Release of phospholipase A and triglyceride lipase from rat liver.
Release of phospholipase A and triglyceride lipase from rat liver.
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从大鼠肝脏中释放磷脂酶 A 和甘油三酯脂肪酶。
DOI：
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发表时间：
1978
影响因子：
4.8
通讯作者：
S. Margolis
中科院分区：
文献类型：
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作者：
G. Sundaram;K. Shakir;G. Barnes;S. Margolis
一种新的，快速的，和灵敏的测定磷脂酶A，利用市售的[14 C]磷脂酰乙醇胺与14 C标记的棕榈酸部分，被用来研究磷脂酶A从灌注的肝脏，肝细胞和肠细胞从大鼠释放。肝素触发了灌注肝脏中磷脂酶A的迅速释放。磷脂酶A和甘油三酯脂肪酶从肝细胞释放的线性速率为1小时和30分钟，分别。肝素（20 u/ml）使肝细胞释放磷脂酶A和甘油三酯脂肪酶加倍。秋水仙碱（0.1 mM），但不是嘌呤霉素（0.2 mM），抑制基础和肝素刺激的磷脂酶A释放40%。由于释放到培养基中的磷脂酶A和甘油三酯脂肪酶的量大大超过细胞内活性，因此分泌可能与酶的非活性形式到活性形式的细胞内转化相结合。二丁酰环AMP（1 mM）抑制磷脂酶A（48%）和甘油三酯脂肪酶（82%）从肝细胞释放。肾上腺素、地塞米松和氯贝特抑制甘油三酯脂肪酶的释放，但不抑制磷脂酶A。肠细胞的磷脂酶A活性大于肝细胞，但无论是肝素还是双丁酰环磷酸腺苷影响肠细胞释放磷脂酶A。这些结果表明，肝脏是肝素后血浆磷脂酶A的主要来源。二丁酰环腺苷酸影响这些酶的释放，这一事实表明，激素调节脂质和脂蛋白代谢的另一种机制。
A new, rapid, and sensitive assay for phospholipase A, utilizing commercially available [14C]phosphatidylethanolamine with 14C label in both palmitic acid moieties, was used to study phospholipase A release from perfused liver, hepatocytes, and intestinal cells from rats. Heparin triggered a prompt release of phospholipase A from perfused liver. Phospholipase A and triglyceride lipase were released from hepatocytes at a linear rate for 1 h and 30 min, respectively. Heparin (20 u/ml) doubled the release of phospholipase A and triglyceride lipase from hepatocytes. Colchicine (0.1 mM), but not puromycin (0.2 mM), inhibited basal and heparin-stimulated phospholipase A release by 40%. Since the amount of phospholipase A and triglyceride lipase released into the medium greatly exceeded intracellular activities, it is possible that secretion is coupled with intracellular conversion from inactive to active forms of the enzymes. Dibutyryl cyclic AMP (1 mM) inhibited phospholipase A (48%) and triglyceride lipase (82%) release from hepatocytes. Epinephrine, dexamethasone, and clofibrate inhibited release of triglyceride lipase but not phospholipase A. Phospholipase A activity of intestinal cells was greater than in hepatocytes, but neither heparin nor dibutyryl cyclic AMP affected phospholipase A release from intestinal cells. These results suggest that the liver is a major source of phospholipase A of postheparin plasma. The fact that dibutyryl cyclic AMP affects the release of these enzymes suggests an additional mechanism for hormonal regulation of lipid and lipoprotein metabolism.