title: Mild zinc deficiency in male and female rats: early postnatal alterations in renal nitric oxide system and morphology.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Cátedra de Fisiología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, IQUIMEFA-CONICET, Buenos Aires, Argentina. atomat@ffyb.uba.ar
authors.forename: Analia Lorena
authors.initials: AL
authors.lastname: Tomat
authors.forename: Luciana Cecilia
authors.initials: LC
authors.lastname: Veiras
authors.forename: Sofía
authors.initials: S
authors.lastname: Aguirre
authors.forename: Héctor
authors.initials: H
authors.lastname: Fasoli
authors.forename: Rosana
authors.initials: R
authors.lastname: Elesgaray
authors.forename: Carolina
authors.initials: C
authors.lastname: Caniffi
authors.forename: María Ángeles
authors.initials: MÁ
authors.lastname: Costa
authors.forename: Cristina Teresa
authors.initials: CT
authors.lastname: Arranz
mesh_terms: D000818:Animals; D017209:Apoptosis; D004032:Diet; D005260:Female; D006973:Hypertension / Q000209:etiology; D007668:Kidney / Q000473:pathology* / Q000503:physiopathology*; D007674:Kidney Diseases / Q000209:etiology; D007774:Lactation; D008297:Male; D008431:Maternal-Fetal Exchange; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D018384:Oxidative Stress; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017208:Rats, Wistar; D012737:Sex Factors; D015032:Zinc / Q000008:administration & dosage / Q000172:deficiency*
chemical_list: D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D015032:Zinc