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J de Ceaurriz

Publications and source records attributed to J de Ceaurriz.

At least 19 recordsLinked to original sources
PubMed2006

Effects of acute prednisolone intake during intense submaximal exercise.

To study the effects of a therapeutical dose of corticosteroid alone or associated with beta-2 agonist on performance and substrate response during intense submaximal exercise, seven healthy moderately trained male volunteers participated in the double-blind randomized cross-over study. An intense endurance exercise test to exhaustion was performed after ingestion of placebo (Pla), 20 mg prednisolone (Pred), and 20 mg prednisolone plus 4 mg salbutamol (Pred-Sal). Blood samples were collected at rest, after 5, 10 min of exercise, at exhaustion, and after 5 (r5), 10 (r10), and 20 (r20) min of passive recovery for ACTH, growth hormone, insulin, blood glucose, and lactate measurements. There were no significant differences in exercise time to exhaustion between the three treatments (Pla: 21.5 +/- 2.9; Pred: 22.0 +/- 2.5; Pred-Sal: 24.2 +/- 2.8 min). ACTH was significantly lowered after Pred and Pred-Sal vs. Pla from the start of exercise to the end of the experiment (p < 0.05). Pred and Pred-Sal increased resting and recovery (r10 and r20) significantly but not exercise blood glucose values. There were no significant differences in growth hormone concentrations between the three treatments whereas insulin was significantly higher at rest, during exercise, and at r20 after Pred-Sal administration vs. Pred and Pla (p < 0.05). Pred and Pred-Sal showed no significant effect on blood lactate compared with Pla treatment. These preliminary results do not support the hypothesis that acute oral therapeutic corticosteroid intake alone or associated with beta-2 mimetic improves performance during intense submaximal exercise, but further studies are necessary with tests of longer duration.

Adrenergic beta-Agonists↗
PubMed2002

Urinary 19-norandrosterone purification by immunoaffinity chromatography: application to gas chromatography/combustion/isotope ratio mass spectrometric analysis.

The detection of exogenous 19-norandrosterone (19-NA) in urines was investigated by using gas chromatography/combustion/isotope ratio mass spectrometry (GC/C/IRMS). 19-NA is, for the first time to our knowledge, isolated from urinary matrix by specific immunoaffinity chromatography (IAC) before analysis. The sample preparation consisted of a preliminary purification of urine by solid-phase extraction after hydrolysis by beta-glucuronidase. Unconjugated 19-NA was thus isolated by IAC and directly analysed by GC/C/IRMS. Optimisation of IAC purification was achieved and the reliability of the technique for anti-doping control is discussed.

Acetylation↗
PubMed2001

Gas chromatography-combustion-isotope ratio mass spectrometry analysis of 19-norsteroids: application to the detection of a nandrolone metabolite in urine.

Determination of whether the major metabolite of nandrolone in urine, 19-norandrosterone (19-NA), is exogenous or endogenous in origin is one of the most exciting challenges for antidoping laboratories. Gas chromatography-combustion-isotope ratio mass spectrometry (GC-C-IRMS) can be used to differentiate these two origins by carbon isotopic ratio analysis. A complete method for purification of 19-NA in urine has been established. Acetylated ketosteroids, and in particular 19-NA, are isolated from the urine matrix before analysis after hydrolysis and purification of urine by reversed-phase and normal solid-phase extraction. The limit of detection for 19-NA was about 60 ng with recoveries of 54-60%. Evidence of exogenous administration of 19-NA may be established from isotope ratio determination from the 13C/12C ratios of several synthetic 19-norsteroids compared to those obtained for endogenous steroids.

Doping in Sports↗
PubMed2001

Detection of perfluorocarbons in blood by headspace solid-phase microextraction combined with gas chromatography/mass spectrometry.

A new method of detection of perfluorocarbon molecules (PFCs) in blood sample has been established. After an extraction and pre-concentration step performed by headspace solid-phase microextraction (HS-SPME), the PFCs are detected by gas chromatography-mass spectrometry (GC/MS) with an ion trap mass spectrometer in MS and MS/MS modes. The influence of different parameters on the SPME process is discussed. The limit of detection and the linearity of the procedure have been determined for two PFCs.

Fluorocarbons↗
PubMed2000

Detection of exogenous intake of natural corticosteroids by gas chromatography/combustion/isotope ratio mass spectrometry: application to misuse in sport.

