CHLOROQUINE IS A POTENT INHIBITOR OF GLUTAMATE DEHYDROGENASE IN LIVER AND KIDNEY-CORTEX OF RABBIT

1997 ◽  
Vol 35 (1) ◽  
pp. 79-84 ◽  
Author(s):  
ROBERT JARZYNAK ◽  
ELŻBIETA LENARCIK ◽  
JADWIGA BRYA
Keyword(s):  
Glutamate Dehydrogenase ◽  
Potent Inhibitor ◽  
Kidney Cortex ◽  
Liver And Kidney

scholarly journals Fate of glutamate carbon and nitrogen in isolated guinea-pig kidney-cortex tubules. Evidence for involvement of glutamate dehydrogenase in glutamine sythesis from glutamate

1980 ◽  
Vol 188 (3) ◽  
pp. 873-880 ◽  
Author(s):  
G Baverel ◽  
C Genoux ◽  
M Forissier ◽  
M Pellet
Keyword(s):  
Guinea Pig ◽  
Glutamate Dehydrogenase ◽  
Carbon Skeleton ◽  
Kidney Cortex ◽  
Glutamate Metabolism ◽  
Carbon And Nitrogen ◽  
Pig Kidney ◽  
Glutamate Concentration ◽  
Rate Limiting Step

1. The pathways and the fate of glutamate carbon and nitrogen were investigated in isolated guinea-pig kidney-cortex tubules. 2. At low glutamate concentration (1 mM), the glutamate carbon skeleton was either completely oxidized or converted into glutamine. At high glutamate concentration (5 mM), glucose, lactate and alanine were additional products of glutamate metabolism. 3. At neither concentration of glutamate was there accumulation of ammonia. 4. Nitrogen-balance calculations and the release of 14CO2 from L-[1-14C]glutamate (which gives an estimation of the flux of glutamate carbon skeleton through alpha-oxoglutarate dehydrogenase) clearly indicated that, despite the absence of ammonia accumulation, glutamate metabolism was initiated by the action of glutamate dehydrogenase and not by transamination reactions as suggested by Klahr, Schoolwerth & Bourgoignie [(1972) Am. J. Physiol. 222, 813-820] and Preuss [(1972) Am. J. Physiol. 222, 1395-1397]. Additional evidence for this was obtained by the use of (i) amino-oxyacetate, an inhibitor of transaminases, which did not decrease glutamate removal, or (ii) L-methionine DL-sulphoximine, an inhibitor of glutamine synthetase, which caused an accumulation of ammonia from glutamate. 5. Addition of NH4Cl plus glutamate caused an increase in both glutamate removal and glutamine synthesis, demonstrating that the supply of ammonia via glutamate dehydrogenase is the rate-limiting step in glutamine formation from glutamate. NH4Cl also inhibited the flux of glutamate through glutamate dehydrogenase and the formation of glucose, alanine and lactate. 6. The activities of enzymes possibly involved in the glutamate conversion into pyruvate were measured in guinea-pig renal cortex. 7. Renal arteriovenous-difference measurements revealed that in vivo the guinea-pig kidney adds glutamine and alanine to the circulating blood.

Lauric acid hydroxylation in human liver and kidney cortex microsomes

1979 ◽  
Vol 28 (23) ◽  
pp. 3385-3390 ◽  
Author(s):  
Richard T. Okita ◽  
Sten W. Jakobsson ◽  
Russell A. Prough ◽  
Bettie Sue Siler Masters
Keyword(s):  
Lauric Acid ◽  
Human Liver ◽  
Kidney Cortex ◽  
Liver And Kidney ◽  
Acid Hydroxylation

scholarly journals Ferrochelatase and δ-aminolaevulate synthetase in brain, heart, kidney and liver of normal and porphyric rats. The induction of δ-aminolaevulate synthetase in kidney cytosol and mitochondria by allylisopropylacetamide

1971 ◽  
Vol 124 (3) ◽  
pp. 633-637 ◽  
Author(s):  
R. Barnes ◽  
M. S. Jones ◽  
O. T. G. Jones ◽  
R. J. Porra
Keyword(s):  
Glutamate Dehydrogenase ◽  
Brain Mitochondria ◽  
Cytosol Fraction ◽  
Kidney Mitochondria ◽  
Liver And Kidney ◽  
Cytochrome Content

1. δ-Aminolaevulate synthetase was detected in liver and kidney mitochondria prepared from normal rats. 2. The administration of allylisopropylacetamide induced an increase in δ-aminolaevulate synthetase in both liver and kidney mitochondria and the enzyme also appeared in the cytosol fraction of both tissues. Comparison with the distribution of glutamate dehydrogenase indicated that this soluble kidney δ-aminolaevulate synthetase was truly of cytosol origin and did not arise from disrupted mitochondria. The kidney cytosol enzyme was inhibited by 50% by 50μm-protohaem. 3. δ-Aminolaevulate synthetase could not be detected in mitochondria or cytosol from heart or brain from normal or porphyric rats. 4. The administration of allylisopropylacetamide caused little or no increase in ferrochelatase or cytochrome content of liver, kidney, heart or brain mitochondria.

Regulation of glutamine metabolism in dog kidney cortex: effect of pH and chronic acidosis

1992 ◽  
Vol 262 (6) ◽  
pp. F1007-F1014
Author(s):  
A. C. Schoolwerth ◽  
B. C. Smith ◽  
K. Drewnowska
Keyword(s):  
Glutamate Dehydrogenase ◽  
Mitochondrial Membrane ◽  
Glutamine Metabolism ◽  
Kidney Cortex ◽  
Cytosolic Ph ◽  
Isolated Mitochondria ◽  
Significant Difference ◽  
Dog Kidney ◽  
Ammonium Production ◽  
Krebs Henseleit Buffer

To examine the interrelationships of proton compartmentation and ammoniagenesis, experiments were performed in tubules and mitochondria isolated from dog kidney cortex. Tubules were incubated in Krebs-Henseleit buffer at different pH (pHe), and cytosolic pH (pHi) was estimated with the fluorescent probe 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Mitochondrial pH (pHm) was determined simultaneously in intact tubules by use of dimethyloxazolidine-2,4-dione. Over the pHe range 6.9-7.7, pHi was similar in control and acidotic dogs and linearly related to pHe. At pHe 7.4 in control tubules. pHm was 7.78 +/- 0.07, and varied little over the pHe range of 7.0-7.7. The pH gradient across the mitochondrial membrane rose at acid pHe. pHm was more alkaline when estimated in tubules from acidotic dogs compared with controls. Ammonium and glucose productions from glutamine were inversely related to pHe and pHi in tubules from both control and acidotic animals and were higher in acidosis. In contrast, ammonium production by isolated mitochondria did not vary as pHe was altered. Enzyme fluxes, calculated from metabolite changes, demonstrated that glutamate dehydrogenase (GDH) flux was altered. Enzyme fluxes, calculated from metabolite changes, demonstrated that glutamate dehydrogenase (GDH) flux was inversely and glutaminase (PDG) flux was linearly related to pHe. Ammonium production was significantly greater in mitochondria from acidotic dogs because of accelerated flux through PDG but not GDH. The present study demonstrates significant difference between proton compartmentation and regulation of ammoniagenesis in kidneys from acidotic dog compared with rat.

scholarly journals Septic shock non-thyroidal illness syndrome causes hypothyroidism and conditions for reduced sensitivity to thyroid hormone

2013 ◽  
Vol 50 (2) ◽  
pp. 255-266 ◽  
Author(s):  
Isabel Castro ◽  
Leah Quisenberry ◽  
Rosa-Maria Calvo ◽  
Maria-Jesus Obregon ◽  
Joaquin Lado-Abeal
Keyword(s):  
Gene Expression ◽  
Septic Shock ◽  
Thyroid Hormone ◽  
Tissue Level ◽  
Binding Activity ◽  
Monocarboxylate Transporter ◽  
Kidney Cortex ◽  
Liver And Kidney ◽  
Response To Stress

Non-thyroidal illness syndrome (NTIS) is part of the neuroendocrine response to stress, but the significance of this syndrome remains uncertain. The aim of this study was to investigate the effect of lipopolysaccharide (LPS)-induced NTIS on thyroid hormone (TH) levels and TH molecular targets, as well as the relationship between septic shock nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) activation and TH receptor β (THRB) gene expression at a multi-tissue level in a pig model. Prepubertal domestic pigs were given i.v. saline or LPS for 48 h. Serum and tissue TH was measured by chemiluminescence and RIA. Expression of THRs and cofactors was measured by real-time PCR, and deiodinase (DIO) activity was measured by enzyme assays. Tissue NF-kB nuclear binding activity was evaluated by EMSA. LPS-treated pigs had decreased TH levels in serum and most tissues. DIO1 expression in liver and kidney and DIO1 activity in kidney decreased after LPS. No changes in DIO2 activity were observed between groups. LPS induced an increase in hypothalamus, thyroid, and liver DIO3 activity. Among the other studied genes, monocarboxylate transporter 8 and THRB were the most commonly repressed in endotoxemic pigs. LPS-induced NF-kB activation was associated with a decrease in THRB gene expression only in frontal lobe, adrenal gland, and kidney cortex. We conclude that LPS-induced NTIS in pigs is characterized by hypothyroidism and tissue-specific reduced TH sensitivity. The role of NF-kB in regulating THRB expression during endotoxemia, if any, is restricted to a limited number of tissues.

Osmotic regulation in isolated liver and kidney slices

1960 ◽  
Vol 199 (6) ◽  
pp. 1227-1231 ◽  
Author(s):  
A. G. Swan ◽  
A. T. Miller
Keyword(s):  
Guinea Pig ◽  
Osmotic Pressure ◽  
Kidney Cortex ◽  
Osmotic Regulation ◽  
Sodium Potassium ◽  
Pig Liver ◽  
Kidney Slices ◽  
Liver And Kidney ◽  
Isolated Liver ◽  
Guinea Pig Liver

Slices of guinea pig liver and kidney cortex were incubated under a variety of metabolic and osmotic conditions and the changes in tissue osmotic pressure and in water and electrolyte distribution were measured. The fresh tissues were approximately isotonic with serum, so that swelling was not due to initially hypertonic cell contents. Autolysis was not an important cause of swelling, probably because of leakage of the autolytic products from the cells. Influx of NaCl was sufficient to account for passage of water into the cells. Based on measured fluxes of sodium, potassium and chloride alone, the water of swelling was isotonic or hypertonic but never hypotonic.

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