Mercury and selenium distribution in human kidney cortex

1994 ◽  
Vol 40 (3) ◽  
pp. 255-265 ◽  
Author(s):  
Lars Björkman ◽  
Brita Palm ◽  
Magnus Nylander ◽  
Monica Nordberg
Keyword(s):  
1975 ◽  
Vol 53 (12) ◽  
pp. 1333-1336 ◽  
Author(s):  
R. Hobkirk ◽  
Mona Nilsen ◽  
Barbara Jennings

Slices of whole kidney and kidney cortex from the female guinea pig catalyzed a marked reduction of estrone 3-sulfate (E13S) and estrone (E1) to 17β-estradiol 3-sulfate (E23S) and 17β-estradiol (E2), respectively, as well as the reverse (dehydrogenation) reactions. Slices of medulla did not appear active in E23S–E13S interconversion but did possess the ability to interconvert E2 and E1, besides possessing considerable sulfatase activity. The use of [3H-35S]E13S and [3H-35S]E23S as substrates, together with a demonstrated lack of estrogen sulfate synthesis by the tissue slices, provided ample evidence that the intact sulfates were involved in direct oxidoreduction. Slices of human kidney cortex catalyzed the reduction of E13S to a very limited extent. Slices of whole kidney and of cortex from guinea pig formed small amounts of estrogen glucuronide(s).


Author(s):  
J. Scherberich ◽  
C. Gauhl ◽  
G. Heinert ◽  
W. Mondorf ◽  
W. Schoeppe

2021 ◽  
Author(s):  
Jin Wook Hwang ◽  
Christophe Desterke ◽  
Julien Loisel-Duwattez ◽  
Frank Griscelli ◽  
Annelise Bennaceur-Griscelli ◽  
...  

AbstractBackgroundIn mammalians, hematopoietic stem cells (HSC) arise in the dorsal aorta from the hemogenic endothelium, followed by their migration to fetal liver and to bone marrow. In zebrafish, kidney is the site of primary hematopoiesis. In humans, the presence of HSC in the fetal or adult kidney has not been established.MethodsWe analyzed the presence of HSC markers in human fetal kidneys by analysis of single-cell datasets. We then analyzed in kidney organoids derived from iPSC, the presence of hematopoietic markers using transcriptome analyses.Results12 clusters were identified of stromal, endothelial, and nephron cell type-specific markers in the two fetal stage (17 weeks) kidney datasets. Among these, expression of hematopoietic cells in Cluster 9 showed expression of primitive markers. Moreover, whole transcriptome analysis of our iPSC-derived kidney organoids revealed induction of the primitive hematopoietic transcription factor RUNX1 as found in the human fetal kidney cortex.ConclusionsThese finding support the presence of cells expressing HSC transcriptome in human kidney. The mechanisms of the appearance of the cells with the same transcriptional features during iPSC-derived kidney organoid generation requires further investigation.


1981 ◽  
Vol 27 (1) ◽  
pp. 68-72 ◽  
Author(s):  
P A Pleban ◽  
J Kerkay ◽  
K H Pearson

Abstract We used polarized Zeeman-effect flameless atomic absorption spectroscopy to quantitatively measure cadmium, copper, lead, and manganese in a nitric acid digest of lyophilized human kidney cortex. Within-run coefficients of variation for cadmium, copper, lead, and manganese, 15.3, 177.2, 84.2, and 56.3 microgram/L, respectively, were 4.1, 6.3, 3.7, and 5.6%, respectively. Between-run coefficients of variation were 6.9, 5.5, 5.9, and 6.3%, respectively, for cadmium, copper, lead, and manganese concentrations of 135.1, 12.8, 2.72, and 3.80 microgram/g, respectively. For cadmium, copper, lead, and manganese digest concentrations (mean +/- SE) of 15.3 +/- 0.6, 41.4 +/- 2.6, 9.4 +/- 0.6, and 20.9 +/- 0.4 microgram/L, respectively, the detection limits were 5.2 microgram/L for copper, 1.2 microgram/L for both cadmium and lead, and 0.8 microgram/L for manganese. Assays were linear to 75 microgram/L for cadmium, 100 microgram/L for manganese, and 200 microgram/L for copper and lead. Average analytical recoveries for the four metals ranged between 95 and 101%. Because these metals were quantitated in the same digest of kidney cortex, the values for each digest gave a trace-metal profile for each autopsy specimen.


