000494:pharmacology; D017392:Thiobarbituric Acid Reactive Substances; D013997:Time Factors; D014131:Trace Elements
chemical_list: D000975:Antioxidants; D016877:Oxidants; D017392:Thiobarbituric Acid Reactive Substances; D014131:Trace Elements; D009569:Nitric Oxide; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D007501:Iron; D005978:Glutathione; D010100:Oxygen