Kidneys cortex

Rcnsl dipcptidflsc (from porcine kidney cortex) [9031-96-3] Mr 47,000 [EC 3.4.13.11]. Purified by homogenising the tissue, extracting with Triton X-100, elimination of insoluble material, and ion-exchange, size exclusion and affinity chromatography. [Hitchcock et al. Anal Biochem 163 219 7957.]... 

Cadmium is effectively accumulated in the kidneys. When the cadmium concentration exceeds 200 gg/g in the kidney cortex, tubular damage will occur in 10% of the population, and proteins begin to leak into urine (proteinuria). When the concentration of cadmium in the kidney cortex exceeds 300 pg/g, the effect is seen in 50% of the exposed population. Typically, excretion of low-molecular weight proteins, such as beta-microglobulin, is increased, due to dysfunction of proximal tubular cells of the kidney. The existence of albumin or other high-molecular weight proteins in the urine indicates that a glomerular injury has also taken place. The excretion of protein-bound cadmium will also be increased. 

The site of accumulation may define tlie point of toxic action. Inorganic mercury accumulation in the kidneys causes sever functional impairment Kidney damage has been shown to occur when the accumulated total of cadmium in the kidney cortex reaches 100-200 ppm... 

Other blockers of epithelial Cl -channels are of the aryl-amino-benzoate type or phenoxy-acetic-acid type [70]. Very few systematic surveys comparing different classes of blockers in one type of Cl -channel are available at this stage. One such study has been performed in membrane vesicles from kidney cortex [80]. In this study IAA-94 and NPPB (cf. Fig. 2) turned out to be the most potent blocker of conductive Cl -flux. In another systematic survey the Cl -conductance of the sweat duct was examined, and it was found that dichloro-DPC (Fig. 2) was the most potent inhibitor of the transepithelial Cl -conductance [90]. 

Meanwhile we have shown that the excision activation of ICOR channels is due to disinhibition [72]. The respective inhibitor, operationally named cytosolic inhibitor (Cl), is present in the cytosol of placenta trophoblast cells HT29- and Tg4-colonic carcinoma cells and RE cells of normal and CF patients. The molecule has an apparent molecular weight of 700-1 500 Da it is amphiphilic heat stable and not digested by trypsin, proteases, nucleotidases, lipases or amylase [72]. Burc-khardt, Fromter and their collaborators [114] have confirmed our results and extracted a similar or identical Cl from kidney cortex. 

Barregard, L., Svalander, C., Schiitz, A., Westberg, G., Blohme, I., Molne, J., Attman, P.-O., and Haglind, P., Cadmium, mercury and lead in kidney cortex of the general Swedish population A study of biopsies from living kidney donors, Environment and Health Perspectives, 107, 867-871, 1999. 

Bertran, J., et al. Expression of Na(+)-independent amino acid transport in Xenopus laevis oocytes by injection of rabbit kidney cortex mRNA. Biochem.J. 1992, 283, 717-723. 

Witzmann FA et al. Differential expression of cytosolic proteins in the rat kidney cortex and medulla preliminary proteomics. Electrophoresis 1998 19 2491-2497. 

EPO in the human adult is synthesized almost exclusively by specialized kidney cells (peritubular interstitial cells of the kidney cortex and upper medulla). Minor quantities are also synthesized in the liver, which represents the primary EPO-producing organ of the foetus. 

Captive animal died after ingesting lead-containing air gun pellets vs. control Kidney cortex 4.2 FW vs. <0.15 FW 181... 

Holterman, W.F.M.O., P. de Voogt, and J.H.J.C. Peereboom-Stegeman. 1984. Cadmium/zinc relationships in kidney cortex and metallothionein of horse and red deer histopathological observations on horse kidneys. Environ. Res. 35 466-481. 

Liver damage due to copper at low Mo (20 mg/kg) diets at 40 and 60 mg Mo/kg, both metals accumulated in kidney cortex but no evidence of liver histopathology or kidney damage (18)... 

No effect on growth of food intake significant increases in levels of kidney cortex copper, liver Mo, and plasma copper major differences in responses among breeds tested (21)... 

Kunz WS, Gellerich FN. Quantification of the content of fluorescent flavoproteins in mitochondria from liver, kidney cortex, skeletal muscle, and brain. Biochem Med Metab Biol 1993 50 103-110. 

Heidrich, H.G. and Dew, M.E. (1977). Homogeneous cell populations from rabbit kidney cortex. J. Cell Biol. 74 780-788. 

Williams, P.D. and Hottendorf, G.H. (1985). Effects of cw-dichlorodiamineplatinum-II (Cisplatin) on organic ion transport in membrane vesicles from rat kidney cortex. Cancer Treat. Rep. 69 875-880. 

Figure 5. Detection of male MSC by Y-PCR. Y chromosome PCR at 24 h after MSC infusion from a male donor into female recipients with AKl. The only organ positive for Y chromosome DNA was the lung (lane 2). Kidney cortex and medulla as well as liver and spleen from 2 animals were negative (lanes 3-11). Lane designation A-female DNA B-male DNA 2 lung 3-kidney cortex 4-kidney medulla 5-liver 6-spleen 7-wound scar 8-lung 9-bone marrow 10-liver 11-spleen.

Fatty acids are released from adipose tissue into the bloodstream, from where they can be taken up and used by aerobic tissues, with the exception of brain and the intestine. In addition, an increase in the plasma fatty acid concentration is one factor that increases the rate of fatty acid oxidation by tissues. Flence, an increase in the mobilisation of fatty acid from adipose tissue is an immediate signal for tissues such as muscle, heart and kidney cortex to increase... 

Since the intracellular concentration of most amino acids is considerably greater than that in the plasma (Table 8.2), the transport of these amino acids is an energy-requiring process. This is achieved via the Na+ gradient across the plasma membrane, which is maintained by the ATP-dependent Na pump the NaVK+ ATPase (Figure 8.5). This is similar to that of the transport of glucose across the luminal membranes of epithelial cells in the gut and in the tubules is the kidney cortex. 

Surface fluorescence of NADH/NADPH can be recorded continuously with a DC fluorimeter and correlated with changes in experimental conditions. A mercury arc lamp (with a 340-375 nm filter in front) is used as a hght source for fluorescence excitation. The fluorescence response of reduced NADH/NADPH was measured at 450-510 nm. The DC fluorimeter and the Hg arc lamp are connected to the kidney by a trifurcated fiber optics light guide. NADH/NADPH fluorescence emission can be corrected for changes in tissue opacity by a 1 1 subtraction of reflectance changes at 340-375 nm from the fluorescence. To determine NADH/NADPH redox state of the total surface area of kidney cortex and to evaluate whether certain areas were insufficiently perfused, fluorescence photographs of the total surface area were taken. The study demonstrated that the surface fluorescence method is simple and provides specific information about the mitochondrial oxidation-reduction state. 

---