Acyl-CoA binding proteins inhibit the nonenzymic S-acylation of cysteinyl-containing peptide sequences by long-chain acyl-CoAs.

Acyl-CoA binding proteins (ACBPs) from rat and bovine liver were found to inhibit the nonenzymic S-acylation of two representative types of peptides by long-chain acyl-CoAs. As demonstrated previously [Quesnel, S. & Silvius, J. R. (1994) Biochemistry 33 13340-13348; Bharadwaj, M., & Bizzozero, O. A. (1995) J. Neurochem. 65, 1805-1815], peptides with the sequences myristoyl-GCG, myristoyl-GCV, and IRYCWLRR-NH2, all representing physiological S-acylation sites in mammalian proteins, become S-acylated at appreciable rates in the presence of long-chain acyl-CoAs and large unilamellar lipid vesicles. Addition of ACBP at physiological molar ratios with respect to long-chain acyl-CoAs strongly inhibits the spontaneous S-acylation reaction, in a manner that can be quantitatively described by assuming that the ACBP sequesters the acyl-CoA with nanomolar affinity in a complex unable to serve as an S-acyl donor. From these results, we calculate that at physiological (intracellular) concentrations of ACBP, long-chain acyl-CoAs, and membrane lipids the expected half-times for spontaneous S-acylation of such protein sequences by long-chain acyl-CoAs will lie in the range of several tens of hours. The nonenzymic reaction of protein cysteine residues with long-chain acyl-CoAs is thus unlikely to contribute significantly to the physiological modification of signaling and other proteins that show relatively rapid rates of S-acylation in mammalian cells. However, it cannot be excluded that a nonenzymic reaction with long-chain acyl-CoAs could contribute to the physiological S-acylation of certain membrane proteins if the latter exhibit very slow kinetics of S-acylation in vivo.

Endocrine-like cells of the pulmonary epithelium of the human adult lung.

The morphological and histochemical characteristics of endocrine-like cells of the pulmonary epithelium of the right lower lobe of 12 human adult lungs were studied. Few cells were reactive to the argyrophil silver method of Grimelius and of Sevier and Munger and cells with a similar morphology and distribution emitted a green or yellow fluorescence after treatment of the lung epithelium with the amine presursors L-DOPA or L-HTP, respectively. A greater number of cells seems to be demonstrated by electron microscopy. The cells were characterized by small, round secretory granules showing a central dense core and a very thin clear halo between the core and the surrounding membrane. The cells are thought to be related to the endocrine-like cells of the pulmonary epithelium of the human foetal lung and to cells of carcinoids of larger bronchi.

Acid-base status before and after arterial clamping.

The necessity of providing alkalizing therapy after re-establishment of the local circulation was studied in 10 otherwise healthy patients with intermittent claudication. No such necessity was found in providing stable peroperative circulation, normo- to slight hypothermia, adequate infusions, and normal acid-base values prior to arterial clamping. It is pointed out that alkalosis can cause circulatory problems that are just as serious as those occurring with acidosis; therefore the routine use of alkalizing agents during vascular surgery is inadvisable. Should unstable circulatory parameters occur and hypoperfusion be suspected, then repeated control of the acid-base values is indicated.