Evolution of liver antioxidant status and iron implication during the development of deoxycorticosterone-saline hypertension in rats

• Published in: Biological trace element research 2005-12, Vol.107 (3), p.263-276
• Main Authors: Elhaïmeur, Fatiha, Nicod, Laurence, Courderot-Masuyer, Carol, Robin, Sophie, Guyon, Catherine, Bouhaddi, Malika, Regnard, Jacques, Richert, Lysiane, Berthelot, Alain
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants; Antioxidants - metabolism; Blood Pressure; Cats; Cytosol; Cytosol - metabolism; Desoxycorticosterone; Desoxycorticosterone - chemistry; Desoxycorticosterone - pharmacology; Glutathione; Glutathione - metabolism; Hypertension; Hypertension - metabolism; Iron; Iron - metabolism; Life Sciences; Liver; Liver - metabolism; Nitric Oxide; Nitric Oxide - metabolism; Oxidants; Oxidants - metabolism; Oxidative Stress; Oxidizing agents; Oxygen; Oxygen - metabolism; Pharmaceutical sciences; Rats; Rats, Sprague-Dawley; Rodents; Salts; Sodium Chloride; Sodium Chloride - pharmacology; Thiobarbituric Acid Reactive Substances; Time Factors; Trace Elements
• ISSN: 0163-4984; 0163-4984; 1559-0720
• DOI: 10.1385/BTER:107:3:263

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.