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Eur J Nutr. 2018 Mar;57(2):569-583. doi: 10.1007/s00394-016-1343-5. Epub 2016 Nov 7.

Cardiac changes in apoptosis, inflammation, oxidative stress, and nitric oxide system induced by prenatal and postnatal zinc deficiency in male and female rats.

Author information

1
Instituto de la Química y Metabolismo del Fármaco (IQUIMEFA). Facultad de Farmacia y Bioquímica, Cátedra de Fisiología, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, 956, piso 7, 1113, Junín, Ciudad Autónoma de Buenos Aires, Argentina.
2
Laboratorio de Terapia Molecular y Celular, Fundación Instituto Leloir, IIBBA-CONICET, Avenida Patricias Argentinas 435, 1405, Buenos Aires, Argentina.
3
Facultad de Farmacia y Bioquímica, Cátedra de Farmacología, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, 956, piso 5, 1113, Junín, Ciudad Autónoma de Buenos Aires, Argentina.
4
Laboratorio Medicina Experimental, Hospital Alemán, Avenida Pueyrredón 1640, C1118 AAT, Buenos Aires, Argentina.
5
Instituto de la Química y Metabolismo del Fármaco (IQUIMEFA). Facultad de Farmacia y Bioquímica, Cátedra de Fisiología, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, 956, piso 7, 1113, Junín, Ciudad Autónoma de Buenos Aires, Argentina. atomat@ffyb.uba.ar.

Abstract

PURPOSE:

Zinc restriction during fetal and postnatal development could program cardiovascular diseases in adulthood. The aim of this study was to determine the effects of zinc restriction during fetal life, lactation, and/or post-weaning growth on cardiac inflammation, apoptosis, oxidative stress, and nitric oxide system of male and female adult rats.

METHODS:

Wistar rats were fed a low- or a control zinc diet during pregnancy and up to weaning. Afterward, offspring were fed either a low- or a control zinc diet until 81 days of life. IL-6 and TNF-α levels, TUNEL assay, TGF-β1 expression, thiobarbituric acid-reactive substances that determine lipoperoxidation damage, NADPH oxidase-dependent superoxide anion production, antioxidant and nitric oxide synthase activity, mRNA and protein expression of endothelial nitric oxide synthase, and serine1177 phosphorylation isoform were determined in left ventricle.

RESULTS:

Zinc deficiency activated apoptotic and inflammatory processes and decreased TGF-β1 expression and nitric oxide synthase activity in cardiac tissue of both sexes. Male zinc-deficient rats showed no changes in endothelial nitric oxide synthase expression, but a lower serine1177 phosphorylation. Zinc deficiency induced an increase in antioxidant enzymes activity and no differences in lipoperoxidation products levels in males. Females were less sensitive to this deficiency exhibiting lower increase in apoptosis, lower decrease in expression of TGF-β1, and higher antioxidant and nitric oxide enzymes activities. A zinc-adequate diet during postnatal life reversed most of these mechanisms.

CONCLUSION:

Prenatal and postnatal zinc deficiency induces alterations in cardiac apoptotic, inflammatory, oxidative, and nitric oxide pathways that could predispose the onset of cardiovascular diseases in adult life.

KEYWORDS:

Cardiac apoptosis; Cardiac nitric oxide system; Cardiac oxidative stress; Moderate zinc deficiency; Prenatal and postnatal growth; Sex differences

PMID:
27822638
DOI:
10.1007/s00394-016-1343-5
[Indexed for MEDLINE]

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