Tou J S, Maier C
Biochim Biophys Acta. 1976 Dec 21;451(2):353-62. doi: 10.1016/0304-4165(76)90130-6.
The effects of dibutyryl cyclic adenosine 3':5'-monophosphate and ATP on isotope incorporation into phospholipids and the release of beta-glucuronidase into the extracellular medium were studied in polymorphonuclear leukocytes from guinea pig peritoneal exudates. Exogenous dibutyryl cyclic adenosine 3':5'-monophosphate (0.1--1.0 mM) reduced beta-glucoronidase release induced by cytochalasin B in the absence of inert particles. It selectively inhibited 32Pi incorporation into phosphatidic acid and the phosphoinositides and the incorporation of myo-[2-3H]inositol into the phosphoinositides. Added ATP (0.1--1.0 MM), but not other nucleotides, was found to potentiate beta-glucuronidase release provoked by cytochasin B, but it impaired the labeling of the phosphoinositides by myo-[2-3H]inositol. The mechanism of the inhibition the isotope incarparation into these acidic phospholipids by the two mucleotides has not been defined. Dibutyryl cyclic adenosine 3':5'-monophosphate at 2--4 mM concentration was not found to appreciably alter the incorporation of [gamma-32P]ATP into phosphatidic acid, phosphatidylinositol, diphosphoinositide, and triphosphoinositide.
在豚鼠腹腔渗出液的多形核白细胞中,研究了二丁酰环腺苷3':5'-单磷酸和ATP对同位素掺入磷脂以及β-葡萄糖醛酸酶释放到细胞外介质中的影响。在没有惰性颗粒的情况下,外源性二丁酰环腺苷3':5'-单磷酸(0.1 - 1.0 mM)减少了细胞松弛素B诱导的β-葡萄糖醛酸酶释放。它选择性地抑制32Pi掺入磷脂酸和磷酸肌醇,以及肌醇-[2-3H]肌醇掺入磷酸肌醇。发现添加的ATP(0.1 - 1.0 mM),而不是其他核苷酸,可增强细胞松弛素B引起的β-葡萄糖醛酸酶释放,但它损害了肌醇-[2-3H]肌醇对磷酸肌醇的标记。尚未确定这两种核苷酸抑制同位素掺入这些酸性磷脂的机制。未发现浓度为2 - 4 mM的二丁酰环腺苷3':5'-单磷酸明显改变[γ-32P]ATP掺入磷脂酸、磷脂酰肌醇、二磷酸肌醇和三磷酸肌醇的情况。