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W Henke

Publications and source records attributed to W Henke.

At least 19 recordsLinked to original sources
PubMed1995

Effects of preservation solutions on cortical and medullary mitochondria of rat kidney.

The mitochondria isolated from cortex and medulla of rat kidneys were examined after storage in either Euro-Collins solution, in Bretschneider's histidine-tryptophan-ketoglutarat solution or in Belzer's University of Wisconsin solution at 25 degrees C or at 4 degrees C for a maximum of 4 to 24 hrs. Independently to the preservation of the solution used, the storage of the kidneys led to a decrease in state 3 respiration and uncoupled respiration as well as to an increase in the rate of state 4 respiration. The decrease in state 3 respiration ran parallelly to a decrease in adenine nucleotides. For the homogeneous protection of the mitochondria as well from the cortex as from the medulla, the Bretschneider's solution had the best preservative effect at a storage temperature of 25 degrees C as shown by the measured mitochondrial parameters. At 4 degrees C storage temperature, the differences in action with the various examined solutions were markedly smaller. However, compared to the other two solutions, the Euro-Collins solution showed a more favourable protective effect on cortical and medullary mitochondria.

Adenine Nucleotides↗
PubMed1993

Comparison of the effects of the immunosuppressive agents FK 506 and cyclosporin A on rat kidney mitochondria.

Interactions of FK 506 with renal cortical mitochondria have been investigated by measuring respiration, ATP net uptake and Ca2+/Pi-induced swelling. Both FK 506 and cyclosporin A (CsA) inhibit the succinate-supported state 3 and uncoupled respiration and are without effect on the glutamate/malate-supported state 3 and uncoupled respiration. FK 506, like CsA, inhibits net uptake of ATP, but, in contrast to CsA, is without effect on Ca2+/Pi-induced swelling.

Adenosine Triphosphate↗
PubMed1992

Cyclosporine A inhibits ATP net uptake of rat kidney mitochondria.

The adenine nucleotide content of mitochondria varies at several physiological and pathological situations. Both net transport and intramitochondrial catabolism of adenine nucleotides has been suggested to be responsible for these changes. Here, the influence of cyclosporine A on the ATP net uptake of isolated rat kidney mitochondria was examined. The ATP net uptake of mitochondria depleted of matrix adenine nucleotides by pyrophosphate treatment was inhibited by cyclosporine A showing a I50 value of about 4 nmol/mg mitochondrial protein. Because intramitochondrial adenine nucleotide content is important for several mitochondrial functions such as oxidative phosphorylation, Ca2+ homoeostasis and mitochondrial biogenesis, it is concluded that the inhibition of adenine nucleotide net transport and a decrease of adenine nucleotide content may be involved in the immunosuppressive and nephrotoxic effects of cyclosporine A.

Adenosine Diphosphate↗
PubMed1992

The contribution of adenine nucleotide loss to ischemia-induced impairment of rat kidney cortex mitochondria.

Adenine nucleotides and respiration were assayed with rat kidney mitochondria depleted of adenine nucleotides by pyrophosphate treatment and by normothermic ischemia, respectively, with the aim of identifying net uptake of ATP as well as elucidating the contribution of adenine nucleotide loss to the ischemic impairment of oxidative phosphorylation. Treatment of rat kidney mitochondria with pyrophosphate caused a loss of adenine nucleotides as well as a decrease of state 3 respiration. After incubation of pyrophosphate-treated mitochondria with ATP, Mg2+ and phosphate, the content of adenine nucleotides increased. We propose that kidney mitochondria possess a mechanism for net uptake of ATP. Restoration of a normal content of matrix adenine nucleotides was related to full recovery of the rate of state 3 respiration. A hyperbolic relationship between the matrix content of adenine nucleotides and the rate of state 3 respiration was observed. Mitochondria isolated from kidneys exposed to normothermic ischemia were characterized by a decrease in the content of adenine nucleotides as well as in state 3 respiration. Incubation of ischemic mitochondria with ATP, Mg2+ and phosphate restored the content of adenine nucleotides to values measured in freshly-isolated mitochondria. State 3 respiration of ischemic mitochondria reloaded with ATP recovered only partially. The rate of state 3 respiration increased by ATP-reloading approached that of uncoupler-stimulated respiration measured with ischemic mitochondria. These findings suggest that the decrease of matrix adenine nucleotides contributes to the impairment of ischemic mitochondria as well as underlining the occurrence of additional molecular changes of respiratory chain limiting the oxidative phosphorylation.

