Studies of the chloride transport in the gastric mucosa of the frog

The unidirectional fluxes of Cl^- and Na⁺ across the frog gastric mucosa in vitro were investigated with radioactive isotopes, and related to the secretory and electrical properties of the normal, and metabolically inhibited, mucosa. The flux of Cl^- from nutrient to secretory surface of the mucosa was observed to rise sharply with increasing acid secretion, while the corresponding flux of Na⁺ did not change appreciably. Lowering [NaCl] in the secretory solution caused a proportional drop in the fluxes from secretory to nutrient surface, of both Cl^- and Na⁺. Under the same conditions, the flux of Cl^- from nutrient to secretory surface fell by nearly the same amount as did the flux of Cl^- in the opposite direction, while the flux of Na⁺ from nutrient to secretory surface remained essentially unchanged. Electrical and hydrodynamic causes for this observation could be excluded. Metabolic inhibitors, including cyanide, azide, DNP, and anaerobiosis depressed Cl^- flux in both directions distinctly below the corresponding values observed with the normal, non-secreting mucosa. At the same time, a decrease in electrical potential difference and conductance was observed under inhibition. The flux of Na⁺ was little changed by metabolic inhibition. The relationship between fluxes and conductance of Cl^- during metabolic inhibition differs markedly from that observed under normal conditions, and is consistent with the view that during metabolic inhibition most of the Cl^- moving across the mucosa does so as a free ion. From the above data it is concluded that Cl^- is normally transported across the mucosa in combination with a carrier, the supply of which is impaired under metabolic inhibition. According to the behavior of the Na⁺ flux, the passive permeability of the mucosa appeared to be little affected by the metabolic inhibition applied, but seemed to rise considerably after death of the mucosa, probably due to structural damage.     

Water flow through frog gastric mucosa

To elucidate the role of protein synthesis in DNA formation, E. coli R2 infected with phage T2 was studed as a model, employing chloramphenicol to inhibit protein synthesis. The following results were obtained. 1. Chloramphenicol inhibited protein synthesis but not synthesis of nucleic acids in uninfected bacteria. 2. Studies of the effect of chloramphenicol on phage maturation indicated a delay of 2 minutes between time of addition and cessation of phage growth. 3. The increase of DNA in phage-infected bacteria was completely suppressed by the addition of chloramphenicol within 2 minutes following infection. Addition at later times showed progressively less inhibitory action depending upon the time interval, and addition after the 10th or 12th minute showed no appreciable effect on DNA synthesis despite the cessation of intracellular phage formation and protein synthesis. 4. When chloramphenicol was added to infected cells the increase of resistance to UV stopped within 2 minutes, whether or not DNA synthesis continued. Thus evolution of resistance paralleled the rate of DNA synthesis achieved, but not the amount of DNA accumulated. 5. We conclude that in infected bacteria, protein synthesis is necessary to initiate DNA synthesis but is not essential for its continuation. The resistance to UV that characterizes infected cells near the midpoint of the latent period is not due to accumulation of DNA, but depends on some chloramphenicol-sensitive process (probably protein synthesis) completed at about the time the rate of DNA synthesis becomes maximal.