Zinc deficiency during growth: Influence on renal function and morphology

Tomat, Analia Lorena; Costa, María A.; Girgulsky, Luciana Carolina; Veiras, Luciana C.; Weisstaub, A.; Inserra, Felipe; Balaszczuk, Ana M.; Arranz, Cristina

doi:10.1016/j.lfs.2006.12.035

Cited by 28 publications

(38 citation statements)

References 46 publications

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“…However, this alteration could not be prevented by an adequate zinc diet after weaning. This degree of blood pressure elevation dramatically increases the risk of cardiovascular events (40,41,42,44,48). Moreover, in the present study, we demonstrated, for the first time, that fetal and postnatal zinc restriction does not modify blood pressure levels in females.…”

Section: Discussionsupporting

confidence: 57%

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

Tomat

Juriol

Gobetto

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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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.

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Section: Discussionsupporting

confidence: 57%

“…Blood from offspring at 6, 21, and 81 days of life and from mothers at weaning was collected to determine serum zinc concentration using atomic absorption spectrophotometry (Varian Spectrophotometer Spectr AA-20, air acetylene flame, 0.5-nm slit, wavelength of 213.9 nm, Perkin-Elmer, Norwalk, CT) (41,44).…”

Section: Methodsmentioning

confidence: 99%

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

Tomat

Juriol

Gobetto

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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“…AGEs decrease phosphorylation activity of eNOS and increase eNOS mRNA degradation, leading to the reduction in eNOS and the subsequent NO production (Rojas and Morales, 2004). Enzymatic activity of eNOS is also sensitive to zinc (Tomat et al, 2007). Zinc is required Fig.…”

Section: Discussionmentioning

confidence: 99%

Effects of zinc and manganese on advanced glycation end products (AGEs) formation and AGEs-mediated endothelial cell dysfunction

et al. 2012

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“…These alterations were associated with decreased activity of the vascular and renal nitric oxide system, an increase in systemic oxidative stress, activation of the renal apoptosis process, and a reduction in the renal filtration surface area (24,25). Therefore, we hypothesize that zinc deficiency during fetal life and early postnatal growth could be an adverse environment for the development of the cardiovascular and renal systems.…”

mentioning

confidence: 99%

Moderate zinc restriction during fetal and postnatal growth of rats: effects on adult arterial blood pressure and kidney

Tomat¹,

Inserra²,

Veiras³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Intrauterine and postnatal zinc restriction may result in an adverse environment for the development of cardiovascular and renal systems. This study evaluated the effects of moderate zinc deficiency during fetal life, lactation, and/or postweaning growth on systolic blood pressure, renal function, and morphology in adult life. Female Wistar rats received low (8 ppm) or control (30 ppm) zinc diets from the beginning of pregnancy up to weaning. After weaning, male offspring of each group of mothers were fed low or control zinc diet. Systolic blood pressure, creatinine clearance, proteinuria, renal morphology, renal apoptosis. and renal oxidative stress state were evaluated after 60 days. Zinc deficiency during pre- and postweaning growth induced an increase in systolic blood pressure and a decrease in the glomerular filtration rate associated with a reduction in the number and size of nephrons. Activation of renal apoptosis, reduction in catalase activity, glutathione peroxidase activity, and glutathione levels and increase in lipid peroxidation end products could explain these morphometric changes. Zinc deficiency through pre- and postweaning growth induced more pronounced renal alteration than postweaning zinc deficiency. These animals showed signs of renal fibrosis, proteinuria, increased renal apoptosis, and higher lipid peroxidation end products. A control diet during postweaning growth did not totally overcome renal oxidative stress damage, apoptosis, and fibrosis induced by zinc deficiency before weaning. In conclusion, zinc deficiency during a critical period of renal development and maturation could induce functional and morphological alterations that result in elevated blood pressure and renal dysfunction in adult life.

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Zinc deficiency during growth: Influence on renal function and morphology

Cited by 28 publications

References 46 publications

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

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

Effects of zinc and manganese on advanced glycation end products (AGEs) formation and AGEs-mediated endothelial cell dysfunction

Moderate zinc restriction during fetal and postnatal growth of rats: effects on adult arterial blood pressure and kidney

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