Assessment of functional activity of cold-stored kidney transplant by proton magnetic resonance spectroscopy.
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Animals↗
Biomedical subjects
C Tallineau
Publications and source records attributed to C Tallineau.
Gentamicin-induced kidney damage and lipid peroxidation in rats.
Although it has been reported that injections of gentamicin induces lipid peroxidation in rat renal cortex (Ramsammy et al. (1985) Biochem. Pharmacol. 34, 3895-3900), our results showed no modification of thiobarbituric-reagent substances (TBARS) or in analysis of the polyunsaturated fatty acid profile. Moreover, endogenous vitamin E and glutathione were not consumed. In in vitro systems, gentamicin incubated with microsomes, homogenates and kidney slices from the normal rat failed to induce lipid peroxidation. We show that the increase in TBARS in vivo detected by Ramsammy et al. was wrongly attributed to the oxidant power of gentamicin. As this antibiotic does react positively to thiobarbituric acid in the presence of a system generating free radicals, it is possible that these authors accidentally introduced such a system into their experiments.
Animals↗
[Auto-oxidation or brain homogenate: research of oxidizing agent and targets. Comparison with liver homogenate].
The aim of this study was to determine: 1) the source of Thiobarbituric Reactive Substances (TBARS) spontaneously produced during rat brain homogenate incubation; 2) the cellular components involved; 3) the reason why brain and liver homogenates did not have the same behaviour. Measurements of TBARS, Polyunsaturated Fatty Acids (PUFAs), aldehydes coming from PUFAS breakdown, vitamin E and Schiff's bases levels were performed on brain and liver homogenates, membrane fractions (Mb) and medium containing soluble cytoplasmic components (CS). Mb and CS were prepared by differential centrifugation. Brain homogenate incubation, contrary to liver homogenate, led to an increase in TBARS amount, while PUFAS, aldehydes and vitamin E levels remained unchanged. No TBARS accumulation arose when Mb or CS were separately incubated. However, it was of interest to note that liver or brain incubation of Mb with CS led to an overproduction of TBARS. These results suggested that spontaneous oxidation of brain homogenate was not due to lipid peroxidation. On the other hand, the fact that, contrary to the liver homogenate, liver Mb incubated with CS led to an increase in TBARS level, supports the idea that a "protective agent" was eliminated during centrifugation. It can be speculated that this "agent" is not effective in the brain.
Aldehydes↗
Evidence of lipoperoxidation induced by lactic acid on kidney homogenates.
Sawas and Gilbert (Arch. Int. Pharmacodyn. Ther., 276 (1985) 301-312) reported that the commercial solution of haloperidol induces lipoperoxidation of kidney homogenates from Sprague-Dawley rats. However, it would appear that this effect is attributable to the excipient, lactic acid, rather than to haloperidol itself. Lactic acid enhances susceptibility to lipoperoxidation of kidney homogenates in a dose- and time-dependent manner by increasing production of thiobarbituric acid-reactive substances and slightly decreasing polyunsaturated fatty acids such as arachidonic acid and docosahexaenoic acid. This stimulation of lipoperoxidation may be attributed to a mechanism less dependent on enzymatic action than on Fe2+ and Fe3+. Lactic acid may facilitate iron release and formation of iron complexes, factors which increase susceptibility to oxidative stress.
Animals↗
Iron- and lactic acid-induced lipid peroxidation in rat kidney homogenates and slices.
Lactic acid 4 mM acted as a lipoperoxidant by increasing production of thiobarbituric acid-reactive substances (TBARS) in rat kidney slices and homogenates. This effect occurred mainly when slices and homogenates were incubated in a pH 5.4 medium conductive to full expression of compound acidity. TBARS increase was only slight when incubation was performed in Krebs buffer, pH 7.4. Moreover, sodium lactate 4 mM increased TBARS production only when homogenates were incubated in the pH 5.4 medium. Deferoxamine (1 mM) inhibited the prooxidant effect of lactic acid 4 mM, and TBARS increase was correlated with iron release. The iron mobilized may come from reserves where it is weakly bound or from ferritin; and ascorbic acid, present in low quantities in kidney, might trigger the release of this product.
