Dolomite was successfully precipitated in culture experiments that simulated microbiogeochemical conditions prevailing during late stages of evaporation in ephemeral, hypersaline dolomitic lakes of the Coorong region, South Australia. Analyses of lake‐ and pore‐water samples document rapid geochemical changes with time and depth in both dolomitic and non‐dolomitic lakes. Extremely high sulphate and magnesium ion concentrations in lake waters decline rapidly with depth in pore waters throughout the sulphate‐reduction zone, whereas carbonate concentrations in pore waters reach levels up to 100 times those of normal sea water. Ultimately, sulphate is totally consumed and no solid sulphate is recorded in the dolomitic lake sediments. ‘Most probable number’ calculations of lake sediment samples record the presence of large populations of sulphate‐reducing bacteria, whereas sulphur‐isotope analyses of lake‐water samples indicate microbial fractionation in all the lakes studied. Viable populations of microbes from the lake sediments were cultured in anoxic conditions in the laboratory. Samples were then injected into vials containing sterilized clastic or carbonate grains, or glass beads, immersed in a solution that simulated the lake water. Falls in the levels of sulphate and rising pH in positive vials were interpreted as indicating active bacterial sulphate reduction accompanied by increased concentrations of carbonate. Within 2 months, sub‐spherical, sub‐micron‐size crystals of dolomite identical to those of lake sediments were precipitated. It is concluded that bacterial sulphate reduction overcomes kinetic constraints on dolomite formation by removing sulphate and releasing magnesium and calcium ions from neutral ion pairs, and by generating elevated carbonate concentrations, in a hypersaline, strongly electrolytic solution. The results demonstrate that bacterial sulphate reduction controls dolomite precipitation in both the laboratory experiments and lake sediments. It is proposed that dolomite formation, through bacterial sulphate reduction, provides a process analogue applicable to thick platformal dolostones of the past, where benthic microbial communities were the sole or dominant colonizers of shallow marine environments.

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Microbially mediated calcification can be traced back for at least 2.6 billion years. Although morphological comparison of fossil and recent microbial carbonates suggests that mineralization processes associated with cyanobacteria and their interactions with heterotrophic bacteria have remained similar from the Archaean until today, the metabolic and chemical details remain poorly constrained. Microbial consortia often exhibit an ability to change solution chemistry and control pH at the microscale, passively or actively. This leads to oversaturation of Ca 2 + and ions and to the removal of kinetic inhibitors to carbonate precipitation, like sulphate or phosphate. The kinetic barriers of low carbonate ion activity, ion hydration and ion complexing, especially in saline waters, inhibit spontaneous carbonate mineral precipitation from saturated solutions but oxygenic photosynthesis and sulphate reduction by sulphate-reducing bacteria can overcome these natural barriers. Sulphate in seawater tends to form pairs with Ca 2 + and Mg 2 + ions. The removal of sulphate reduces complexing, raises carbonate alkalinity, and along with pyrite formation, enhances carbonate precipitation. Cyanobacteria can store Ca 2 + and Mg 2 + ions in organic envelopes and precipitate carbonates within their sheaths and extracellular polymeric substances, thus, triggering sedimentary carbonate production. We propose that this interplay of cyanobacteria and heterotrophic bacteria has been the major contributor to the carbonate factory for the last 3 billion years of Earth history.

Epithelial cells lining respiratory airways can participate in inflammation in a number of ways. They can act as target cells, responding to exposure to a variety of inflammatory mediators and cytokines by altering one or several of their functions, such as mucin secretion, ion transport, or ciliary beating. Aberrations in any of these functions can affect local inflammatory responses and compromise pulmonary defense. For example, oxidant stress can increase secretion of mucin and depress ciliary beating efficiency, thereby affecting the ability of the mucociliary system to clear potentially pathogenic microbial agents. Recent studies have indicated that airway epithelial cells also can act as "effector" cells, synthesizing and releasing cytokines, lipid mediators, and reactive oxygen species in response to a number of pathologically relevant stimuli, thereby contributing to inflammation. Many of these epithelial-derived substances can act locally, affecting both neighboring cells and tissues, or, via autocrine or paracrine mechanisms, affect structure and function of the epithelial cells themselves. Studies in our laboratories utilized cell cultures of both human and guinea pig tracheobronchial and nasal epithelial cells, and isolated human nasal epithelial cells, to investigate activity of respiratory epithelial cells in vitro as sources of cytokines and inflammatory mediators. Primary cultures of guinea pig and human tracheobronchial and nasal epithelial cells synthesize and secrete low levels of IL-6 and IL-8 constitutively. Production and release of these cytokines increases substantially after exposure to specific inflammatory stimuli, such as TNF or IL-1, and after viral infection.

Reactive oxygen species (ROS) have been implicated in the pathogenesis of numerous disease processes. Epithelial cells lining the respiratory airways are uniquely vulnerable regarding potential for oxidative damage due to their potential for exposure to both endogenous (e.g., mitochondrial respiration, phagocytic respiratory burst, cellular oxidases) and exogenous (e.g., air pollutants, xenobiotics, catalase negative organisms) oxidants. Airway epithelial cells use several nonenzymatic and enzymatic antioxidant mechanisms to protect against oxidative insult. Nonenzymatic defenses include certain vitamins and low molecular weight compounds such as thiols. The enzymes superoxide dismutase, catalase, and glutatione peroxidase are major sources of antioxidant protection. Other materials associated with airway epithelium such as mucus, epithelial lining fluid, and even the basement membrane/extracellular matrix may have protective actions as well. When the normal balance between oxidants and antioxidants is upset, oxidant stress ensues and subsequent epithelial cell alterations or damage may be a critical component in the pathogenesis of several respiratory diseases. Oxidant stress may profoundly alter lung physiology including pulmonary function (e.g., forced expiratory volumes, flow rates, and maximal inspiratory capacity), mucociliary activity, and airway reactivity. ROS may induce airway inflammation; the inflammatory process may serve as an additional source of ROS in airways and provoke the pathophysiologic responses described. On a more fundamental level, cellular mechanisms in the pathogenesis of ROS may involve activation of intracellular signaling enzymes including phospholipases and protein kinases stimulating the release of inflammatory lipids and cytokines. Respiratory epithelium may be intimately involved in defense against, and pathophysiologic changes invoked by, ROS. -Environ Health Perspect 1 02(Suppl 1 0): 85-90 (1994)

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