Biological methylation and hydride formation of metals and metalloids are ubiquitous environmental processes that can lead to the formation of chemical species with significantly increased mobility and toxicity. While much is known about the interaction of metal(loid)s with microorganisms in environmental settings, little information has been gathered on respective processes inside the human body as yet. Here, the biotransformation and excrDie Biomethylierung und die Hydridbildung von Metall(oid)en sind ubiquitäre Prozesse in der Umwelt, die zur Bildung von chemischen Spezies mit erhöhter Mobilität und Toxizität führen können. Während viel über die Wechselwirkung von Metall(oid)en mit Mikroorganismen unter Umweltbedingungen ermittelt wurde, sind bisher nur wenige Informationen über vergleichbare Prozesse im Menschen vorhanden. Diese Arbeit stellt einen Beitrag zur Biotransformation und Eliminierung von Bismut im Menschen dar, die in zwei Probandenstudien mit massenspektrometrischen Kopplungstechniken (GC/ICP-MS, GC/EI-MS/ICP-MS, GC/MS und ICP-MS) untersucht wurden. Weiterhin wurden humane Hepatozyten (HepG2) mit Bismut-haltigen Reagenzien (CBS, Bismutcystein und Bismutglutathion) inkubiert, um durch die Detektion der Metaboliten in vitro Hinweise auf die Beteiligung der humanen Leber an der Biomethylierung des Bismuts zu erhalten. Bei der ersten Probandenstudie wurde 20 männlichen Probanden eine Dosis von 215 mg Bismut in Form von Bismutsubcitrat oral verabreicht und die Biotransformation und Eliminierung des Bismut beobachtet. Die sehr geringe Bismut-Resorption im Magen uetion of bismuth following ingestion of bismuth in two studies were investigated with hyphenated mass spectrometric techniques (GC/ICP-MS, GC/EI-MS/ICP-MS, GC/MS and ICP-MS). In addition, human hepatoma cells (HepG2) were incubated with bismuth containing compounds (CBS, bismuth cysteine, bismuth glutathione) in order to investigate the involvement of the human liver in the biomethylation of bismuth in vitro. In the first study the biotransformation and excretion of bismuth following ingestion of bismuth subcitrate (215 mg bismuth) to 20 male human volunteers were investigated. Bismuth absorption in the stomach and upper intestine was very low, as evidenced by the small quantity of bismuth eliminated via the renal route. Total bismuth concentrations in blood increased rapidly in the first hour following ingestion. Most of the ingested bismuth was excreted via feces during the study period. Trace levels of the metabolite trimethylbismuth ((CH3)3Bi) were detected via low temperature-gas chromatography/inductively coupled plasma-mass spectrometry (LT-GC/ICP-MS) in blood samples and in exhaled air samples. Concentrations were in the range of up to 2.50 pg/ml (blood) and 0.8-458 ng/m3 (exhaled air), with high inter-individual variation. Elimination routes of bismuth were exhaled air (up to 0.03 ‰), urine (0.03-1.2 %), and feces. In the second study the biotransformation and excretion were observed with a higher time resolution. Here, in three experiments 215 mg bismuth (twice) and 430 mg bismuth (single) were given to the same male volunteer. The results of the first study were basically confirmed and, moreover, a few characteristic (CH3)3Bi concentration maxima were detected in exhaled air – each time after food intake. This observation indicates the involvement of enzymes in the biotransformation of bismuth, which were activated by food intake. In addition to this result (CH3)3Bi was detected in feces samples in a range from 1738 ng/kg to 5679 ng/kg. The headspace analysis of human hepatoma cells (HepG2) which were incubated with bismuth containing compounds (CBS, bismuth cysteine, bismuth glutathione) indicated that (CH3)3Bi was not detectable in any of the samples. After ethylation with sodium tetraethylborate at pH 7 monomethyl diethyl bismuth was found in cell lysates of cell cultures which were incubated with CBS or bismuth cysteine. In contrast, no monomethyl diethyl bismuth was not detectable after incubation with bismuth glutathione. These results show that human hepatoma cells have the potential to methylate bismuth and that the permethylated species is not generated within the observed time period. If methylation was not observed as in the case of bismuth glutathione, this might result from the low uptake of this compound into the hepatoma cells. In conclusion, it was shown in these studies that bismuth is methylated in the human body. It appears from the results that both the intestinal microflora and the liver are involved in this biotransformation.