[Structure of side-chain-3-substituted indoles and color intensity in reaction with glyoxylic acid-sulfuric acid].
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The oxidation of sulfite by Thiobacillus thiooxidans was studied at various pH values with changing concentrations of potassium sulfite. The optimal pH for sulfite oxidation by cells was a function of sulfite concentrations, rising with increasing substrate concentrations, while that by the cell extracts was unaffected. The sulfite oxidation by cells was inhibited at high sulfite concentrations, particularly at low pH values. The results from kinetic studies show that the fully protonated form of sulfite, sulfurous acid or sulfur dioxide, is the form which penetrates the cells for the oxidation.
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Despite the widespread occurrence of acidic sulfur oxides in the ambient environment and their potential risks to human health, effects associated with pulmonary immune defenses have been poorly studied. The current in vivo study was designed to provide some insight into this relatively unexplored area by investigating the impact of inhaled sulfuric acid on immune defense mechanisms critical for maintaining pulmonary resistance against infectious diseases. Results of this study demonstrate that repeated inhalation of sulfuric acid reduces the uptake and intracellular killing of pathogenic bacteria by exposed pulmonary macrophages, and depresses the activity/production of important biological modifiers critical for maintaining pulmonary immunocompetence. These findings have important implications for human health, and may contribute to a better understanding of the possible mechanism(s) underlying the epidemiological evidence which suggests an association between total sulfates in the ambient air and increased incidence of acute bronchitis and lower respiratory illness in school-age children.
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Gas-liquid scattering experiments provide direct observations of the fate of hydrogen-bonding molecules striking the surfaces of acidic liquids. Collisions of gaseous formic acid with concentrated sulfuric acid show that impinging monomers (HCOOH and DCOOD) scatter inelastically from the interface or become trapped by surface H2SO4. Most trapped DCOOD molecules undergo proton exchange before desorbing from the acid, indicating that gas-surface accommodation almost always leads to reaction with H2SO4 molecules. This proton transfer is not inhibited by dimerization of the formic acid: The dimers readily undergo intramolecular hydrogen bond cleavage and D-H exchange before desorbing from the acid.
Previous studies have suggested that the increment in renal acid excretion caused by sulfuric acid feeding is mediated solely by an interplay between the sulfate-induced increase in distal sodium delivery and the gradual augmentation of distal sodium reabsorption that occurs as sodium losses accumulate. This hypothesis predicts that if distal sodium reabsorption were stimulated sufficiently prior to the administration of sulfuric acid, excretion of the hydrogen ion load would occur promptly, thus obviating the fall in plasma bicarbonate or loss of cation that normally occurs. To test this prediction, we fed sulfuric acid (7 mEq of H+/kg/day) to dogs in which distal sodium avidity had been enhanced prior to acid feeding either by diuretic-induced sodium depletion (N = 6) or by deoxycorticosterone acetate 7.5 mg, twice a day and a low-sodium diet (N = 8). Contrary to expectation, over the first 3 days of acid feeding there was a significant fall in plasma bicarbonate (7.1 and 7.5 mEq/liter) and an increase in urinary sodium excretion (48 mEq in both groups). Moreover, changes in both plasma bicarbonate and urinary sodium excretion were similar to those observed previously (5.9 mEq/liter and 46 mEq, respectively) in normal dogs fed the same dose of sulfuric acid.
Sulfuric acid (H2SO4) aerosols are common in both ambient and occupational environments. This study examined the numbers and selected in vitro functional properties of alveolar macrophages recovered from rabbits undergoing inhalation exposure to 0.5 mg/m3 submicrometer (0.3 micron) H2SO4 for 2 hr/day. Bronchoalveolar lavage was performed on Days 3, 7, and 14 during the exposure period (specifically, 24 hr after either 2, 6, or 13 exposures). Total cell numbers and macrophage counts were increased on Day 3, but returned to control levels by Day 7; no change in polymorphonuclear leukocytes was observed at any time point. Macrophage substrate attachment was not affected by exposures to H2SO4, but random mobility was severely depressed at Days 7 and 14. The numbers of phagocytically active macrophages and the level of such activity were increased on Day 3, but became depressed by Day 14. These results demonstrate significant alterations in important functional properties of alveolar macrophages due to short-term intermittent exposures to H2SO4 aerosols; these changes have implications for the ability of the lungs to maintain adequate defense against deposited viable and nonviable particles.
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