title: Behaviour of the anti-oxidant defence system and heme oxygenase-1 protein expression in fructose-hypertensive rats.
abstract: 1. Addition of fructose to a rat diet for various periods of time leads to hypertension, hyperinsulinaemia and dyslipidaemia and provides a model for testing oxidative stress parameters in the animals. 2. In the present study, oxidative stress generation, the soluble and enzymatic defence system and heme oxygenase-1 (HO-1) protein expression were investigated in the heart, liver and kidney of rats fed fructose for a period of 1 or 8 months. 3. Compared with the control group, fructose-hypertensive rats showed increased in lipid peroxidation only in the heart after both 1 and 8 months of fructose treatment. Changes in the behaviour of the soluble and enzymatic defence system and HO-1 protein expression were different depending on the organ. Increased or unaltered activities of anti-oxidant enzymes were found in the liver and kidney, respectively. Induction of HO-1 prevented the generation of oxidative stress in the liver, where the activity of anti-oxidant defence enzymes was not reduced. Increased expression of HO-1 protein was not able to prevent the generation of oxidative stress in the heart, where fructose treatment diminished the activity of anti-oxidant enzymes. 4. The results of the present study demonstrate that upregulation of HO-1 may prevent the generation of oxidative stress only when the anti-oxidant defence system is still operative.
authors.affiliation: Departamento de Química Biológica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
authors.forename: Ariel H
authors.initials: AH
authors.lastname: Polizio
authors.forename: Soledad
authors.initials: S
authors.lastname: Gonzales
authors.forename: Marina C
authors.initials: MC
authors.lastname: Muñoz
authors.forename: Clara
authors.initials: C
authors.lastname: Peña
authors.forename: María L
authors.initials: ML
authors.lastname: Tomaro
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001794:Blood Pressure; D002374:Catalase / Q000378:metabolism; D004040:Dietary Carbohydrates / Q000008:administration & dosage; D005632:Fructose / Q000008:administration & dosage; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism*; D006973:Hypertension / Q000139:chemically induced / Q000201:enzymology* / Q000503:physiopathology; D007668:Kidney / Q000201:enzymology; D008099:Liver / Q000201:enzymology; D008297:Male; D023421:Models, Animal; D009206:Myocardium / Q000201:enzymology; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D000975:Antioxidants; D004040:Dietary Carbohydrates; D017392:Thiobarbituric Acid Reactive Substances; D005632:Fructose; D002374:Catalase; D005979:Glutathione Peroxidase; D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat; D013482:Superoxide Dismutase; D005978:Glutathione