Gomez N N, Ojeda M S, Gimenez M S
Department of Biochemistry and Biological Sciences, Faculty of Chemistry, Biochemistry and Pharmacy, National University of San Luis, Argentina.
Lipids. 2002 Mar;37(3):291-6. doi: 10.1007/s11745-002-0893-3.
There have been a limited number of studies investigating surfactant lipid changes in lung with trace elements. The present investigation was designed to examine the effect of moderate zinc deficiency on the lipid metabolism in rat lung. We also evaluated whether zinc deficiency, which is a wide-spread problem, could play a role in adult respiratory distress syndrome (ARDS). For that purpose, adult male Wistar rats were fed two diets differing in zinc concentration. The rats were divided into two groups. One group was fed a zinc-deficient diet containing 3 mg Zn/kg, and the other group received a zinc-adequate control diet with 30 mg Zn/kg according to AIN 93-M. After 2 mon of treatment, we observed that in the zinc-deficient group (i) total lipids, phospholipids, and cholesterol increased whereas TG decreased in whole lung; (ii) phospholipid (PC) concentration increased in lamellar bodies and alveolar macrophages and decreased in extracellular surfactant but did not change in microsomes; (iii) protein concentration decreased in whole lung, extracellular surfactant, lamellar bodies, and macrophages; (iv) the incorporation of [Me-14C]choline into PC (phospholipids) of lung slices increased; and (v) the activity of CTP/phosphocholine cytidylyltransferase bound to the microsomes increased in the lung. These results suggest that the lipid concentration in the lung (especially the phospholipids) is modified directly or indirectly by a zinc-deficient diet. In a zinc-deficient diet, the lung changes the pattern of PC for an adaptive or recovery stage. Therefore, zinc deficiency implications are important for the design of therapies and public health interventions involving targeted zinc supplementation for high-risk groups or groups with certain diseases, such as ARDS.
研究微量元素对肺表面活性物质脂质变化的数量有限。本研究旨在探讨中度锌缺乏对大鼠肺脂质代谢的影响。我们还评估了广泛存在的锌缺乏问题是否可能在成人呼吸窘迫综合征(ARDS)中起作用。为此,成年雄性Wistar大鼠喂食两种锌浓度不同的饲料。大鼠分为两组。一组喂食含锌量为3mg/kg的缺锌饲料,另一组根据AIN 93-M标准喂食含锌量为30mg/kg的锌充足对照饲料。治疗2个月后,我们观察到在缺锌组中:(i)全肺总脂质、磷脂和胆固醇增加,而甘油三酯减少;(ii)板层小体和肺泡巨噬细胞中的磷脂(PC)浓度增加,细胞外表面活性物质中的磷脂浓度降低,而微粒体中的磷脂浓度未变化;(iii)全肺、细胞外表面活性物质、板层小体和巨噬细胞中的蛋白质浓度降低;(iv)[甲基-14C]胆碱掺入肺切片PC(磷脂)中的量增加;(v)肺中与微粒体结合的CTP/磷酸胆碱胞苷转移酶活性增加。这些结果表明,缺锌饮食直接或间接改变了肺中的脂质浓度(尤其是磷脂)。在缺锌饮食中,肺会改变PC模式以进入适应或恢复阶段。因此 zinc deficiency implications对于为高危人群或患有某些疾病(如ARDS)的人群设计针对性补锌的治疗方法和公共卫生干预措施具有重要意义。