A detailed procedure for the analysis of exogenous hydrocortisone and cortisone in urine by gas chromatography/combustion/isotope ratio mass spectrometry (GC/C/IRMS) is proposed. As urinary levels of hydrocortisone are rather low for GC/C/IRMS analysis, the focus is on the main corticosteroid metabolites, tetrahydrocortisone (THE) and tetrahydrocortisol (THF). Following different solid phase extraction purifications, THE and THF are oxidized to 5beta-androstanetrione before analysis by GC/C/IRMS. Significant differences in delta(13)C per thousand values of synthetic natural corticosteroids and endogenous human corticosteroids have been observed. Therefore, a positive criterion, to detect exogenous administration of synthetic corticosteroids in anti-doping control, is proposed.

Adrenal Cortex Hormones↗
PubMed1996

Formation of GSH-derivatives as a pathway for inactive intermediates in vinylidene chloride-treated rats.

The two conjugates, S-[N-(2-hydroxyethyl)carbamoylmethyl]glutathione (GSAAE), and its corresponding mercapturic derivative N-acetyl-S-[N-(2-hydroxyethyl)carbamoylmethyl]cysteine (NCySAAE) were administered to fasted Sprague-Dawley rats as putative metabolites of vinylidene chloride (VDC). Methylthioacetylaminoethanol (MAAE) was identified in the urine of GSAAE- or NCySAAE-treated rats (0.5-2.0 mmol/kg, i.p.), as well as in the urine of VDC-treated rats (0.5-2.0 mmol/kg, p.o.). The effects of VDC, GSAAE and NCySAAE on the kidney and liver were also examined using aspartate aminotransferase (ASAT). N-acetyl-beta-D-glucosaminidase (NAG) and beta 2-microglobulin (beta 2-m) as urinary parameters of nephrotoxicity, and glutamate dehydrogenase (GLDH), sorbitol dehydrogenase (SDH) and alanine aminotransferase (ALAT) as serum parameters of hepatotoxicity. Unlike treatment with VDC, treatment with both GSAAE and NCySAAE failed to cause kidney and liver toxicity. The results support the hypothesis that MAAE originates from the formation of GSAAE and further metabolization to NCySAAE, and that MAAE excretion does not reveal a pathway of reactive intermediates.

Acetylglucosaminidase↗
PubMed1995

An attempt to explain interindividual variability in 24-h urinary excretion of inorganic arsenic metabolites by C57 BL/6J mice.

Forty C57 BL/6J mice, injected subcutaneously with 0.5 mg/kg arsenic as sodium arsenite, were examined for 24-h urinary excretion of total arsenic metabolites, creatinine and S-adenosylmethionine (SAM) and for 24-h faecal excretion of arsenic and levels of arsenic in the blood, liver, kidneys, lung, skin, spleen and bone at 24-h post-dose. Total urinary arsenic metabolites were calculated by summing up the inorganic (Asi), monomethylated (MMA) and dimethylated (DMA) derivatives directly measured by selective arsine generation-atomic absorption spectrometry (AG-AAS) or were measured by AG-AAS following complete mineralization. Both sets of results showed interindividual differences varying by as much as 7-fold and correlated with the 24-h urinary excretion of both SAM (r = 0.84 and r = 0.86, respectively) and creatinine (r = 0.82 and r = 0.87, respectively). There was interindividual variability of about a 30-fold range in 24-h faecal excretion of arsenic which correlated inversely with 24-h urinary excretion of arsenic metabolites (r = -0.69) and 24-h urinary excretion of both creatinine (r = -0.70) and SAM (r = -0.67). Body tissue levels of arsenic were low and not related to 24-h urinary excretion of arsenic metabolites, SAM and creatinine. Taken together, the results indicate that differences in the profile of urinary arsenic excretion and in the retention of arsenic in a particular organ do not contribute to interindividual variability in 24-h urinary excretion of arsenic metabolites by C57 BL/6J mice, but that variability in faecal excretion does, at least in part. It is speculated that there is most likely a predominant contribution from a diffuse tissue retention of arsenic or from a third route of arsenic elimination, i.e. respiratory, to this phenomenon in view of the small faecal contribution.

Animals↗
PubMed1995

Interindividual variability in the urinary excretion of inorganic arsenic metabolites by C57 BL/6J mice: possible involvement of a thiol/disulfide exchange mechanism.

