Biomedical subjects

J de Ceaurriz

Publications and source records attributed to J de Ceaurriz.

At least 37 records · Page 2Linked to original sources

PubMed1991

Interdependence of polymorphonuclear neutrophils and macrophages stained for N-acetyl-beta-glucosaminidase in lavage effluents from toluene diisocyanate-exposed rat lungs.

Male Sprague-Dawley rats were exposed to toluene diisocyanate (TDI) concentrations between 0.082 and 1.087 ppm for 4 h, and pulmonary lavage was carried out 24 h after initiation of the exposure. Cells recovered from the lavage effluents of TDI-exposed rat lungs were identified and counted, then pulmonary macrophages (PMs) resulting from cytocentrifuged preparations were examined for N-acetyl-beta-glucosaminidase (NAG) cytochemical staining. Exposure to TDI led to a parallel and concentration-dependent increase in the number of polymorphonuclear neutrophils (PMNs) and the proportion of PMs stained for NAG, suggesting that the same primary event initiates the two cell responses.

Acetylglucosaminidase↗

PubMed1990

Pregnancy-associated changes in renal toxicity of cadmium-metallothionein: possible role of intracellular metallothionein.

Nulliparous female, 10-day and 20-day pregnant rats were injected intraperitoneally with saline or labelled cadmium-metallothionein (109Cd-MTh) at a single dose of 25 or 250 micrograms Cd as cadmium-metallothionein (Cd-MTh)/kg and sacrificed at 24 h. The renal toxicity was manifested by increased 24-h urinary excretion of beta 2-microglobulin (beta 2-m) and the increased number of damaged convoluted proximal tubules at 24 h. The renal excretion of 109Cd and 109Cd content in the maternal liver and kidney and in the foeto-placental unit were determined. The binding of 109Cd to kidney proteins and the level of intracellular metallothionein (MTh) in livers and kidneys were also determined. It was found that the nephrotoxicity of injected Cd-MTh did not differ in nulliparous and 10-day pregnant rats. This result was consistent with the absence of difference in the renal uptake of 109Cd, its binding to kidney proteins and in the content of endogenous MTh in the kidneys between nulliparous and 10-day pregnant rats. In contrast, 20-day pregnant rats exhibited much more nephrotoxicity than nulliparous rats. The most prominent finding in relation to the extreme sensitivity of 20-day pregnant rats was a lower basal level of intracellular MTh in the kidneys and the accumulation of 109Cd in the high molecular weight proteins in the soluble fraction. It is suggested that the decrease of intracellular MTh in the kidneys of 20-day pregnant rats is the reason for the low protection against the renal toxicity of injected Cd-MTh.

Animals↗

PubMed1990

Adrenal-dependent leucopenia after short-term exposure to various airborne irritants in rats.

Leucopenia without any change in differential or red blood cell counts was observed in rats exposed for 4 h to increasing concentrations of the following airborne irritants: acetic acid, benzyl chloride, 1,2-dichlorobenzene, ethyl acetate, ethyl acrylate, formaldehyde, isophorone, mesityl oxide, phenol, styrene, toluene diisocyanate and vinyl toluene. This effect was abolished by adrenalectomy. Vinyl toluene and 1,2-dichlorobenzene induced leucopenia at levels as low as their current occupational standards of 50 ppm. With the exception of 1,2-dichlorobenzene, the tested compounds caused leucopenia only when exposure reached the irritant level. It is discussed that stress associated with the irritative effect of chemicals can confound specific haematological effects.

Adrenal Glands↗

PubMed1990

Diethylbenzene-induced sensorimotor neuropathy in rats.

The commercial isomer mixture of diethylbenzene (DEB mixture), 1,2-diethylbenzene (1,2-DEB), 1,3-diethylbenzene (1,3-DEB) and 1,4-diethylbenzene (1,4-DEB) were administered orally to male Sprague-Dawley rats. The experimental rats and the appropriate controls were examined electrophysiologically for motor and sensory conduction velocities (MCV and SCV), and for the amplitude of the sensory action potential (ASAP) of the tail nerve, at weekly or bi-weekly intervals. Oral administration of DEB mixture (750 or 500 mg kg-1, once daily, 5 days per week for 10 weeks) and 1,2-DEB (100 mg kg-1, once daily, 4 days per week for 8 weeks) produced a time-dependent decrease in MCV, SCV and ASAP. Rats treated with DEB mixture and 1,2-DEB exhibited a blue discoloration of tissues and urine. No changes in MCV, SCV and ASAP developed in rats administered orally with 1,3-DEP and 1,4-DEB (500 mg kg-1, once daily, 5 days per week for 8 weeks). The results indicate that 1,2-DEB is the isomer responsible for neurotoxicity and suggest that a metabolic pathway giving rise to coloured compounds is involved in the neurotoxicity of DEB.

Animals↗

PubMed1990

Decrease in the rat bronchial acetylcholinesterase activity after toluene diisocyanate inhalation.

Acetylcholinesterase (AChE) activity was measured in bronchial tissue homogenate and blood from rats subjected to single and repeated 4-h daily inhalation exposure to toluene diisocyanate (TDI) or control atmospheres. A single 4-h exposure to TDI in the concentration range of 0.7-4.3 ppm did not decrease AChE activity in bronchial tissue but a 4-h exposure to 0.6 ppm TDI, or greater, for two consecutive days did reduce this activity (19% to 33% of the controls). Increasing the level of exposure to TDI for two consecutive days from 0.6 to 4.0 ppm and extending the length of exposure to 1.2 ppm TDI from 2 to 4, 9 or 14 days produced no further decrease in bronchial ACHE activity. Throughout these experiments, blood AChE activity remained unchanged. In rats exposed to 0.3 or 1 ppm TDI for 3 weeks, staining of the bronchial smooth muscle for AChE was reduced (36% of the controls) after exposure to 1 ppm TDI. These results support, for the first time, in vivo and localized anti-AChE activity by TDI.

Acetylcholinesterase↗

PubMed1990

Role of gamma-glutamyltranspeptidase and beta-lyase in the nephrotoxicity of hexachloro-1,3-butadiene and methyl mercury in mice.

Male Swiss OF1 mice received a single oral dose of either 80 mg/kg hexachloro-1,3-butadiene (HCBD) or 80 mg/kg methyl mercury (MeHg). Examination of cryostat kidney sections stained for alkaline phosphatase (APP) revealed damage to about 50% of the proximal tubules after 8 h. Pretreatment with the gamma-glutamyltranspeptidase (gamma-GT) inactivator AT-125 (Acivin, 50 mg/kg i.p., plus 50 mg/kg p.o., reduced the number of damaged tubules by 59 and 58% in mice treated with HCBD and MeHg, respectively. Pretreatment with the two beta-lyase inhibitors, amino-oxyacetic acid (AOAA, 3 x 100 mg/kg p.o.) and DL-propargylglycine (PPG, 300 mg/kg i.p. plus 300 mg/kg p.o.), reduced HCBD nephrotoxicity by 46 and 59%, respectively, but did not protect against MeHg nephrotoxicity. The results support a role for gamma-GT and beta-lyase in the mouse renal toxicity of HCBD and implicate gamma-GT but not beta-lyase in MeHg-induced nephrotoxicity in mice.

Acute Kidney Injury↗

PubMed1990

Assessment of urinary rat beta 2-microglobulin by enzyme immunoassay.

An enzyme immunoassay (EIA) was developed using unlabelled and peroxidase-labelled rabbit antibodies to assess urinary rat beta 2-microglobulin (beta 2-m) excretion. It consisted in the adsorption of rabbit anti-rat beta 2-m immunoglobulin to a polystyrene surface, the addition of beta 2-m samples or standard and the addition of peroxidase-labelled rabbit anti-rat beta 2-m immunoglobulin. After addition of hydrogen peroxide and o-phenylenediamine, the enzyme activity of the solid phase was measured photometrically at 490 nm. Analytical recovery of pure beta 2-m in urine was 102%. From determinations made on normal female and male rats, the ranges of 24-h urine beta 2-m individually excreted were found to be 0.84-4.77 and 3.7-17.3 micrograms, respectively. The means +/- SEM were 2.49 +/- 0.17 and 10.2 +/- 0.55 micrograms. EIA was of value in evidencing the tubule-damaging properties of sodium chromate and hexachloro-1,3-butadiene in rats.

Animals↗

PubMed1989

Nasal irritation and pulmonary toxicity of aliphatic amines in mice.

