Tomat Analía Lorena, Costa María Angeles, Girgulsky Luciana Carolina, Veiras Luciana, Weisstaub Adriana Ruth, Inserra Felipe, Balaszczuk Ana María, Arranz Cristina Teresa
Cátedra de Fisiología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, IQUIMEFA-CONICET, Junín 956, Piso 7, 1113 Ciudad Autónoma de Buenos Aires, Argentina.
Life Sci. 2007 Mar 13;80(14):1292-302. doi: 10.1016/j.lfs.2006.12.035. Epub 2007 Jan 20.
This study was designed to investigate the effects of moderate zinc deficiency during growth on renal morphology and function in adult life. Weaned male Wistar rats were divided into two groups and fed either a moderately zinc-deficient diet (zinc: 8 mg/kg, n=12) or a control diet (zinc: 30 mg/kg, n=12) for 60 days. We evaluated: renal parameters, NADPH-diaphorase and nitric oxide synthase activity in kidney, renal morphology and apoptotic cells in renal cortex. Zinc-deficient rats showed a decrease in glomerular filtration rate and no changes in sodium and potassium urinary excretion. Zinc deficiency decreased NADPH diaphorase activity in glomeruli and tubular segment of nephrons, and reduced activity of nitric oxide synthase in the renal medulla and cortex, showing that zinc plays an important role in preservation of the renal nitric oxide system. A reduction in nephron number, glomerular capillary area and number of glomerular nuclei in cortical and juxtamedullary areas was observed in zinc deficient kidneys. Sirius red staining and immunostaining for alpha-smooth muscle-actin and collagen III showed no signs of fibrosis in the renal cortex and medulla. An increase in the number of apoptotic cells in distal tubules and cortical collecting ducts neighboring glomeruli and, to a lesser extent, in the glomeruli was observed in zinc deficient rats. The major finding of our study is the emergence of moderate zinc deficiency during growth as a potential nutritional factor related to abnormalities in renal morphology and function that facilitates the development of cardiovascular and renal diseases in adult life.
本研究旨在调查生长期间中度锌缺乏对成年期肾脏形态和功能的影响。将断奶雄性Wistar大鼠分为两组，分别给予中度缺锌饮食（锌含量：8毫克/千克，n = 12）或对照饮食（锌含量：30毫克/千克，n = 12），持续60天。我们评估了：肾脏参数、肾脏中NADPH-黄递酶和一氧化氮合酶活性、肾脏形态以及肾皮质中的凋亡细胞。缺锌大鼠的肾小球滤过率降低，尿钠和尿钾排泄无变化。锌缺乏降低了肾小球和肾单位肾小管段中的NADPH黄递酶活性，并降低了肾髓质和皮质中一氧化氮合酶的活性，表明锌在维持肾脏一氧化氮系统中起重要作用。在缺锌肾脏中，观察到皮质和近髓区域的肾单位数量、肾小球毛细血管面积和肾小球细胞核数量减少。天狼星红染色以及α-平滑肌肌动蛋白和III型胶原蛋白的免疫染色显示肾皮质和髓质无纤维化迹象。在缺锌大鼠中，观察到与肾小球相邻的远端小管和皮质集合管中的凋亡细胞数量增加，在肾小球中也有程度较轻的增加。我们研究的主要发现是，生长期间出现的中度锌缺乏是一种潜在的营养因素，与肾脏形态和功能异常有关，这可能促使成年期心血管和肾脏疾病的发生。