The 24-h urine of 75 C57 BL/6J mice injected s.c. with 0.5 mg/kg arsenic as sodium arsenite were examined for creatinine, S-adenosylmethionine (SAM), urea and inorganic arsenic metabolites including inorganic arsenic (ASi), monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA). There was interindividual variability of about a 10-fold range in the 24-h urinary excretion of creatinine (80-642 micrograms/24 h, variability (cv) of 33%), SAM (7.5-67.2 micrograms/24 h, cv of 38%), urea (9.5-89.7 mg/24 h, cv of 36%), ASi (0.1-1.6 microgram/24 h, cv of 48%), MMA (0.17-2.1 micrograms/24 h, cv of 50%), DMA (0.73-8.13 micrograms/24 h, cv of 32%) and total arsenic metabolites (1.0-10.4 micrograms/24 h, cv of 31%). Interindividual differences, varying by as much as 5-7-fold, were also found in the urinary proportion of ASi (3-23%, cv of 41%) and MMA (5-22%, cv of 37%), but not in the urinary proportion of DMA (64-90%, cv of 7%). The 24-h urinary excretion of all arsenic metabolites correlated with the 24-h urinary excretion of urea (r = 0.81), creatinine (r = 0.88) and SAM (r = 0.83) as did the 24-h urinary excretion of urea with creatinine (r = 0.94) and SAM (r = 0.86), and the 24-h urinary excretion of creatinine with SAM (r = 0.94). Taken together, these results suggest that the overall intracellular glutathione (GSH)-dependent redox state, as reflected by the 24-h urinary excretion of SAM and creatinine, is involved in the interindividual variability in total arsenic metabolite excretion by C57 BL/6J mice. These preliminary results were also discussed with regard to the involvement of intracellular GSH-dependent redox state in the regulation of the reduction and of the methylation steps of arsenic, and to interindividual variability in the urinary excretion of total arsenic metabolites as a possible complicating factor in the biological monitoring of occupational exposure to arsenic.

Animals↗
PubMed1993

Relative developmental toxicities of inhaled aliphatic mononitriles in rats.

The developmental toxicities of eight aliphatic mononitriles were studied in Sprague-Dawley rats after inhalation exposure for 6 hr/day, during Days 6 to 20 of gestation. The range of exposure concentrations for acetonitrile was 900 to 1800 ppm; for propionitrile and n-butyronitrile, 50 to 200 ppm; for isobutyronitrile, 50 to 300 ppm; for acrylonitrile and methacrylonitrile, 12 to 100 ppm; for allylnitrile 12 to 50 ppm; and for 2-chloroacrylonitrile, 1 to 12 ppm. Embryolethality was observed after exposure to 1800 ppm acetonitrile, 200 ppm propionitrile, 300 ppm isobutyronitrile; fetotoxicity was observed after exposure to 200 ppm propionitrile, n-butyronitrile, or isobutyronitrile, or to 25 ppm acrylonitrile in the presence of overt signs of maternal toxicity. In the absence of significant maternal toxicity, allylnitrile caused embryolethality, fetotoxicity, and clear teratogenicity at 50 ppm, and n-butyronitrile and methacrylonitrile caused fetotoxicity at 200 ppm and 100 ppm, respectively. While maternal toxicity was observed for 2-chloroacrylonitrile, it did not cause significant embryonal or fetal toxicity up to 12 ppm.

Acetonitriles↗
PubMed1993

Modulation of acrylonitrile-induced embryotoxicity in vitro by glutathione depletion.

The effects of glutathione (GSH) depletion on the embryotoxicity of acrylonitrile were assessed in vitro using the rat whole-embryo culture system. Day 10 rat embryos were cultured in rat serum medium for 6 h in the presence of 250 microM L-buthionine-S,R-sulfoximine (BSO), a specific inhibitor of GSH synthesis, to deplete GSH in both embryo and visceral yolk sac. Following pretreatment, conceptuses were cultured for an additional 21 h in the presence of 152, 228, or 304 microM acrylonitrile. At the end of the culture period, conceptuses were assessed for survival, growth and development, malformations, and the protein and glutathione content of embryos and yolk sacs were assayed. Acrylonitrile alone produced concentration-related and statistically significant decreases in yolk sac diameter, crown-rump length, head length and number of somite pairs, as well as in embryonic and yolk sac proteins. The chemical also caused dysmorphogenesis of the brain and of the caudal extremity, and a concentration-related and statistically significant increase in GSH content in the yolk sac. Pretreatment with BSO significantly enhanced the embryotoxic effects of acrylonitrile. The conceptuses displayed further decreases in functional yolk sac circulation, yolk sac diameter, crown-rump and head length, when compared to either acrylonitrile or BSO alone. The incidence of caudal malformations and the severity of brain malformations produced by acrylonitrile were also increased. Marked decreases in embryonic and yolk sac GSH contents were observed after exposure to BSO alone or in combination with acrylonitrile.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Drug-Induced↗
PubMed1993

Urinary excretion of porphyrins by smelter workers chronically exposed to arsenic dust.