Animals↗
[Shoulder prosthesis].
In our department, 25 shoulder prostheses were laid in 24 patients. The main indication remains omarthritis with or without necrosis (13). Fifteen Neer's prostheses (13 total, 2 simple humeral ones) were laid. The posterior approach was chosen in 14 cases. Out of the 20 shoulders reviewed, 8 presented with preoperative muscle atrophy, 8 with no postoperative muscle atrophy, including 8 with posterior approaches. In 4 cases of posterior approach, postoperative atrophy of the infraspinatus muscle was noted, but these four patients were all satisfied or very satisfied. The analysis was carried out according to our grading (0 to 20) of Neer's prostheses. The overall results are excellent for simple humeral prostheses on traumatic lesions. In the other cases, the main benefit is obtained for shoulders in a stable state. The improvement remains poor for the mobility and function of the shoulder. The patients are satisfied on a whole, especially with the improvement of pain.
Adult↗
Cu(2+)-induced lipid oxidation in plasma: questionable relation between cholesterol oxidation and LDL modification.
Oxidatively modified low-density lipoproteins (LDL) may be involved in the process of cholesterol deposition in arteries. Because of their cytotoxicity, oxysterols resulting from cholesterol oxidation could be a contributing factor in this process. Studies in this area have generally been performed on purified LDL, but in our research whole plasma was exposed to the oxidizing action of copper. Oxidation of the ring structure, which is at the origin of oxysterols, apparently occurs once most polyunsaturated fatty acids have disappeared. Hydrated LDL density reaches a value identical to that obtained during oxidation of LDL by endothelial cells, whereas the ring structure remains unmodified.
Adult↗
Cholesterol-lowering effect of continuous enteral nutrition in man.
We have studied the effect of polymeric cholesterol-free enteral nutrition (EN) on serum lipid and apolipoprotein levels in 30 consecutive non-diabetic, non-hyperlipaemic gastrointestinal patients. EN-40 +/- (SEM) 2 kcal/kg/day including 35% vegetable lipids (50% highly polyunsaturated fat, 50% medium chain triglycerides)-was delivered continuously (24h) via the gastric route for at least 2 weeks (mean duration: 35 +/- 4 days). In the entire group, serum total cholesterol decreased by 10.5% (p < 0.01) on day 7 and 17.5% (p < 0.01) on day 28 (n = 12); this was accompanied by 21% and 20% decreases in LDL-cholesterol and apolipoprotein B (p < 0.05) levels respectively, on day 28. In the 19 patients who were normocholesterolaemic on day 0, serum total cholesterol decreased by 15% (p < 0.01) on day 7 and by 28% (p < 0.05) on day 28 (n = 7). Conversely, in the other 11 patients with a low (<3.7 mmol/L) pre-EN serum total cholesterol level, no significant changes were observed during EN. We conclude that continuous, cholesterol-free EN has, in normocholesterolaemic patients, a marked cholesterol-lowering effect; the respective role of the composition of the diet and the continuous delivery of nutrient within the gut have yet to be investigated.
Journal Article↗
Polyunsaturated fatty acid profiles and alpha-tocopherol levels in plasma and whole blood incubated with copper. Evidence of inhibition of lipoperoxidation in plasma by hemolysate.
Polyunsaturated fatty acid (PUFA) profiles and alpha-tocopherol levels were studied in human plasma and whole blood incubated with copper under air or nitrogen. In plasma, both PUFAs and alpha-tocopherol disappeared. The results were completely different in whole blood: (i) in plasma, while alpha-tocopherol decreased in the same manner as in plasma incubated alone, profiles of PUFA were only slightly modified. So, in spite of the absence of alpha-tocopherol, lipoperoxidation was not very marked. That is why the release of a protective factor from erythrocytes during hemolysis was under consideration. This was confirmed by the complete inhibition of degradation of PUFAs in plasma when hemolysate was added; (ii) In erythrocytes, no modification in PUFA profiles could be detected while alpha-tocopherol decreased slightly. Thus, not only do erythrocytes resist the copper-dependent oxidative stress in an incredible manner, but they also seem to protect plasma at the time of hemolysis.
