PubMed · 4414782
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E Heikkinen, T K Larmi, R Huttunen. 1974. Necrotizing colitis.. https://doi.org/10.1016/0002-9610(74)90174-3
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Mitochondrial cytochromes c from spinach, cucumber, and sweet potato have been investigated through direct electrochemical measurements and electronic and 1H NMR spectroscopies, under conditions of varying temperature and pH. The solution behaviors of these plant cytochromes closely resemble, but do not fully reproduce, those of homologous eukaryotic species. The reduction potentials (E0') at pH 7 and 25 degrees C are +0.268 V (spinach), +0.271 V (cucumber), and +0.274 V (sweet potato) vs SHE. Three acid-base equilibria have been determined for the oxidized proteins with apparent pKa values of 2.5, 4.8, and 8.3-8.9, which are related to disruption of axial heme ligation, deprotonation of the solvent-exposed heme propionate-7 and replacement of the methionine axially bound to the heme iron with a stronger ligand, respectively. The most significant peculiarities with respect to the mammalian analogues include: (i) less negative reduction enthalpies and entropies (Delta S0'rc and Delta H0'rc) for the various protein conformers [low- and high-T native (N1 and N2) and alkaline (A)], whose effects at pH 7 and 25 degrees C largely compensate to produce E degrees ' values very similar to those of the mammalian proteins; (ii) the N1 --> N2 transition that occurs at a lower temperature (e.g., 30-35 degrees C vs 50 degrees C at pH 7. 5) and at a lower pH (7 vs 7.5); and (iii) a more pronounced temperature-induced decrease in the pKa for the alkaline transition which allows observation of the alkaline conformer(s) at pH values as low as 7 upon increasing the temperature above 40 degrees C. Regarding the pH and the temperature ranges of existence of the various protein conformers, these plant cytochromes c are closer to bacterial cytochromes c2.
The effect of membrane chemical composition and drug chemical structure on the localisation of several benzodiazepines (BZDs) (DZ, diazepam; CZ, clonazepam; CX, chlordiazepoxide) within model membranes was investigated. We used a spectrophotometric method presented in a previous paper (B.A. García, M.A. Perillo, Biochim. Biophys. Acta 1324 (1997) 76-84) based on the study of BZD acid-base equilibrium. 'Intrinsic pK' values (pKi) were calculated according to the theory of M.S. Fernández and P. Fromherz (J. Phys. Chem. 81 (1977) 1755-1761). Homogeneous media of known dielectric constant (dioxane 0-80% v/v in water) were used to construct a curve of DeltapKi (pKi-pKw) vs. dielectric constant (D) where DeltapKi values obtained in lipidic dispersions were interpolated. In heterogeneous media consisting of aqueous dispersions of Triton X-100 micelles we determined the relative localisation depth of BZDs according to their DTriton values (36, 37 and 62 for DZ, CX and CZ respectively) taking into account that lower D values correspond to deeper localisation. pKi determined in dispersions of dipalmitoylphosphatidylcholine (dpPC) and egg phosphatidylcholine (egg-PC) mixed multilamellar vesicles showed that, when cholesterol content increased from 0 to 20 mole%, D values decreased (from 59 to 40) in dpPC vesicles and increased (from 51 to 72) in egg-PC vesicles, indicating a tendency of BZDs to penetrate deeper into less ordered interfaces. These results should be considered to understand the non-specific pharmacological effects of BZDs as well as to evaluate the actual relevance of their pharmacological concentrations.
Thermal stress is known to impair endurance capacity during moderate prolonged exercise. However, there is relatively little available information concerning the effects of thermal stress on the performance of high-intensity short-duration exercise. The present experiment examined human power output during repeated bouts of short-term maximal exercise. On two separate occasions, seven healthy males performed two 30-s bouts of sprint exercise (sprints I and II), with 4 min of passive recovery in between, on a cycle ergometer. The sprints were performed in both a normal environment [18.7 (1.5) degrees C, 40 (7)% relative humidity (RH; mean SD)] and a hot environment [30.1 (0.5) degrees C, 55 (9)% RH]. The order of exercise trials was randomised and separated by a minimum of 4 days. Mean power, peak power and decline in power output were calculated from the flywheel velocity after correction for flywheel acceleration. Peak power output was higher when exercise was performed in the heat compared to the normal environment in both sprint I [910 (172) W vs 656 (58) W; P < 0.01] and sprint II [907 (150) vs 646 (37) W; P < 0.05]. Mean power output was higher in the heat compared to the normal environment in both sprint I [634 (91) W vs 510 (59) W; P < 0.05] and sprint II [589 (70) W vs 482 (47) W; P < 0.05]. There was a faster rate of fatigue (P < 0.05) when exercise was performed in the heat compared to the normal environment. Arterialised-venous blood samples were taken for the determination of acid-base status and blood lactate and blood glucose before exercise, 2 min after sprint I, and at several time points after sprint II. Before exercise there was no difference in resting acid-base status or blood metabolites between environmental conditions. There was a decrease in blood pH, plasma bicarbonate and base excess after sprint I and after sprint II. The degree of post-exercise acidosis was similar when exercise was performed in either of the environmental conditions. The metabolic response to exercise was similar between environmental conditions; the concentration of blood lactate increased (P < 0.01) after sprint I and sprint II but there were no differences in lactate concentration when comparing the exercise bouts performed in a normal and a hot environment. These data demonstrate that when brief intense exercise is performed in the heat, peak power output increases by about 25% and mean power output increases by 15%; this was due to achieving a higher pedal cadence in the heat.