Liver cells transform inorganic bismuth into potentially toxic methylated species, according to observations from scientists in Germany.

Inorganic bismuth is known to have low toxicity and is often used as a lead substitute, for example in paints and alloys; it is even used in medicine as an antigastric and antiulcer agent. However, there is evidence that intestinal microflora can convert inorganic bismuth compounds into multiply-methylated species, which are highly toxic and can cause brain disfunction. Now Markus Hollmann and colleagues, at the University of Duisberg-Essen, have shown that human hepatic cells can also convert inorganic bismuth to organic bismuth. 

Hepatic cells could play a role in bismuth methylation in vivo

The researchers incubated the cells with various bismuth complexes and trapped the resulting volatile bismuth species by mixing the cell lysate with sodium tetraethylborate to form heavier ethylated derivatives. They could then analyse the mixture using a combined gas chromatography-mass spectrometry technique. They found that some bismuth species were methylated but bismuth glutathione was not, indicating that cell uptake of bismuth is species-dependent. 

'As far as we know, this study is the first to show bismuth methylation using mammalian cells and our work provides another piece in the puzzle of bismuth toxicology and bismuth metabolism,' says Hollmann.

Yasumitsu Ogra, an expert in chemical toxicology from Showa Pharmaceutical University, Tokyo, Japan, agrees.

'The evidence for bismuth methylation may give novel toxicological insight,' he says. 'The technique paves a road to speciation of other volatile metal/metalloid-containing metabolites in biological samples,' he adds. 

The German team plans to pursue several avenues in future research. These include investigating the methylation process and its time dependency and kinetics, and eventually the cellular distributions of the bismuth compounds.

Carl Saxton

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