Adenine Nucleotides↗
PubMed1992

Inhibition of skin allograft rejection and acute graft-versus-host disease by cis-urocanic acid.

Ultraviolet B radiation initiates a suppression of the delayed-type hypersensitivity response accompanied by a generation of antigen-specific suppressor cells and an alteration of antigen-presenting function. In previous studies we and other investigators could achieve a prolongation of graft survival by a treatment of the recipient with UVB light or 8-methoxy-psoralen plus UVA light (PUVA). One of the mediators of the systemic immunomodulatory effects of ultraviolet light or PUVA may be urocanic acid, which is isomerized in the skin by ultraviolet light from its cis- to the trans-isomer. In this work we present evidence that cis-urocanic acid, generated in vitro by a treatment with UVB light or PUVA, is able to prolong the survival of allogeneic MHC disparate skin grafts in mice. In contrast, the rejection of second set grafts was not suppressed. Unirradiated (trans-urocanic acid) had no effect on allograft rejection. In a murine model cis-, but not trans-urocanic acid, prevented or delayed an acute lethal graft-versus-host disease. These experiments demonstrate the potent systemic immunomodulatory effects of cis-urocanic acid in vivo.

Animals↗
PubMed1992

Adaptational increase of liver glutathione content during long-term application of cyclosporine A may attenuate toxic side effects.

The concentrations of reduced and oxidized glutathione and of adenine nucleotides were determined in liver, kidney and heart of rats during long-term (four weeks), high-dose therapy with cyclosporine A. In liver and kidney the concentration of oxidized glutathione increased following 4 weeks-therapy suggesting increased formation of free radicals and accelerated lipid peroxidation processes. These processes may be due to an increased activity of the cytochrome P-450 system. Compensatory levels of reduced glutathione were also increased. The adaptational increase of the tissue level of reduced glutathione, presumably the response to a chronic oxidative stress, was more distinct in the liver. The liver did not lose adenine nucleotides. In contrast the kidney, after 4 weeks of cyclosporine A therapy, lost 25% of the adenine nucleotides. These findings suggest that the liver is characterized by a greater potential for effective adaptation to oxidative stress conditions compared to the kidney. These adaptations may prevent distortions of energy and nucleotide metabolism in the liver which is in agreement with the minor ultrastructural changes we have observed.

Adaptation, Physiological↗
PubMed1992

Practical approach for determining glomerular filtration rate by single-injection inulin clearance.

We compared the glomerular filtration rate as measured by a single-injection inulin clearance with that measured by a standard isotope method with 99mTc-labeled diethylenetriaminopentaacetic acid in 21 subjects with glomerular filtration rates greater than 35 mL/min. After a bolus injection of 5 g of inulin, blood samples were taken 20, 45, 90, 120, 145, 180, and 240 min afterwards. Inulin was measured by optimized chemical or enzymatic methods of high analytical sensitivity to determine inulin at low concentrations. We used the one-compartment model and inulin concentrations measured at two sampling times to calculate the glomerular filtration rate from the data of the disappearance curve of inulin. Inulin concentrations at 20 and 240 min after injection of the inulin bolus were suited to estimate glomerular filtration rate by this procedure, resulting in values (y) comparable with those obtained by isotope technique (x). The relationship to the isotope technique was characterized by the equation y = +4.80 mL/min + 0.92x (r = 0.97). The single-injection inulin clearance determination can detect a decrease of glomerular filtration rate at the beginning of kidney damage, given that our study included subjects with glomerular filtration rates greater than 35 mL/min. We conclude that the glomerular filtration rate can be determined by analyzing only two blood samples after a bolus injection of inulin.

Adult↗
PubMed1992

Cis-urocanic acid as a mediator of ultraviolet-light-induced immunosuppression.

