title: Ovariectomy exacerbates oxidative stress and cardiopathy induced by adriamycin.
abstract: Ovarian hormone depletion in ovariectomized experimental animals is a useful model with which to study the physiopathological consequences of menopause in women. It has been suggested that menopause is a risk factor for the induction of several cardiovascular disorders. In the present study we analyzed the effects of ovarian hormone depletion by ovariectomy (OVX) in a model of oxidative stress and cardiopathy induced by adriamycin (AD). To evaluate these effects, we measured parameters related to cardiac damage (creatinine kinase, lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase) and oxidative stress (malondialdehyde, catalase, superoxide dismutase, glutathione peroxidase, reduced glutathione, nitric oxide and carbonyl proteins) in cardiac tissue and erythrocytes. OVX was found to alter all markers of oxidative stress and cell damage in cardiac tissue. Similarly, the OVX-derived loss of ovarian hormones enhanced cardiac damage and oxidative stress induced by AD. Our results suggest that antioxidant status in cardiac tissue and erythrocytes is seriously compromised by OVX during the cardiomyopathy induced by AD in experimental animals. In conclusion, the absence of hormones caused by OVX or menopause may induce or accelerate pre-existing cardiovascular dysfunctions.
authors.affiliation: Department of Biochemistry and Molecular Biology, School of Medicine, Reina Sofia University Hospital, Cordoba, Spain. juanr.munoz.exts@juntadeandalucia.es
authors.forename: Juan Rafael
authors.initials: JR
authors.lastname: Muñoz-Castañeda
authors.forename: Jordi
authors.initials: J
authors.lastname: Muntané
authors.forename: Carmen
authors.initials: C
authors.lastname: Herencia
authors.forename: Maria C
authors.initials: MC
authors.lastname: Muñoz
authors.forename: Inmaculada
authors.initials: I
authors.lastname: Bujalance
authors.forename: Pedro
authors.initials: P
authors.lastname: Montilla
authors.forename: Issac
authors.initials: I
authors.lastname: Túnez
mesh_terms: D000818:Animals; D002374:Catalase / Q000097:blood / Q000378:metabolism; D004317:Doxorubicin / Q000633:toxicity*; D004912:Erythrocytes / Q000737:chemistry / Q000201:enzymology; D005260:Female; D005978:Glutathione / Q000032:analysis / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood / Q000378:metabolism; D006331:Heart Diseases / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D015227:Lipid Peroxidation; D008593:Menopause; D023421:Models, Animal; D009206:Myocardium / Q000737:chemistry / Q000201:enzymology; D010052:Ovariectomy; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000097:blood / Q000378:metabolism
chemical_list: D004317:Doxorubicin; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione