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Impact of Moderate Zinc Deficiency During Fetal Life and Postnatal Growth on Cardiac Nitric Oxyde System, Inflammatory and Oxidative Markers in Adult Male Rats
Author(s) -
Juriol Lorena,
Gobetto Natalia,
Mendes Garrido Facundo,
Pineda Gonzalo,
Dasso Marina,
Toblli Jorge,
Carranza Andrea,
Elesgaray Rosana,
Tomat Analía,
Arranz Cristina
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.957.3
Subject(s) - endocrinology , medicine , enos , nitric oxide synthase , endothelial nos , tbars , zinc deficiency (plant disorder) , proinflammatory cytokine , oxidative stress , nitric oxide , chemistry , biology , inflammation , lipid peroxidation , zinc , organic chemistry
Moderate zinc deficiency during fetal and postnatal growth programs cardiovascular dysfunction and hypertension. Male zinc deficient rats showed reduced left ventricular (LV) wall thickness and ejection fraction. Aim: to evaluate nitric oxide (NO) system, pro‐inflammatory cytokines and oxidative state in LV of adult male rats exposed to this deficiency. Wistar rats received during pregnancy up to weaning low (L:8 ppm) or control (C:30 ppm) zinc diet. After weaning, male offspring fed low (l) or control (c) zinc diet during 60 days (Cc, Ll, Lc). At day 81, we evaluated in LV: Interleukin‐6 and Tumor Necrosis Factor‐α (IL‐6;TNF‐α), basal NO synthase (NOS) and endothelial, neuronal and inducible (eNOS;nNOS;iNOS) isoforms activities; eNOS and Ser1177 eNOS phosphorylation protein expression (eNOS/β‐actin; p Ser1177 eNOS/eNOS), mRNA expression (eNOS/GAPDH) and lipid peroxidation end products (TBARS). Means±SEM, n=6/group. One way ANOVA, Bonferroni post‐test.Cc Ll Lc TNF‐α (immunohistochemistry;% of positive staining/area) 1.4±0.4 20.4±2.0* 1.7±0.3 IL‐6 (immunohistochemistry; % of positive staining/area) 1.8±0.3 21.1±1.7* 2.8±0.8 Basal NOS Activity (pmol 14 C L‐citrulline/g tissue.min) 204±6 164±10* 157±11* Basal NOS+iNOS inhibitor (Aminoguanidine; pmol 14 C L‐citrulline/g tissue.min) 216±7 166±8* 163±9* Basal NOS+nNOS inhibitor (7‐nitroindazole; pmol 14 C L‐citrulline/g tissue.min) 209±10 166±8* 164±9* Basal NOS+Ca 2+ ‐calmodulin inhibitor (Calmidazolium; pmol 14 C L‐citrulline/g tissue.min) 47±2# 52±2# 49±2# pSer1177eNOS/eNOS (Western Blot; optical density relative to Cc) 1.00±0.02 0.74±0.03* 1.02±0.16 TBARS (nmol/mg protein) 0.21±0.02 0.78±0.08* 0.47±0.02*†No differences were found in eNOS protein and mRNA expression. *p<0.01vsCc;†p<0.01vsLl;#p<0,01vs basal NOS. Zinc deficiency during fetal and postnatal life programs a lower production and bioavailability of cardiac NO due to decreased activity and p Ser1177 of eNOS and increased TBARS. These alterations, jointly with higher levels of IL‐6 and TNF‐α, could contribute to the cardiac disorders previously observed. Supported by:UBA‐CONICET