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Proximal tubular regions

The gastrointestinal compartment is less complicated. Calcium binding ligands administered in the fasting state would be present in the absoprtive area primarily in the unchelated form. [Pg.386]

The local pH and the presence of endogenous cations and metal binding ligands would determine the extent of calcium chelation. [Pg.386]

ACS Symposium Series American Chemical Society Washington, DC, 1980. [Pg.386]

Nitrilotriacetlc acid was supplied by the Hampshire Chemical Co., Division of W. R. Grace Co., Nashua, New Hampshire. For feeding studies It was neutralized with 1 M sodium hydroxide to provide a 1% NTA solution. Ethyl nltrllotrlacetate was obtained as a clear colorless viscous oil by refluxing 30g of nltrllotrl-acetlc acid In 1 liter of absolute alcohol In the presence of 3g of toluenesulphonlc acid for forty-eight hours. The alcohol was removed by distillation from a water bath in vacuo, the residue mixed with 100 ml of 0.5 percent sodium bicarbonate solution and extracted with one liter of benzene. The benzene solution was extracted twice more with bicarbonate solution, washed with water and concentrated from a water bath In vacuo. The clear colorless residual oil was dissolved by shaking with an aqueous solution of 1.5 M citric acid and the volume adjusted by addition of distilled water to provide a final solution of 1% NTA ethyl ester as citric acid salt. [Pg.387]

One of the two remaining groups was continued as a control on the regular diet while the other was now fed the treatment [Pg.387]


In male Fischer 344 rats treated intraperitoneally with 0, 10, 20, 40, 60 or 80 mg/kg bw acrylonitrile, significant increases in urinary volume and glucose were observed 24 h after treatment with 20 mg/kg bw (Rouisse et al., 1986). Increased levels of urinary N-acetyl-P-D-glucosaminidase were detected after treatment with 60 mg/kg bw acrylonitrile. Symptoms of nephrotoxicity were also observ ed after a 4-h exposure to 200 ppm [434 mg/m3] acrylonitrile. Histopathological examination revealed lesions in the proximal tubular region of the kidney. [Pg.79]

Cephaloridine is actively taken up from the blood into proximal tubular cells by the OAT 1 (Fig. 7.35). This requires a hydrophobic region as well as an anionic group, is specifically... [Pg.332]

Compound A is nephrotoxic in rats at thresholds estimated at 180 ppm/hour [67]. Renal toxicity is characterized histologically by proximal tubular cell degeneration and necrosis in the corticomedullar region of die kidney and biochemically by proteinuria, glucosuria, and enzymuria (NAG and a-GST) with increased serum creatinine and BUN concentrations occurring with severe toxicity [67-70]. [Pg.540]

In most studies, a combination of more than two or three enzymes has provided better information than the measurement of a single enzyme, with measurements based on regional and cellular location. Urinary enzymes have been particularly useful in detection of acute renal damage and, specihcally, proximal tubular damage however, they are correspondingly less valuable in providing information about chronic injury. [Pg.85]

More simply, in the early regions of the tubule (proximal tubule and Loop of Henle), Na+ ions leave the lumen and enter the tubular epithelial cells by way of passive facilitated transport mechanisms. The diffusion of Na+ ions is coupled with organic molecules or with other ions that electrically balance the flux of these positively charged ions. In the latter regions of the tubule (distal tubule and collecting duct), Na+ ions diffuse into the epithelial cells through Na+ channels. [Pg.319]

Water reabsorption. Water is reabsorbed passively by way of osmosis from many regions of the tubule. As with sodium and chloride, 65% of the filtered water is reabsorbed from the proximal tubule. An additional 15% of the filtered water is reabsorbed from the descending limb of the Loop of Henle. This reabsorption occurs regardless of the water content of the body. The water enters the tubular epithelial cells through water channels, also referred to as aquaporins. These channels are always open in the early regions of the tubule. [Pg.320]


See other pages where Proximal tubular regions is mentioned: [Pg.205]    [Pg.306]    [Pg.331]    [Pg.388]    [Pg.148]    [Pg.95]    [Pg.242]    [Pg.9]    [Pg.199]    [Pg.199]    [Pg.1496]    [Pg.1497]    [Pg.36]    [Pg.1689]    [Pg.468]    [Pg.709]    [Pg.127]    [Pg.645]    [Pg.90]    [Pg.109]    [Pg.105]    [Pg.40]    [Pg.60]    [Pg.709]    [Pg.386]    [Pg.344]    [Pg.202]    [Pg.53]    [Pg.284]    [Pg.37]    [Pg.38]    [Pg.273]    [Pg.162]    [Pg.163]    [Pg.221]    [Pg.563]    [Pg.200]    [Pg.201]    [Pg.496]    [Pg.2413]    [Pg.1673]    [Pg.1679]    [Pg.90]   
See also in sourсe #XX -- [ Pg.386 ]




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Proximal

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