Stable isotope fractionation by Clostridium pasteurianum. 3. Effect of SeO32- on the physiology and associated sulfur isotope fractionation during SO32- and SO42- reductions.
Increased SeO32- concentration reduced H2S evolution from SO32- during whole cell and cell-free extract reductions by Clostridium pasteurianum. H2S production from SO42- was completely inhibited by SeO32- in stationary phase cells. Generation times increased with greater SeO32- concentration, the increase with 1 mM SeO32- being a factor of 2.5 for 1 mM SO32-, and over 3 for 1 mM SO42- reductions. In vitro and in vivo experiments with proposed intermediates of the SO32- reduction pathway show that SeO32- inhibited both the S3O62- to S2O32- and S2O32- to S2- reaction sequences with the latter being more pronounced in growth experiments. Both extracts and whole cells reduced SeO32- to Se0 but Se0 granules were not found in the cell's cytoplasm. The formation of S2O32- by an extracellular chemical mechanism appears not to have occurred in these experiments. Increased SeO32- concentration had the effect of compressing the isotopic release pattern for H2S along the H2S production axis and did not significantly alter the maximum and minimum values of delta 34S. Thus, inhibition by SeO32- limited the conversions of sulfur species without altering the isotopic selectivity of rate-controlling steps in the pathway.
D002474:Cell-Free System; D003013:Clostridium / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D006862:Hydrogen Sulfide / Q000378:metabolism; D012643:Selenium / Q000494:pharmacology*; D018036:Selenium Compounds; D064588:Selenium Oxides; D013431:Sulfates / Q000378:metabolism*; D013447:Sulfites / Q000378:metabolism*
D018036:Selenium Compounds; D064588:Selenium Oxides; D013431:Sulfates; D013447:Sulfites; D012643:Selenium; D006862:Hydrogen Sulfide