Sauerstoffzufuhr zu den Wurzeln von Pflanzen aus Feuchtgebieten

Aquatic macrophytes or plants living in wet soils have to cope with oxygen shortage around their roots and rhizomes. These organs are not able to take up oxygen from the surrounding medium and have to rely internal oxygen supply through aerenchymatous spaces in the plants. The present study tries to elucidate the mechanism of oxygen supply to the roots of Acorus calamus, Iris pseudacorus, and Phragmites communis. Release of oxygen out of the roots could be of special importance because the species could contribute in the aeration of sewage sludges. Gas escape from the plants roots was found to be species specific: in Acorus and Phragmites rates of 1-2 ml of air h high -1 were calculated, whereas Iris was found to emit not more than 0.2 ml air h high -1 per plant. The reasons for the differences in diffusion are discussed

Metabolism of 1,3-butadiene to toxicologically relevant metabolites in single-exposed mice and rats.

1,3-Butadiene (BD) was carcinogenic in rodents. This effect is related to reactive metabolites such as 1,2-epoxy-3-butene (EB) and especially 1,2:3,4-diepoxybutane (DEB). A third mutagenic epoxide, 3,4-epoxy-1,2-butanediol (EBD), can be formed from DEB and from 3-butene-1,2-diol (B-diol), the hydrolysis product of EB. In BD exposed rodents, only blood concentrations of EB and DEB have been published. Direct determinations of EBD and B-diol in blood are missing. In order to investigate the BD-dependent blood burden by all of these metabolites, we exposed male B6C3F1 mice and male Sprague-Dawley rats in closed chambers over 6–8 h to constant atmospheric BD concentrations. BD and exhaled EB were measured in chamber atmospheres during the BD exposures. EB blood concentrations were obtained as the product of the atmospheric EB concentration at steady state with the EB blood-to-air partition coefficient. B-diol, EBD, and DEB were determined in blood collected immediately at the end of BD exposures up to 1200 ppm (B-diol, EBD) and 1280 ppm (DEB). Analysis of BD was done by GC/FID, of EB, DEB, and B-diol by GC/MS, and of EBD by LC/MS/MS. EB blood concentrations increased with BD concentrations amounting to 2.6 ?mol/l (rat) and 23.5 ?mol/l (mouse) at 2000 ppm BD and to 4.6 ?mol/l in rats exposed to 10000 ppm BD. DEB (detection limit 0.01 ?mol/l) was found only in blood of mice rising to 3.2 ?mol/l at 1280 ppm BD. B-diol and EBD were quantitatively predominant in both species. B-diol increased in both species with the BD exposure concentration reaching 60 ?mol/l at 1200 ppm BD. EBD reached maximum concentrations of 9.5 ?mol/l at 150 ppm BD (rat) and of 42 ?mol/l at 300 ppm BD (mouse). At higher BD concentrations EBD blood concentrations decreased again. This picture probably results from a competitive inhibition of the EBD producing CYP450 by BD, which occurs in both species