Adult↗
Copper-induced lipid peroxidation and hemolysis in whole blood: evidence for a lack of correlation.
In order to establish a possible relationship between hemolytic and peroxidant activities of copper ions, lipid peroxidation was studied in plasma and whole blood incubated for 24 h with different concentrations of copper. The lipid peroxidation was investigated by the determination of thiobarbituric acid-reactive species, conjugated dienes and fluorescent lipid chromophores. The copper-induced lipoperoxidation was clearly demonstrated in plasma incubated with high concentrations of copper (12.10(-4) and 20.10(-4) M); in whole blood, all the lipoperoxidation products were increased in the plasma, while the fluorescent lipid chromophores remained unchanged in red cells. With a copper concentration similar to that found in acute copper intoxication (4.10(-4) M) no lipoperoxidation was observed and yet hemolysis occurred, reduced glutathione (GSH) decreased dramatically and methemoglobin (MetHb) increased. From these results, we assume that, despite its prooxidant activity and its capacity to produce lipoperoxidation, it has not been proven that copper ions at pathophysiological concentrations induce hemolysis by an oxidative mechanism.
Adult↗
[Current surgical indications in amebic abscess of the liver. Apropos of a series of 270 cases].
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Humans↗
[Urinary neopterin: its value in the study of various neoplasms].
A systematic study of urinary Neopterin was carried out, gathering two thousand five hundred measurements, on a hospital population of patients supposedly affected by tumors and the concentrations obtained were compared to the usual values determined at the same time on patients apparently free from any disease. Malignant tumors appear to be associated with high concentration of urinary Neopterin and this increase seems well correlated with the severity of the disease. Benign tumors correspond, on the contrary, to an appreciably normal excretion of Neopterin. A clinic study of Neopterin elimination specifies, however, that each elevated value must be followed with other determinations in order to rule out the possibility of an eventual viral infection at the incubation stage. The authors think that this dosage could represent a mean of discovery of professional cancers in high risk populations as well as an element in the supervision of anti-neoplastic treatments.
Adolescent↗
[Value of the assay of urinary neopterin in multiple myeloma. Preliminary study].
Urinary neopterin was assayed by HPLC (high performance liquid chromatography). 75 assays were performed in a population of 21 patients with multiple myeloma. There was a significant correlation between the urinary neopterin level and the electrophoretic peak, the R beta-2 microglobulinaemia ratio and the calculated tumour mass (Tbmc). This study demonstrates the value of this assay in the monitoring of patients with multiple myeloma.
Aged↗
Evidence for the involvement of (Cu-ATP)2- in the inhibition of human erythrocyte (Ca2+ + Mg2+)-ATPase by copper.
The effects of copper on the activity of erythrocyte (Ca2+ + Mg2+)-ATPase have been tested on membranes stripped of endogenous calmodulin or recombined with purified calmodulin. The interactions of copper with Ca2+, calmodulin and (Mg-ATP)2- were determined by kinetic studies. The most striking result is the potent competitive inhibition exerted by (Cu-ATP)2- against (Mg-ATP)2- (Ki = 2.8 microM), while free copper gives no characteristic inhibition. Our results also demonstrate that copper does not compete with calcium either on the enzyme or on calmodulin. The fixation of calmodulin on the enzyme is not altered in the presence of copper as shown by the fact that the dissociation constant remains unaffected. It may be speculated that (Cu-ATP)2- is the active form of copper, which could plausibly be at the origin of some of the pathological features of erythrocytes observed in conditions associated with excess copper.
Adenosine Triphosphate↗
Decreased red cell enolase activity in a 40-year-old woman with compensated haemolysis.
