Carbon monoxide conversion with Clostridium aceticum.

Carbon monoxide concentrations in syngas are often high, but tolerance toward CO varies a lot between homoacetogenic bacteria. Analysis of the autotrophic potential revealed that the first isolated acetogenic bacterium Clostridium aceticum was able to use CO as sole carbon and energy source for chemolithoautotrophic carbon fixation but simultaneously showed little tolerance to high CO concentrations. Not yet reported, autotrophic ethanol production by C. aceticum was discovered with CO as a substrate in batch processes. Growth rates estimated in batch processes at varying CO partial pressures were used to identify the CO inhibition kinetics of C. aceticum, using a substrate inhibition model. C. aceticum shows a strong CO inhibition with an optimum CO partial pressure of only 5.4 mbar in the gas phase at cell dry weight concentrations of up to 0.5 g·L -1 . At optimum conditions, growth and acetate formation rates were estimated to be 0.24 hr -1 and 0.52 g·g -1 ·hr -1 , respectively. Syngas fermentation at high partial pressures of up to 280 mbar CO in the inlet gas phase was enabled by applying a continuously operated stirred-tank bioreactor with submerged membranes with total cell retention. Around 70% CO conversion was achieved continuously in the membrane bioreactor with strongly CO inhibited C. aceticum resulting in space-time yields of up to 0.85 g·L -1 ·hr -1 acetate.

A timeline of hydrogen sulfide (H2S) research: From environmental toxin to biological mediator.

The history of H2S - as an environmental toxin - dates back to 1700, to the observations of the Italian physician Bernardino Ramazzini, whose book "De Morbis Artificum Diatriba" described the painful eye irritation and inflammation of "sewer gas" in sewer workers. The gas has subsequently been identified as hydrogen sulfide (H2S), and opened three centuries of research into the biological roles of H2S. The current article highlights the key discoveries in the field of H2S research, including (a) the toxicological studies, which characterized H2S as an environmental toxin, and identified some of its modes of action, including the inhibition of mitochondrial respiration; (b) work in the field of bacteriology, which, starting in the early 1900s, identified H2S as a bacterial product - with subsequently defined roles in the regulation of periodontal disease (oral bacterial flora), intestinal epithelial cell function (enteral bacterial flora) as well as in the regulation of bacterial resistance to antibiotics; and (c), work in diverse fields of mammalian biology, which, starting in the 1940s, identified H2S as an endogenous mammalian enzymatic product, the functions of which - among others, in the cardiovascular and nervous system - have become subjects of intensive investigation for the last decade. The current review not only enumerates the key discoveries related to H2S made over the last three centuries, but also compiles the most frequently cited papers in the field which have been published over the last decade and highlights some of the current 'hot topics' in the field of H2S biology.

Regulation of mitochondrial bioenergetic function by hydrogen sulfide. Part I. Biochemical and physiological mechanisms.

Until recently, hydrogen sulfide (H2 S) was exclusively viewed a toxic gas and an environmental hazard, with its toxicity primarily attributed to the inhibition of mitochondrial Complex IV, resulting in a shutdown of mitochondrial electron transport and cellular ATP generation. Work over the last decade established multiple biological regulatory roles of H2 S, as an endogenous gaseous transmitter. H2 S is produced by cystathionine γ-lyase (CSE), cystathionine ß-synthase (CBS) and 3-mercaptopyruvate sulfurtransferase (3-MST). In striking contrast to its inhibitory effect on Complex IV, recent studies showed that at lower concentrations, H2 S serves as a stimulator of electron transport in mammalian cells, by acting as a mitochondrial electron donor. Endogenous H2 S, produced by mitochondrially localized 3-MST, supports basal, physiological cellular bioenergetic functions; the activity of this metabolic support declines with physiological aging. In specialized conditions (calcium overload in vascular smooth muscle, colon cancer cells), CSE and CBS can also associate with the mitochondria; H2 S produced by these enzymes, serves as an endogenous stimulator of cellular bioenergetics. The current article overviews the biochemical mechanisms underlying the stimulatory and inhibitory effects of H2 S on mitochondrial function and cellular bioenergetics and discusses the implication of these processes for normal cellular physiology. The relevance of H2 S biology is also discussed in the context of colonic epithelial cell physiology: colonocytes are exposed to high levels of sulfide produced by enteric bacteria, and serve as a metabolic barrier to limit their entry into the mammalian host, while, at the same time, utilizing it as a metabolic 'fuel'.