Treatment of an organism with UVB light or PUVA (8-methoxypsoralen + UVA light) not only leads to alterations in the irradiated skin but also to systemic immunomodulation, due to the release of several chemical mediators of immunosuppression like prostaglandins, acute-phase proteins, IL-1 inhibitor, alpha-melanocyte-stimulating hormone, propiomelanocorticotropin or other cytokines. A recently described mediator is urocanic acid, which is transformed by UV light in the skin from the trans- to the cis-isomer and that exerts a systemic immunomodulatory effect. In our experiments, treatment with PUVA or with cis-urocanic acid prevents the rejection of rat heart allografts in 50% and 40% of cases, respectively. Control grafts are rejected in fewer than 10 days. PUVA treatment of donor leukocytes before transfusion into the prospective recipient inhibits only their sensitizing, not their graft-protecting, effect on subsequent skin grafts in mice. PUVA treatment also prevents acute lethal GVH disease in mice after irradiation with a sublethal dose of x-rays and transfusion of semiallogeneic spleen cells. Treatment of recipient mice with cis-urocanic acid has the same effect. The humoral immune response to sheep erythrocytes is not influenced by cis-urocanic acid. These results demonstrate that PUVA treatment or its chemical mediator, cis-urocanic acid, may be used in transplantation and hematology as naturally occurring immunosuppressive agents, especially for the control and manipulation of GVH leukemia reaction.

Animals↗
PubMed1991

Ischemia decreases the content of the adenine nucleotide translocator in mitochondria of rat kidney.

The activity of the adenine nucleotide translocator is decreased at ischemia. Studies were undertaken to elucidate changes in the adenine nucleotide translocator by determining its content in mitochondria of ischemic rat kidney. After 60 min of ischemia, the content of the adenine nucleotide translocator amounted only to about 55%, of that measured in control mitochondria. At the same time, the flux control coefficient was increased. These changes paralled the well-known effects of ischemia: the decrease in oxidative phosphorylation and in adenine nucleotides. It is supposed that the decrease in the adenine nucleotide translocatar content accounts, at least partially, for the ischemia-induced impairment of mitochondria.

Animals↗
PubMed1991

Methods compared for determining activity of N-acetyl-beta-D-glucosaminidase in urine without pretreatment of sample: different sensitivity and species effect.

N-Acetyl-beta-D-glucosaminidase (NAG) activities in the urine of men and rats were measured with methods recommended as procedures without pretreatment of the urine sample. Four different derivatives of NAG were compared for determination: 4-nitrophenyl; 3,3-dichlorophenylsulfonphthaleinyl; 3-cresolsulfonphthaleinyl, and 2-methoxy-4-(2-nitro-vinyl)phenyl. The conventional test using the 4-nitrophenyl derivative showed the highest activities and correlated very well with the other tests. There are method-dependent differences between NAG activities measured in men and rats due to the different Km values and inhibitory effects by urea.

Acetylglucosamine↗
PubMed1991

Evaluation of methods for determining N-acetyl-beta-D-glucosaminidase in urine of rats without purification of urine samples.

N-Acetyl-beta-D-glucosaminidase (NAG) activities in urine of rats were measured with methods recommended as procedures without the pretreatment of urine sample. Four different derivatives [4-nitrophenyl; 3-cresolsulfonephthaleinyl; 3,3'-dichlorophenylsulfonephthaleinyl; 2-methoxy-4-(2-nitrovinyl)phenyl] of N-acetyl-beta-D-glucosaminide were compared for determination. The conventional test using the 4-nitrophenyl derivative showed the highest activities and was very well correlated with the other tests. The test using the 3,3'-dichlorophenylsulfonephthaleinyl substrate is most convenient and practical to determine NAG in small animals because it is, in contrast to the other three discontinuous (endpoint) tests, a continuous (kinetic) assay which can be easily adapted to clinical chemistry analyzers.

Acetylglucosaminidase↗
PubMed1991

Kinetic evidence that the sodium-dependent high-affinity and the sodium-independent low-affinity dopamine uptake are mediated by one carrier.

In synaptosomes of the rat striatum the dopamine uptake was measured in a concentration range of 0.03 microM to 100 microM. In the presence of sodium the uptake exhibited a non-Michaelis-Menten kinetics and in a sodium-free medium the uptake kinetics was sigmoid. According to these findings a novel model for the dopamine uptake is proposed. Its main assumption is one carrier with two dopamine binding sites.

Animals↗
PubMed1991

Characterization of a hexammineruthenium-stimulated external NADH oxidase from rat liver mitochondria.

The existence of an external hexammineruthenium-stimulated NADH oxidase in rat liver mitochondria is postulated. This enzyme is localized on the outer surface of the inner mitochondrial membrane, is specific for NADH and requires oxygen. The apparent affinity of the enzyme for NADH amounts to about 4 microM. Furthermore, the enzyme is characterized by an alkaline pH optimum and a linear Arrhenius plot (14 kJ/mol). The electron transfer from NADH to oxygen is not linked with the respiratory chain but is connected with the formation of superoxide radicals.

Animals↗