A 40-year-old woman splenectomized 17 years previously for hereditary haemolytic anaemia was investigated in our laboratory because of persistent conjunctival subicterus associated with compensated haemolysis. The results of the autohaemolysis and osmotic fragility tests were similar to those usually observed in hereditary spherocytosis. Red cell enzyme assays indicated a decreased amount of kinetically normal enolase. The genetic transmission of this defect could not be established since the only other affected member of the family was the proposita's father who died several years ago after splenectomy for an undefined haemolytic disorder.
Adult↗
Intoxication by benzodiazepines: studies with diazepam used as a model compound suggest an interaction with red blood cells calmodulin dependent (Ca2+, Mg2+) ATPase.
20 patients under therapy or intoxicated by benzodiazepines were studied. A partial inhibition of (Ca2+, Mg2+)ATPase on 'B' membranes (CaM rich membranes) was evident in 2 cases. A total inhibition of (Ca2+, Mg2+) ATPase on both 'B' and 'A' (CaM depleted) membranes was noted in 1 case: the patient who was severely intoxicated had pronounced hemolysis. As an attempt to elucidate the mechanism of this action, the effect of diazepam chosen as model compound was studied on 'B' and 'A' membranes prepared from normal human RBC previously incubated with diazepam. A high concentration of diazepam, corresponding to a 20-fold therapeutic level results in a 50% inhibition of the maximal activity of the enzyme on 'B' membranes. It may be speculated from these experiments that the effect of high concentration of benzodiazepines on CaM dependent (Ca2+, Mg2+) ATPase leads to accelerated RBC destruction.
Benzodiazepines↗
Lack of correlation between TBARS production and PUFA degradation during incubation of membrane erythrocytes in an OH. (Fe2+/H2O2) generator system.
We investigated the effects of an OH. (Fe2+/H2O2) generator system on erythrocyte membrane, particularly the time-course of lipid peroxidation as estimated by measurement of conjugated dienes, thiobarbituric reactive substances (TBARS), lipofuscin-like pigments, and alpha-tocopherol. Polyunsaturated fatty acids (PUFAs), especially arachidonic acid (20:4 omega 6) and docosahexenoic acid (22:6 omega 3), were also measured. Erythrocyte membranes were suspended in phosphate buffer containing Fe2+ (200 microM) and H2O2 (1.42 mM), and incubated in a shaking water bath at 37 degrees C. Initially, there was an increase in TBARS and lipofuscin-like pigments, two well-known end products of PUFA oxidative degradation, whereas PUFAs remained unchanged (incubation time: 1 h). After two or more hours of incubation, marked lipid peroxidation was noted, with the appearance of conjugated dienes and a decrease of PUFAs, indicating that lipid peroxidation had occurred after a lag phase during which TBARS were not produced from PUFAs. This suggests that another OH. target was involved.
Arachidonic Acid↗
Age-related changes in ethanolamine glycerophospholipid fatty acid levels in rat frontal cortex and hippocampus.
Morphological and biochemical alterations are associated with a progressive age-related cognitive deficit. Plasmenylethanolamine, the major brain plasmalogen, may be modified during aging because of a possible antioxidant role and involvement in synaptic transmission. Two- and 18-month-old rats were used to study the effect of aging on the levels and acyl composition of plasmenylethanolamine (PmE), phosphatidylethanolamine (PE), and phosphatidylserine (PS) in the frontal cortex and hippocampus. Aging only reduced significantly the PE levels in the frontal cortex. In 18-month-old rats, the fatty acid composition of the three phospholipid classes studied showed an increase of monounsaturated fatty acid (18:1 n-9 and 20:1 n-9) and a decrease in polyunsaturated fatty acid (PUFAs), essentially docosahexaenoic acid (DHA). DHA was markedly decreased in hippocampus PE. DHA, but also arachidonic acid, were considerably lower in frontal cortex PmE. PS modifications were similar in both regions. Hippocampus and frontal cortex underwent specific age-induced modifications in PmE and PE acyl composition. This could produce different effects on the functional ability of these two structures involved in the processes of specific memorization.
Aging↗