Urinary arsenic (inorganic arsenic and methylated metabolites), uroporphyrin and coproporphyrin I and III isomers were determined in 84 smelter workers exposed to arsenic trioxide and in 22 non-exposed controls. Both 'high' and 'low' exposure groups were defined, based on individual's work area (arsenic recovery plant and maintenance) and mean urinary excretion of arsenic was compared to the control group (257 and 129 micrograms/g creatinine against 9.9 micrograms/g creatinine). Total coproporphyrin (I+III) increased in each exposure group as compared to control (63.3 and 59 micrograms/g creatinine against 27.2 micrograms/g creatinine), as a consequence of a 2-fold increase in each coproporphyrin isomer. The mean concentration of uroporphyrin in each exposure group was very similar to that of the non-exposed controls (9.5 and 8.8 micrograms/g creatinine against 10.7 micrograms/g creatinine). These results suggest that long-term occupational exposure of humans to arsenic is associated with coproporphyrinuria and raise the question of the use of this parameter in addition to urinary arsenic for biological monitoring.

Adult↗
PubMed1992

Indirect and lactation-associated changes in renal alkaline phosphatase of newborn rats prenatally exposed to cadmium chloride.

Pregnant Sprague-Dawley rats were intraperitoneally injected with physiological saline solution (vehicle) or cadmium chloride (CdCl2) at 2.5 mg kg-1 body wt. on days 8, 10, 12 and 14 of gestation. Offspring were examined for renal alkaline phosphatase activity (ALP) on postnatal days (PND) 3 and 12, and for kidney metallothionein (MTh) and for liver, kidney and entire gastrointestinal tract 109Cd content at birth and on PND 3 and 12. No effects were observed on neonatal survival or on body, liver and kidney weights of pups up to PND 12. Newborns born and fed by mothers exposed to CdCl2 during pregnancy exhibited a significant decrease in ALP activity on PND 3. Conversely, no significant changes were observed in newborns lactated by surrogate non-treated mothers. Renal MTh increased with age but was not influenced by maternal treatment. Traces of 109Cd were present in the liver at birth (5-7 ng). Thereafter, 109Cd was mainly found in the gastrointestinal tract of newborns lactated by their biological mothers (610-690 ng on PND 12), with a marginal uptake in the liver (10-12 ng on PND 12). 109Cd was not detectable in the kidneys at any age (less than 4 ng). These results show that prenatal exposure to Cd cannot be the sole aetiological agent in the induction of the subtle and transitory changes in renal biochemistry observed in offspring born and fed by female rats intraperitoneally injected with 2.5 mg CdCl2 kg-1 body wt. on days 8, 10, 12 and 14 of gestation. The results also contradict the role of a direct effect on the kidney.

Alkaline Phosphatase↗
PubMed1992

Evaluation of the interaction of benzene and toluene on the urinary excretion of t,t-muconic acid in rats.

The influence of simultaneous exposure to benzene and toluene on the urine excretion of t,t-muconic acid (t,t-MA) was examined in rats. t,t-MA was measured from 24-h urine of rats subjected to a single 4-h exposure to 5 or 20 ppm benzene and/or 50, 100, 200 or 1000 ppm toluene. Coexposure lowered t,t-MA excretion in a concentration-dependent manner, especially in the 20 ppm benzene group where the decrease averaged 28, 44 and 85% after exposure to 100, 200 and 1000 ppm toluene, respectively, as compared to benzene-exposed groups alone. The data confirm the sensitivity of t,t-MA as an indicator of benzene exposure and point out that measurement of t,t-MA may underestimate the exposure to benzene in the presence of toluene.

Administration, Inhalation↗
PubMed1991

Changes in urinary proximal tubule parameters in neonatal rats exposed to cadmium chloride during pregnancy.

