Morphological and functional effects on cardiac tissue induced by moderate zinc deficiency during prenatal and postnatal life in male and female rats

Abstract

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.

Developmental programming of vascular dysfunction by prenatal and postnatal zinc deficiency in male and female rats

“…These alterations were related to changes in apoptosis, inflammatory cytokines, growth factors expression, oxidative stress and NO system. On the other hand, females would be less sensitive to this micronutrient deficiency since they exhibited no significant structural or functional cardiac alterations and lower changes in NO system [22,23,56].…”

“…In both 6-and 81-day-old rats, Picrosirius Red staining allowed us to measure perivascular collagen area (CA), expressed as the CA/LA ratio ((μm 2 /μm 2 )*100) in 5-μmthick aortic sections [23]. Collagen fibers in aortic tunica media of 81-day-old rats were evaluated on a subjective scale ranging from 0 to 4 (0: very poor staining of collagen fibers, 1: poor, 2: moderate, 3: intense, 4: very intense).…”

Perinatal Protein Undernutrition and Cardiovascular System: A Systematic Review

“…However, the cardiomyocytes continue to proliferate for a while in the postnatal period. 2 Several elements are important to maintain the integrity of this system, such as zinc, which is necessary for the cardiac development, 3 and tryptophan, which is important for the development of the cardiorespiratory center in the medulla oblongata. 4 Thus, a balanced diet is essential for pregnant women to promote a healthy development of the fetus.…”

Early-in-life dietary zinc deficiency and supplementation and mammary tumor development in adulthood female rats

“…Thus, marginal zinc deficiency intake in adulthood can also induce zinc accumulation and oxidative stress in the mammary tissue [20]. Other experimental studies have showed that moderate-tosevere zinc deficiency during fetal life and lactation has shown adverse effects on rat blood pressure and renal and cardiac function in adult life [21][22][23].…”