We performed an electrophysiological study to investigate ion transport of pendrin and thereby understand the pathogenesis of Pendred syndrome. Using pendrin-transfected COS-7 cells, we could show that pendrin transports both iodide and chloride measured as voltage-dependent inward and outward membrane currents. Chloride in the culture medium, [Cl-]o, was efficiently exchanged with cytoplasmic iodide, [I-]i, under physiological concentrations, indicating that pendrin is important for chloride uptake and iodide efflux. Although exchange of iodide in the medium, [I-]o, with cytoplasmic chloride, [Cl-]i, was observed, a significantly high concentration of iodide (10 mm) was required. In addition, either iodide or chloride was required on both sides of the cell membrane for the anion exchange activity of pendrin, indicating that iodide and chloride activate the exchange activity of pendrin while they are transported. The present study further supports that pendrin is responsible for the iodide efflux in thyroid cells where intracellular iodide concentration is high and that the general function of pendrin in other tissues is to transport chloride through exchange with other anions.
Two patients with primary hyperparathyroidism had hyperuricemia due to the decrease in urate clearance. In analysis by 4-component model system, the tubular secretion of urate commonly decreased without changes in either filtered urate or presecretory reabsorption of urate. Both patients had a reduction of urea clearance, and both parathyroidectomy in the former case and intravenous infusion of saline in the latter case could reduce the serum urate level associated with the increase in the ratio of urate clearance to creatinine clearance. It is of interest that the former case with a higher serum urate level had a relatively higher postsecretory reabsorption, even with the decrease in tubular secretion of urate. However, the latter patient with a lower serum urate level had a decrease in postsecretory reabsorption of urate in pro portion to the decrease in tubular secretion. These results suggest that in hyperuricemia patients with primary hyperparathyroidism, the reduction of tubular urate secretion via hypoperfusion of the capillary network is typically present, however, the severity of the hyperuricemia might be dependent on the dysfunction of the postsecretory reabsorption of urate. (Internal Medicine 31: 807-811, 1992)
1. Membrane fraction containing halorhodopsin was prepared from the lysate of a mutant strain of Halobacterium halobium, Y1, which is defective in bacteriorhodopsin synthesis. 2. Irradiation of the membrane with red light at 0 degrees C decreased the absorbance intensities over the whole range of 500--600 nm and a new absorption peak appeared at about 400 nm. This process was reversed either by irradiation with blue light or simply by incubation in the dark. The wavelength at which the red light-induced absorbance decrease became maximum was 566 nm in the absence of NaCl and moved to 576 nm upon addition of NaCl. The midpoint for the conversion was at about 0.1 M NaCl. 3. Even though the membrane containing halorhodopsin was prepared in the absence of NaCl, this pigment was photochemically active in the sense that it could form a bathochromic photoproduct, a batho-intermediate, at -196 degrees C. 4. Retinal isomer composition during irradiation with red light at 0 degrees C was determined. Unirradiated halorhodopsin had predominantly all-trans retinal. With the increase of the blue-shifted product on irradiation, 13-cis content increased.
Cerebral blood flow was almost normal in one case and decreased in the basal ganglia and watershed area in the other case due to infarcts occurring before surgery. In both cases, F-fluorodeoxyglucose positron emission tomography revealed elevated glucose metabolism in the corresponding side of the striatum, which reverted to normal after recovery from chorea. Magnetic resonance angiography revealed a dilated and extended lenticulostriate artery at the exact site of the hypermetabolic lesion.
A cross-sectional study was performed on 165 male lead-exposed workers to clarify the quantitative relationships between less severe exposure to lead and its effects on renal function in 1985. Mean and range of blood lead concentration (Pb-B) were 36.5 ƒÊg/
Abstract— Using two kinds of rhodopsin preparations (digitonin extract and rod outer segments suspension), we measured changes in absorption spectra during the conversion of rhodopsin or isorhodopsin to a photosteady state mixture composed of rhodopsin, isorhodopsin and bathorhodopsin by irradiation with blue light (437 nm) at 77 K and during the reversion of bathorhodopsin to a mixture of rhodopsin and isorhodopsin by irradiation with red light (> 650 nm) at 77 K. The reaction kinetics could be expressed with only one exponential in the former case and with two exponentials in the latter case. These data suggest that both rhodopsin and isorhodopsin are composed of a single molecular species, while bathorhodopsin is composed of two molecular species, designated as bathorhodopsin1 and bathorhodopsin2. The absorption spectra of these bathorhodopsin were calculated by two different methods (kinetic method and warming‐cooling method). The former was based on the kinetics of the conversion of two forms of bathorhodopsin by irradiation with the red light. The spectra obtained by this method were consistent with those obtained by the warming‐cooling method. Bathorhodopsin1 and bathorhodopsin2 have Λmax at 555 and 538 nm, respectively. The two forms of bathorhodopsin are interconvertible in the light, but not in the dark. Thus, we suggest that a rhodopsin molecule in the excited state relaxes to either bathorhodopsin1 or bathorhodopsin2 through one of the two parallel pathways.
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