The expiratory bradypnoea indicative of upper airway irritation in mice was evaluated during a 15-min oronasal exposure to increasing concentrations of twenty aliphatic amines. The airborne concentration resulting in a 50% decrease in the respiratory rate of mice (RD50) was calculated for each test compound. Moreover, eight out of the twenty amines were tested for pulmonary toxicity in mice and for the effects of a 120-min exposure on the respiratory rates of non-anaesthetized, tracheally cannulated mice (RD50TC). Both allylamine and diallylamine showed RD50 values of 9 ppm and 4 ppm, respectively, while the RD50 values associated with exposure to saturated amines ranged from 50 to 200 ppm. Among the eight amines tested for both upper airway irritation and pulmonary toxicity, diisopropylamine and di-n-butylamine showed a RD50TC/RD50 ratio of less than 1, indicating that the respiratory toxicity induced by these two amines would be related primarily to pulmonary effects. On the basis of prior predictions proposed for upper airway irritants, tentative standards are given for ten amines. Moreover, it is suggested that the basis of standards for industrial exposure to diisopropylamine and di-n-butylamine should be specified.

Amines↗

PubMed1989

The effects of maternally inhaled formaldehyde on embryonal and foetal development in rats.

Sprague-Dawley rats were exposed to 0, 5, 10, 20 or 40 ppm formaldehyde for 6 hr/day from day 6 to 20 of gestation. On day 21 of gestation the rats were killed for evaluation of maternal reproductive and foetal parameters. No effect on embryonic or foetal lethality, nor significant alterations in the external, visceral or skeletal appearance of the foetuses were noted in any of the exposed groups. Significant concentration-related reduction of foetal body weight occurred at 20 and 40 ppm, and at 40 ppm foetal body weights were 20% less than those of the controls. Maternal toxicity, indicated by significant reduction in body weight and absolute weight gain, was observed at 40 ppm. The results of this study show that formaldehyde is slightly foetotoxic at 20 ppm. Neither embryolethal nor teratogenic effects were observed following inhalation exposure at levels up to 40 ppm.

Animals↗

PubMed1989

Effects of prenatal methylmercury exposure on urinary proximal tubular enzyme excretion in neonatal rats.

The basal developmental pattern of excretion of 3 proximal tubular enzymes was determined in 8-h urinary specimens from neonatal rats. Gammaglutamyltransferase (GGT), alkaline phosphatase (ALP), and N-acetyl-beta-glucosaminidase (NAG) activities were measured at 3, 6, 9 and 12 days after birth. Subsequently, methylmercury chloride (CH3HgCl), known to induce foetotoxic changes in the proximal tubule was administered on days 8, 10 and 12 of gestation at 3 or 6 mg/kg and its effects on the enzyme activities were examined. Dose-related increases in the 3 enzyme activities occurred at dose levels that produced no maternal or postnatal toxicity, nor overt morphological malformation of the kidney. The peak of enzyme activities averaged about 200% and 130% of the control values for GGT, ALP, and NAG respectively, and occurred on days 3 and 6 in the treated groups. Urinary enzyme activities returned to the control levels from days 6 to 12. Our data point to the possibility of detecting CH3HgCl-induced prenatal effect on the kidney by measuring the 8-h urinary excretion of enzymes by rats in the early postnatal period.

Acetylglucosaminidase↗

PubMed1989

Acetone compared to other ketones in modifying the hepatotoxicity of inhaled 1,2-dichlorobenzene in rats and mice.

The ability of acetone and 3 other ketone vapours to influence the hepatotoxicity of inhaled 1,2-dichlorobenzene (DCB) was examined in rats and mice. Methylethylketone, methylisobutylketone or cyclohexanone increased liver cytochrome P-450 content and glutathione-S-transferase (GST) activity, but did not affect serum glutamate dehydrogenase (GLDH) activity in rats. Pre-exposure to these ketones enhanced DCB-induced increase in serum GLDH activity (8-63-fold), while the increases in cytochrome P-450 content (33-86%) and GST activity (42-64%) were identical to those resulting from exposure to ketones alone. Each of the 3 levels of exposure to acetone elicited cytochrome P-450 and GST responses comparable with those caused by the other ketones. In spite of that, acetone pre-exposure potentiated (4785 ppm), reduced (10670 ppm) or suppressed (14790 ppm) DCB-induced liver toxicity. In mice, the 3 ketones mentioned above interacted with DCB on centrolobular liver glucose-6-phosphatase (G-6-Pase) while acetone pre-exposure elicited an interactive G-6-Pase response in the mediolobular area alone, suggesting topographic change.

