Eskelson C D, Chvapil M, Strom K A, Vostal J J
Department of Surgery, University of Arizona Health Sciences Center, Tucson 85724.
Environ Res. 1987 Dec;44(2):260-71. doi: 10.1016/s0013-9351(87)80235-9.
Rats chronically exposed to diesel particulates (dp) or given intratracheally a single dose of dp show increased levels of phospholipids in the lungs and in pulmonary lavage fluid. Pulmonary phospholipidosis is accompanied by increased lecithin levels and by increased palmitate content in lecithin of both lungs and pulmonary lavage fluid. A de novo increase of pulmonary and hepatic phospholipid (PL) formation was detected 5 days after rats were treated with dp. We hypothesize that a dp-stressed lung releases a pulmonary lipogenic factor (PLF), which stimulates hepatic lipogenesis. This was further tested by an in vitro study in which primary cultures of free hepatocytes were incubated with [2-14C]acetate and various molecular weight fractions of a pulmonary homogenate from rats. The results from these studies indicated that in rat lung homogenates a PLF exists of greater than 100,000 Da molecular mass. The results also indicate that respired air containing a dp concentration of greater than 750 micrograms dp/m3 of air would result in a mild phospholipidosis in the lung, whereas a dp dose in respired air of 250 micrograms dp/m3 of air for 2 years did not alter pulmonary PL content in rats.
长期暴露于柴油颗粒（dp）的大鼠或经气管内给予单次剂量dp的大鼠，其肺和肺灌洗液中的磷脂水平会升高。肺磷脂沉着症伴有肺和肺灌洗液中卵磷脂水平升高以及卵磷脂中棕榈酸含量增加。在用dp处理大鼠5天后，检测到肺和肝磷脂（PL）的从头合成增加。我们假设，受dp应激的肺会释放一种肺脂肪生成因子（PLF），该因子会刺激肝脂肪生成。通过一项体外研究进一步对此进行了测试，在该研究中，将原代游离肝细胞培养物与[2-¹⁴C]乙酸盐以及来自大鼠肺匀浆的各种分子量级分一起孵育。这些研究结果表明，在大鼠肺匀浆中存在一种分子量大于100,000 Da的PLF。结果还表明，吸入空气中dp浓度大于750微克dp/m³的空气会导致肺部出现轻度磷脂沉着症，而吸入空气中dp剂量为250微克dp/m³持续2年不会改变大鼠肺部的PL含量。
