Morphological and functional effects on cardiac tissue induced by moderate zinc deficiency during prenatal and postnatal life in male and female rats.
The aim of this study was to evaluate whether moderate zinc restriction in rats throughout fetal life, lactation, and/or postweaning growth results in early changes in cardiac morphology predisposing the onset of cardiac dysfunction in adult life as well as sex-related differences in the adaptation to this nutritional injury. Female Wistar rats received low or control zinc diets from the beginning of pregnancy up to offspring weaning. After being weaned, offspring were fed either a low or control zinc diet until 81 days. Systolic blood pressure was measured. Echocardiographic and electrocardiographic examinations, morphological experiments, and apoptosis by TUNEL assay were performed in the left ventricle. In the early stages, zinc-deficient male and female offspring showed an increase in cardiomyocyte diameter, probably associated with an increase in cardiac apoptotic cells, but smaller myocyte diameters in adulthood. In adult males, this nutritional injury induced decreased contractility and dilatation of the left ventricle, not allowing the heart to compensate the higher levels of blood pressure, and hypertrophic remodeling of coronary arteries associated with increased blood pressure. Adequate zinc intake during postweaning life did not overcome blood pressure levels but reversed some of the detrimental effects of earlier zinc deficiency in cardiac morphology and function. Females were less sensitive to this deficiency, exhibiting normal levels of blood pressure and no structural or functional heart alterations in adult life. The present study demonstrates that the effects of zinc deficiency on blood pressure, cardiac morphology, and function differ between sexes, with males more predisposed to develop cardiovascular diseases in adulthood.
Cátedra de Fisiología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Instituto de Química y Metabolismo del Fármaco-Consejo Nacional de Investigaciones Científicas y Técnicas, Ciudad Autónoma de Buenos Aires, Argentina; and.
Analia Lorena
AL
Tomat
Lorena Vanesa
LV
Juriol
María Natalia
MN
Gobetto
Luciana Cecilia
LC
Veiras
Facundo
F
Mendes Garrido Abregú
Judith
J
Zilberman
Héctor
H
Fasoli
Rosana
R
Elesgaray
María Ángeles
MÁ
Costa
Cristina Teresa
CT
Arranz
D000367:Age Factors; D000818:Animals; D001794:Blood Pressure; D003331:Coronary Vessels / Q000378:metabolism* / Q000473:pathology; D004032:Diet; D005260:Female; D005865:Gestational Age; D006331:Heart Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006352:Heart Ventricles / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007774:Lactation / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017208:Rats, Wistar; D012307:Risk Factors; D012737:Sex Factors; D016277:Ventricular Function, Left; D015430:Weight Gain; D015032:Zinc / Q000097:blood / Q000172:deficiency*
D015032:Zinc
heart morphology and function; moderate zinc deficiency; prenatal and postnatal growth; sex differences