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.

Mild zinc deficiency in male and female rats: early postnatal alterations in renal nitric oxide system and morphology.

OBJECTIVE: Fetal and postnatal zinc deficiencies induce an increase in arterial blood pressure and impair renal function in male adult rats. We therefore hypothesized that these renal alterations are present in early stages of life and that there are sexual differences in the adaptations to this nutritional injury. The aim was to study the effects of moderate zinc deficiency during fetal life and lactation on renal morphology, oxidative stress, apoptosis, and the nitric oxide system in male and female rats at 21 d of life. METHODS: Female Wistar rats received low (8 ppm) or control (30 ppm) zinc diets from the beginning of pregnancy to weaning. Glomerulus number, morphology, oxidative stress, apoptotic cells, nitric oxide synthase activity, and protein expression were evaluated in the kidneys of offspring at 21 d. RESULTS: Zinc deficiency decreased the nephron number, induced glomerular hypertrophy, increased oxidative damage, and decreased nitric oxide synthase activity in the male and female rat kidneys. Nitric oxide synthase activity was not affected by inhibitors of the neuronal or inducible isoforms, so nitric oxide was mainly generated by the endothelial isoenzyme. Gender differences were observed in glomerular areas and antioxidant enzyme activities. CONCLUSION: Zinc deficiency during fetal life and lactation induces an early decrease in renal functional units, associated with a decrease in nitric oxide activity and an increase in oxidative stress, which would contribute to increased arterial blood pressure and renal dysfunction in adulthood. The sexual differences observed in this model may explain the dissimilar development of hypertension and renal diseases in adult life.