The American journal of physiology
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The intracellular supply of O2 to mitochondria was studied in single-cell suspensions of rat hepatocytes by measuring the O2 dependence of oxidation of cytochromes. Values were obtained by adding standardized O2-containing solutions to anaerobic cell suspensions and observing absorbance changes at wavelength pairs specific for cytochromes a + a3, c + c1, and b561 + b566. ⋯ Analysis of these data indicate that the diffusion coefficient in the region of mitochondria in situ is considerably smaller than the extracellular diffusion coefficient and suggests that a significant O2 gradient in the vicinity of mitochondria occurs under hypoxic conditions. These results suggest that the rate of O2 diffusion may be a critical factor for intracellular O2 supply to mitochondria during hypoxia.
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Metiamide-inhibited fundic mucosa of bullfrog secreted alkali (OH-) at 0.1-0.2 mueq.cm-2.h-1. OH- was abolished by dinitrophenol (DNP) and was decreased significantly by 4,4-didsothiocyano-2,2-disulfonate stilbene (DIDS), anoxia, or HCO3(-)-free nutrient solution. In Na+ solutions, increasing nutrient, [HCO3(-)] augmented OH- and Isc linearly while resistance (R) decreased. ⋯ In the absence of secretory Cl-, OH- and Isc were linearly related to varying nutrient [Cl-]. In tissues with nutrient solutions on the secretory side and vice versa, apparent OH- was 0.4-0.5 mueq.cm-1.h-1 and was dependent on secretory [HCO3(-)] but was not affected by DNP, DIDS, or replacement of Cl- on secretory or nutrient solutions. We conclude that 1) OH- secretion is dependent on nutrient HCO3(-) and Na+ and oxidative metabolism, 2) endogenous HCO3(-) does not contribute significantly, and 3) adequate tissue Cl- must be present for normal OH-.