Pregnant Sprague-Dawley rats were injected intraperitoneally with physiological saline solution (vehicle) or cadmium chloride (CdCl2) at 2.0 or 2.5 mg kg-1 on days 8, 10, 12 and 14 of gestation. On postnatal day (PND) 3, 12 or 49, the offspring were examined for 8- or 24-h urinary excretion of beta 2-microglobulin (beta 2-m), metallothionein (MT) and urinary activity of three proximal tubular enzymes: gammaglutamyl transferase (GGT), alkaline phosphatase (ALP) and N-acetyl-beta-glucosaminidase (NAG). Treatment with CdCl2 did not affect growth or survival of offspring. Significant decreases in the urinary excretion of GGT, ALP and NAG were observed on PND 3, at both doses. Exposure to 4 x 2.5 mg kg-1 resulted in functional deficit of the proximal tubule on PND 3, as evidenced by the significant increase in beta 2-m. Except for a slight but significant increase of beta 2-m in 49-day-old males, all the other urinary parameters returned to control values on PND 12. There was no effect on MT. Results from this study show that prenatal exposure to CdCl2 can induce significant changes in the kidney biochemistry of rats in the early postnatal period.

Alkaline Phosphatase↗
PubMed1991

Difference in liver and serum malathion carboxylesterase and glucose-6-phosphatase in detecting carbon tetrachloride-induced liver damage in rats.

Microsome, cytosol and serum malathion carboxylesterase (MaCEst) activity was assessed in rats after single i.p. administration of carbon tetrachloride (CCl4) in doses ranging from 0.05 to 1 ml kg-1. MaCEst activities were compared with those of glucose-6-phosphatase (G6-Pase) as an indicator of endoplasmic reticulum damage and serum glutamate dehydrogenase (GLDH) and sorbitol dehydrogenase (SHD) as indicators of liver cytolysis. The data showed a dose-dependent increase in GLDH and SDH serum activities (175% and 68%) from 0.05 ml kg-1; an increase in serum G6-Pase (31%) and a decrease in microsomal G6-Pase (38%) was apparent only after 0.5 or 1.0 ml kg-1 doses. MaCEst activity was unaffected. The results demonstrate that, under these experimental conditions, serum and subcellular measurements of MaCEst activity failed to reveal the liver toxicity of CCl4.

Animals↗
PubMed1991

Biliary excretion of hexachloro-1,3-butadiene and its relevance to tissue uptake and renal excretion in male rats.

Renal, biliary, pulmonary and faecal excretion experiments were carried out with labelled hexachloro-1,3-butadiene [( 14C]HCBD) in male Sprague-Dawley rats, given orally (p.o.) and intravenously (i.v.) in doses of 1 and 100 mg kg-1 as a solution in polyethylene glycol. The radioactivity excreted over 72 h was determined in rats fitted with exteriorized biliary cannulae and in rats whose bile ducts remained fully functional, respectively. In addition, bile duct-duodenum cannula-linked rats, of which the donor was given 100 mg kg-1 [14C]HCBD orally and the recipient had also a bile fistula, were examined within 30 h for radioactivity in the excreta, the kidney, the liver and the plasma. In non-cannulated rats, fractional urinary excretion decreased when the dosage increased and amounted to 23% and 8.6% after i.v. injection or 18.5% and 8.9% after p.o. administration of 1 and 100 mg kg-1, respectively. Pulmonary excretion of radioactivity was less than 9% and was not affected by the increase in dosage. In bile duct-cannulated rats, fractional urinary excretions were similar irrespective of the dose and the route of administration and amounted to ca. 7.5% of the dose. Decrease in fractional biliary excretion occurred with increase in dosage (88.7% vs 72%) after i.v. injection and (66.8% vs 58%) after gavage. In cannulated rats, faecal excretion was less than 0.5% after i.v. injection and accounted for 3% and 16% of the dose after p.o. administration of 1 and 100 mg kg-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Difference in the developmental toxicity of ethylenethiourea and three N,N'-substituted thiourea derivatives in rats.

Sprague-Dawley rats were administered ethylenethiourea (ETU), 1,3-dimethyl-2-thiourea (DMT), 1,3-dibutyl-2-thiourea (DBT), or 1,3-diphenyl-2-thiourea (DPT) by gavage from Days 6 to 20 of gestation. Daily dosage levels (mg/kg/day) were ETU at 0, 15, 25 and 35; DMT at 0, 15, 25, 50, 100, and 200; DBT at 0, 15, 25, 50, 100, and 200; and DPT at 0, 25, 50, 100, and 200. There was evidence of maternal toxicity at all doses of DMT and at doses greater than or equal to 50 mg DBT/kg/day. DPT was embryolethal at 200 mg/kg/day. Fetotoxicity was observed at doses greater than or equal to 15 mg DMT/kg/day, greater than or equal to 15 mg DBT/kg/day, and greater than or equal to 100 mg DPT/kg/day. ETU was the only chemical tested that proved to be teratogenic.

Animals↗