1992 ◽  
Vol 262 (4) ◽  
pp. C1069-C1076 ◽  
Author(s):  
K. Takaichi ◽  
D. Wang ◽  
D. F. Balkovetz ◽  
D. G. Warnock

Two types of Na(+)-H+ antiporter with different sensitivities to amiloride analogues have been identified in mammalian plasma membranes. A human Na(+)-H+ antiporter cDNA was obtained by Sardet and co-workers (C. Sardet, L. Counillon, A. Franchi, and J. Pouyssegur. Cell 56: 271-280, 1989) using mutant mouse fibroblasts lacking Na(+)-H+ antiporter transformed with human genomic DNA. However, the amiloride sensitivity of this cloned Na(+)-H+ antiporter was not precisely determined. Furthermore, the reported cDNA sequence may be a chimera of human and mouse genes. Hence we isolated a Na(+)-H+ antiporter cDNA actually expressed in human tissues and characterized its amiloride sensitivity. Our 4 kb cDNA obtained from human kidney cortex contained the identical open reading frame to that previously reported and the entire 3' terminus, which was quite different from that reported. This discrepancy was not due to differences in tissue-specific expression because cDNAs from different human tissues were identical, and single bands were observed under high stringency on Northern blots of various human tissues. Na(+)-H+ antiporter activity of mutant mouse fibroblasts deficient in Na(+)-H+ antiporter activity transfected with the cloned cDNA was very sensitive to amiloride and 5-N substituted analogues of amiloride. Thus the cloned cDNA represents the NHE-1 isoform of the Na(+)-H+ antiporter.


1998 ◽  
Vol 106 (4) ◽  
pp. 175-178 ◽  
Author(s):  
L Friis ◽  
L Petersson ◽  
C Edling
Keyword(s):  

Metabolism ◽  
1973 ◽  
Vol 22 (1) ◽  
pp. 67-76 ◽  
Author(s):  
Stanton Segal ◽  
Myron Genel ◽  
Philip Holtzapple ◽  
Claire Rea
Keyword(s):  

Author(s):  
Jin Wook Hwang ◽  
Christophe Desterke ◽  
Julien Loisel-Duwattez ◽  
Frank Griscelli ◽  
Annelise Bennaceur-Griscelli ◽  
...  

BackgroundIn mammalians, hematopoietic stem cells (HSCs) arise in the dorsal aorta from the hemogenic endothelium, followed by their migration to the fetal liver and to the bone marrow. In zebrafish, the kidney is the site of primary hematopoiesis. In humans, the presence of HSCs in the fetal or adult kidney has not been established.MethodsWe analyzed the presence of HSC markers in the human fetal kidneys by analysis of single-cell datasets. We then analyzed in kidney organoids derived from induced pluripotent stem cells (iPSCs) the presence of hematopoietic markers using transcriptome analyses.ResultsTwelve clusters were identified as stromal, endothelial, and nephron cell type-specific markers in the two fetal stage (17 weeks) kidney datasets. Among these, the expression of hematopoietic cells in cluster 9 showed an expression of primitive markers. Moreover, whole transcriptome analysis of our iPSC-derived kidney organoids revealed induction of the primitive hematopoietic transcription factor RUNX1 as found in the human fetal kidney cortex.ConclusionThese finding support the presence of cells expressing HSC transcriptome in the human kidney. The mechanisms of the appearance of the cells with the same transcriptional features during iPSC-derived kidney organoid generation require further investigation.


2001 ◽  
Vol 12 (8) ◽  
pp. 1615-1623
Author(s):  
LAURENCE DUBOURG ◽  
CHRISTIAN MICHOUDET ◽  
PIERRE COCHAT ◽  
GABRIEL BAVEREL

Abstract. The nephrotoxic effects of the antineoplastic drug ifosfamide have been attributed to its hepatic metabolite chloroacetaldehyde. The effects of chloroacetaldehyde on isolated human kidney cortex tubules metabolizing lactate (a physiologic substrate in human kidneys) were investigated. At concentrations of ≥0.5 mM, chloroacetaldehyde was toxic to the human kidney tubules, as demonstrated by a dramatic decrease in cellular ATP levels and a large increase in lactate dehydrogenase release; chloroacetaldehyde also stimulated pyruvate accumulation and inhibited lactate removal and glucose synthesis. These effects, which were associated with incomplete disappearance of chloroacetaldehyde and extensive depletion of the cellular CoA, acetyl-CoA, and glutathione contents, were prevented by the addition of thiol-protecting drugs (mesna and amifostine). Human kidney tubules were demonstrated to metabolize chloroacetaldehyde at high rates, presumably via aldehyde dehydrogenase, which is very active in human kidneys. Carbon-13 nuclear magnetic resonance spectroscopy measurements indicated that human kidney tubules converted [2-13C]chloroacetaldehyde to [2-13C]chloroacetate, the further metabolism of which was very limited. At equimolar concentrations, chloroacetate was much less toxic than chloroacetaldehyde, indicating that chloroacetate synthesis from chloroacetaldehyde by human kidney tubules represents a detoxification mechanism that could play a role in vivo in preventing or limiting the nephrotoxic effects observed during ifosfamide therapy.


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