Ovariectomy exacerbates oxidative stress and cardiopathy induced by adriamycin.
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.
Muñoz-Castañeda
Juan Rafael
JR
Department of Biochemistry and Molecular Biology, School of Medicine, Reina Sofia University Hospital, Cordoba, Spain. juanr.munoz.exts@juntadeandalucia.es
Muntané
Jordi
J
Herencia
Carmen
C
Muñoz
Maria C
MC
Bujalance
Inmaculada
I
Montilla
Pedro
P
Túnez
Issac
I
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
D004317:Doxorubicin; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione