Effect of cigarette smoking on pentane excretion in alveolar breath.

The concentrations of acetone, isoprene, and pentane in alveolar breath were examined in 50 smokers and 50 nonsmokers by gas chromatography. The baseline pentane in smokers was 0.17 +/- 0.03 nmol/L (mean +/- SE), which was not different from pentane in nonsmokers (0.23 +/- 0.03 nmol/L). There were also no differences between smokers and nonsmokers in the concentrations of acetone and isoprene. Serial breath samples were obtained from 15 smokers before smoking and at 5, 15, and 60 min after smoking. Although acetone was not altered by smoking, isoprene increased by 86% +/- 26% 5 min after smoking (P <0.001) and returned to baseline 10 min later. Pentane increased by 456% +/- 156% 5 min after smoking (P <0.001) and remained increased 10 min later (204% +/- 73% of baseline, P <0.05). Isoprene concentrations in mainstream cigarette smoke were >5000 times greater than breath concentrations, whereas pentane could not be detected in mainstream smoke. Because pentane is produced from the peroxidation of n-6 polyunsaturated fatty acids, the results provide evidence that cigarette smoking causes an immediate increase in lipid peroxidation.

Regulation of the membrane attack complex of complement. Evidence that C8 gamma is not the target of homologous restriction factors.

Inability of the membrane attack complex of C (C5b-9) to efficiently lyse E from the same species has been attributed to one or more membrane-associated proteins that are collectively called homologous restriction factors. These include a 65,000 Mr protein referred to as the C8 binding protein or homologous restriction factor and a 20,000 Mr protein referred to as P-18, HRF20, CD59 Ag, or MIRL. Both are found on nucleated cells as well as E and both protect against complement-mediated lysis by interfering with C8 and/or C9 function within C5b-9. The exact mechanism by which these factors restrict activity is unknown but studies with purified C8 binding protein suggest they may interact specifically with the gamma subunit of C8. To determine directly if gamma is the target of restriction factors, a derivative of human C8 lacking this subunit was evaluated for its potential to lyse homologous cells. This derivative (C8') was previously shown to be functionally equivalent to normal C8 in a heterologous sheep E system. Here, it is compared to normal C8 by using human E as target cells. Results indicate no difference between the ability of C8 and C8' to incorporate into HuEAC1-7, to mediate subsequent C9 binding and to promote hemolysis. Thus, the presence or absence of gamma has no effect on homologous restriction of C5b-9, therefore gamma cannot be the primary target of homologous restriction factors.