PubMed · 14425215
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P B MUMFORD. 1960. Dihydroxyacetone.. https://doi.org/10.1111/j.1365-2133.1960.tb13891.x
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Dermal contact with some organic disinfection by-products (DBPs) such as trihalomethanes in chlorinated drinking water has been established to be an important exposure route. We evaluated dermal absorption of two haloketones (1,1-dichloropropanone and 1,1,1-trichloropropanone) and chloroform while bathing, by collecting and analyzing time profiles of expired breath samples of six human subjects during and following a 30-min bath. The DBP concentrations in breath increased towards a maximum concentration during bathing. The maximum haloketone breath concentration during dermal exposure ranged from 0.1 to 0.9 microg / m(3), which was approximately two orders of magnitude lower than the maximum chloroform breath concentration during exposure. Based on a one-compartment model, the in vivo permeability of chloroform, 1,1-dichloropropanone, and 1,1,1-trichloropropanone were approximated to be 0.015, 7.5 x 10(- 4), and 4.5 x 10(- 4) cm / h, respectively. Thus, haloketones are much less permeable across human skin under normal bathing conditions than is chloroform. These findings will be useful for future assessment of total human exposure and consequent health risk of these DBPs.
Analysis of breath acetone has been used as a diagnostic tool for diabetes. Due to its nature of volatility and activity, it is very difficult to accurately measure the concentration of acetone in human breath by gas chromatography-mass spectrometry (GC-MS). To overcome this problem, we developed a new method using GC-MS and solid-phase microextraction (SPME) with on-fiber derivatization to determine acetone in human breath. Breath gas from controls and diabetic patients was collected in 3-l Tedlar bags. O-2,3,4,5,6-(Pentafluorobenzyl) hydroxylamine hydrochloride (PFBHA) in solution was firstly adsorbed on the SPME fiber of 65 microm polydimethylsiloxane-divinylbenzene (PDMS-DVB), and then the fiber was further headspace exposed in exhaled gas in the Tedlar bag at 40 degrees C for 4 min. Finally, the formed acetone oxime on the fiber was desorbed and analyzed by GC-MS. Using external standard method, acetone in the human breath was quantitatively analyzed by measurement of its oxime. The method provided a low detection limit of 0.049 ppbv for acetone in breath, relative standard deviation (R.S.D.) value of 3.4%, excellent accuracy. In addition, the method required simple sample preparation and no organic solvent. Acetone in diabetic breath was found to be higher than 1.71 ppmv, while its concentration in normal breath was lower than 0.76 ppmv. The results show that GC-MS and SPME with on-fiber derivatization is a simple, rapid and sensitive and solvent-free method for determination of low concentration acetone in breath and analysis of breath acetone can be used as supplementary tool for diagnosis of diabetes.
Aminoacetone (AA) is a threonine metabolite accumulated in threoninemia, cri-du-chat, and diabetes, where it contributes toward the formation of cytotoxic and genotoxic methylglyoxal (MG). Oxyradicals yielded from iron-catalyzed AA aerobic oxidation to MG are shown here to promote Ca2+ -mediated mitochondrial membrane permeabilization in an AA dose-dependent way. The inhibitory effect of added EGTA, cyclosporin A, Mg2+, and DTT observed in this study suggests the formation of transition pores in the inner mitochondrial membrane by AA, associated with thiol protein aggregation. That the mitochondrial iron pool plays a coadjutant role in the transition of mitochondrial permeability is indicated by the dramatic inhibitory effect of added o-phenanthroline. Iron released from ferritin by AA oxidation products--superoxide anion and AA enolyl radicals--is shown to act as an alternative source of ferrous iron, intensifying the mitochondrial damage. These findings may contribute to clarify the role of accumulated AA and iron overload in the mitochondrial oxidative damage reportedly occurring in diabetes mellitus.