Acetone↗

PubMed1989

Inhalation teratology study on hexachloro-1,3-butadiene in rats.

Pregnant rats were exposed to 0, 2, 5, 10 or 15 ppm hexachloro-1,3-butadiene (HCBD) 6 h/d during days 6-20 of gestation. Maternal reproduction and fetal parameters were evaluated on gestational day 21. A significant reduction in maternal weight gain and in fetal body weight occurred at 15 ppm. The incidences of external, visceral and skeletal alterations were not significantly increased in any of the HCBD-exposed groups. It is concluded that exposure of pregnant rats to HCBD by inhalation of concentrations high enough to cause maternal and slight fetal toxicity is neither embryotoxic nor teratogenic.

Animals↗

PubMed1989

Effects of inhalation exposure to carbon disulfide and its combination with hydrogen sulfide on embryonal and fetal development in rats.

Pregnant rats were exposed to 0, 100, 200, 400 or 800 ppm of carbon disulfide (CS2), 100 ppm of hydrogen sulfide (H2S) alone or in combination with 400 and 800 ppm CS2, 6 h/d during days 6-20 of gestation. Maternal reproduction and fetal parameters were evaluated on gestational day 21. Treatment with 100 or 200 ppm CS2 or with 100 ppm H2S caused no maternal toxicity or adverse effects on the developing embryo or fetus. Exposure to 400 or 800 ppm CS2 resulted in a low incidence of club foot and in a significant reduction of maternal weight gain. Significant increases in unossified sternebrae occurred at 800 ppm CS2 and reduction of fetal body weight at 400 and 800 ppm CS2. The latter effect was enhanced by combination with 100 ppm H2S. These results support the conclusion that, at levels of exposure associated with maternal toxicity, CS2 leads to an increase in incidence of club foot and to fetal toxicity which is enhanced by simultaneous exposure to H2S.

Administration, Inhalation↗

PubMed1988

A sensitive cadmium-affinity assay for the determination of thionein in urine.

A sensitive cadmium-affinity assay was developed for measurement of urinary thionein (Th) level. Acidification with HCl (2.5 M) was used to remove metal ions from purified urinary metallothionein (MTh), adsorbed on activated polystyrene tubes. It was found that the amount of 109Cd bound to standard Th (rabbit Th) was proportional to that of Th in the concentration range of 20-6000 ng/ml. The method exhibited a sensitivity below 20 ng/ml and a precision of about 5%. The results of the Cd-affinity assay were unaffected by dilution of, or addition of standard Th to urine samples. Under the latter circumstances, the Cd-affinity assay was performed with a mean analytical recovery of 100.3 +/- 4%. Addition of Cd, Zn, Hg and Cu (50 micrograms each) or glutathione and cysteine (0.1 mmol) to urine specimens (1 ml) did not interfere with the determination of Th. The mean values of urinary Th in healthy subjects were 200 +/- 53 micrograms/g creatinine (n = 9) and 256 +/- 97 micrograms/g creatinine (n = 8) for men and women respectively. The mean daily excretions of Th by non-fasting female and male healthy adult rats were 9.95 +/- 2.7 micrograms (n = 10) and 18.2 +/- 3.9 micrograms, respectively. The Cd-affinity assay succeeded in indicating Cd exposure and/or development of Cd toxicity in rats.

Animals↗

PubMed1988

Toluene diisocyanate-induced airway hyperresponsiveness to intravenous acetylcholine: a study on single and repeated exposure in guinea-pigs.

We examined the changes in airway responsiveness to increasing doses of intravenous acetylcholine (ACh), in groups of 10 anaesthetized and tracheotomized spontaneously breathing guinea-pigs, 20 h after inhalation exposure to toluene diisocyanate (TDI). TDI exposure consisted of a single 4-h exposure to 1.2 ppm, intermittent exposures to 1.078 and 0.126 ppm for 4 h daily for 2 consecutive days, and continuous exposures to 0.118 ppm for 48 h or to 0.045 and 0.023 ppm for 1 week. Airway resistance (Raw) of the corresponding control groups, which inhaled clean filtered air, was used as baseline, and was similar for air and TDI groups. All the patterns of exposure, except exposure to 0.126 ppm TDI for 4 h daily for 2 consecutive days, significantly reduced by 28-60% the dose of ACh calculated to cause a 200% increase in Raw (ED200). The results indicate that TDI-induced airway hyperresponsiveness to ACh in guinea-pigs can occur at a level of exposure as low as 0.023 ppm for 1 week, and is consistent with the hypothesis of a cumulative effect.

