Moderate zinc restriction during fetal and postnatal growth of rats: effects on adult arterial blood pressure and kidney.
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.
Cátedra de Fisiología, Facultad de Farmacia y Bioquímica, Junín 956, piso 7, Ciudad Autónoma de Buenos Aires, Argentina.
Analía Lorena
AL
Tomat
Felipe
F
Inserra
Luciana
L
Veiras
María Constanza
MC
Vallone
Ana María
AM
Balaszczuk
María Angeles
MA
Costa
Cristina
C
Arranz
D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D017209:Apoptosis; D001794:Blood Pressure; D002374:Catalase / Q000378:metabolism; D003404:Creatinine / Q000378:metabolism; D005260:Female; D005355:Fibrosis; D005919:Glomerular Filtration Rate; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D007668:Kidney / Q000201:enzymology / Q000254:growth & development / Q000473:pathology / Q000503:physiopathology*; D007774:Lactation; D015227:Lipid Peroxidation; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D009929:Organ Size; D018384:Oxidative Stress; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011507:Proteinuria / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase; D013997:Time Factors; D014886:Weaning; D015032:Zinc / Q000172:deficiency*
D003404:Creatinine; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D015032:Zinc