Mild zinc deficiency in male and female rats: early postnatal alterations in renal nitric oxide system and morphology

TOMAT AL; VEIRAS LC; AGUIRRE S; FASOLI H; ELESGARAY, R; CANIFFI C; COSTA M.A; ARRANZ C

NUTRITION

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2013 vol. 29 p. 568 - 573

0899-9007

Objective: Fetal and postnatal zinc deficiency induces an increase in arterial blood pressure and impairs renal function in male adult rats. We therefore hypothesized that these renal alterations are already present in early stages of life and that there are gender 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 days of life. Methods: Female Wistar rats received low (8 ppm) or control (30 ppm) zinc diets from the beginning of pregnancy up to weaning. Glomeruli number, morphology, oxidative stress, apoptotic cells, nitric oxide synthase activity and protein expression were evaluated in kidneys of offspring at 21 days. Results: Zinc deficiency decreased nephron number, induced glomerular hypertrophy, increased oxidative damage and diminished nitric oxide synthase activity in male and female kidneys. Nitric oxide synthase activity was not affected by inhibitors of the neuronal or inducible isoforms, so nitric oxide is mainly generated via the endothelial isoenzyme. Gender differences were observed in glomerular areas and antioxidant enzymes activity. Conclusion: 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. Gender differences observed in this model may explain dissimilar development of hypertension and renal diseases in adult life.