Acetylcholine↗

PubMed1986

Assessment of tail nerve function in rats chronically exposed to vinyltoluene.

In male Sprague-Dawley rats, motor and sensory conduction velocities (MNCV and SNCV) of the tail nerve decreased significantly as a result of oral administration of 400 and 200 mg/kg of 2,5 hexanedione (2,5-HD) once daily, 5 days a week for up to 7 and 15 weeks, respectively; and of whole-body exposure to 300 ppm of vinyltoluene for 6 h daily, 5 days a week for up to 21 weeks. Exposure to 100 ppm of vinyltoluene did not cause any significant impairment of tail nerve function throughout the 21-week exposure period. Significant changes in MNCV and SNCV were consistently observed from weeks 4 and 2, respectively, in 2,5-HD-treated rats. Changes resulting from exposure to 300 ppm of vinyltoluene were reported intermittently from week 15. Significant linear relationships were established between the length of treatment with 2,5-HD, length of exposure to 300 ppm of vinyltoluene, and the extent of impairment of tail nerve function. Structural damage to the sciatic nerves was only seen in 2,5-HD-treated rats. It is concluded that vinyltoluene can be regarded as an airborne chemical which leads to the development of a borderline experimental neuropathy at a level of 300 ppm.

Action Potentials↗

PubMed1984

Testing natural indigo for genotoxicity.

The genotoxicity of indigo has been assessed by two short-term tests. The mutagenicity of natural indigo was compared with that of synthetic indigo. Both chemicals were tested using the standard procedure of the Salmonella/microsome mutagenicity test as described by Ames. The substance exhibits mutagenicity towards strains TA1538 and TA98 when S9 preparations of rat liver induced with Aroclor 1254 were present in the medium. The clastogenic potential was evaluated by the micronucleus test in the bone marrow of male mice. The test compound was administered twice with an interval of 24 h, the animals were killed 30 h and 54 h after the first treatment. When the test compound was given by oral gavage as two equal dosages of 0.1, 1 and 1.2 g/kg body weight, no statistically significant increase in the percentage of polychromatic erythrocytes with micronuclei was observed for any group treated with natural indigo.

Animals↗

PubMedDate not supplied

Role of cysteine conjugation in vinylidene chloride-induced nephrotoxicity and hepatotoxicity in fasted rats.

Pretreatment of fasted rats with aminooxyacetic acid (AOAA, 0.25 mmol kg-1, i.p.), methimazole (MTZ, 0.35 mmol kg-1, i.p.) and acivicin (AT-125, 56 mumol kg-1, i.p.) 30 min prior to a 4-h inhalation exposure to 180-200 ppm or 150-180 ppm vinylidene chloride (VDC) was used to study the role of cysteine beta-lyase, cysteine conjugate S-oxidase and gamma-glutamyltranspeptidase (gamma-GT) in VDC-induced liver and kidney toxicity. Pretreatment with AOAA reduced by 65-95% those increases in serum alanine aminotransferase (ALAT), glutamate dehydrogenase (GLDH) and sorbitol dehydrogenase (SDH) caused by exposure to 180-200 ppm VDC. This pretreatment also prevented VDC-induced increases in aspartate aminotransferase (ASAT) and N-acetyl-beta-d-glucosaminidase (NAG) activities and in the concentration of beta 2-microglobulin (beta 2-m) in 24-h urine samples. There was only a slight potentiation of VDC-induced liver and renal toxicities by MTZ given before exposure to 180-200 ppm VDC, but potentiation became significant (40-80%) when MTZ was administered before a slightly lower level of exposure (150-180 ppm). Pretreatment with AT-125 did not significantly change the liver and renal effects of exposure to 180-200 ppm VDC. These results suggest that the formation of a cysteine conjugate may be involved in the renal and liver toxicity of VDC in fasted rats.

Animals↗