Biomedical subjects

S Laham

Publications and source records attributed to S Laham.

At least 19 recordsLinked to original sources

PubMed1991

Subacute inhalation toxicity of benzaldehyde in the Sprague-Dawley rat.

Benzaldehyde was administered by inhalation to female and male Sprague-Dawley rats for 14 consecutive days (low level: 500 ppm; medium level: 750 ppm; high level: 1000 ppm). Effects of this chemical were investigated during and at the end of the exposure period. Throughout the experiment, significant hypothermia and a reduction of motor activity were observed in all rats exposed to benzaldehyde and were accompanied in high-level rats by a severe impairment of the central nervous system, as evidenced by abnormal gait, tremors, and a positive Straub sign. Histopathologic examination of tissues from exposed rats showed a goblet cell metaplasia that was largely confined to the respiratory epithelium lining the nasal septum in male rats. No other abnormal microscopic changes were observed. A no effect level was not observed in these studies.

Administration, Inhalation↗

PubMed1987

Biological conversion of benzaldehyde to benzylmercapturic acid in the Sprague-Dawley rat.

The metabolism of benzaldehyde was investigated in Sprague-Dawley rats. After repeated oral administration of this compound (0.4-1.0 g/kg) for 13 consecutive days, urine was collected and analyzed for the presence of metabolites. The acidification of the pooled urine samples (pH:2.0) with 6 N H2SO4 was followed by ethyl acetate extraction, evaporation of the extract and methylation with diazomethane. Identification of the metabolite by comparison with a synthetic sample of benzylmercapturic acid (BENZM) was conducted by gas chromatography. Mass spectrometry examination of this metabolite revealed the following peaks characteristic of benzylmercapturic acid: m/z (%), 91(100), 176(27), 208(23), 43(20), 88(13), 117(10), 134(9), M+ 267(2). Monitoring of urines from both female and male rats showed a dose-related increase of benzylmercapturic acid which was found to be a reliable indicator of exposure to benzaldehyde.

Acetylcysteine↗

PubMed1985

Dose-response toxicity studies on tributoxyethyl phosphate orally administered to Sprague-Dawley rats.

The response of the peripheral nervous system to various dose levels of tributoxyethyl phosphate (TBOP) was investigated in Sprague-Dawley rats. Groups of randomized female and male rats (10 rats/gender/dose level) were administered a single oral dose of TBOP (1.0 to 3.2 g/kg for females; 1.0 to 9.0 g/kg for males). Physiological parameters were measured in surviving rats three weeks following TBOP administration. A significant reduction (p less than 0.05) in caudal nerve conduction velocity (NCV) was observed in both female and male rats. Light and electron microscopic examination of sciatic nerve sections showed degenerative changes in both myelinated and unmyelinated fibers of female (2.0 g/kg) and male (6.8 g/kg) groups. Advanced degeneration was observed only in the highest dose level of both genders (3.2 g/kg for females; 8.0 and 9.0 g/kg for males). Although similar morphological changes were observed in both genders, females were more susceptible than males to the toxic effects of this compound.

Administration, Oral↗

PubMed1984

Induction of electrophysiological and morphological changes in Sprague-Dawley rats fed tributoxyethyl phosphate.

The effects of a widely used trialkyl phosphate (TP), tributoxyethyl phosphate (TBOP), on the peripheral nervous system of Sprague-dawley (SD) rats were investigated. Male and female SD rats were administered this chemical by gavage over a period of 18 weeks (low dose: 0.25 ml kg-1; high dose: 0.50 ml kg-1). Electrophysiological changes observed at 18 weeks in all test animals included a significant reduction (P less than 0.001) in nerve conduction velocity and an important increase (P less than 0.001) of both relative (RRP) and absolute refractory period (ARP). Light and electron microscopic examination of sciatic nerve from all test animals showed the presence of degenerating myelin sheaths accompanied by axonal swelling. An advanced stage of degeneration was indicated by the presence of lamellated electron dense inclusions in unmyelinated nerve fibres.

Animals↗

PubMed1984

Subacute oral toxicity of tri-n-butyl phosphate in the Sprague-Dawley rat.

Tri-n-butyl phosphate was administered by gavage to male and female Sprague-Dawley rats for 14 consecutive days (low dose: 0.14 ml kg-1; high dose: 0.42 ml kg-1). Effects of this chemical were investigated at the end of the feeding period. Histopathological examination of the testes (high-dose group) showed the presence of microscopic degenerative changes in the seminiferous tubules. No other abnormal microscopic changes were observed.

Administration, Oral↗

PubMed1983

Biological conversion of N-phenyl-2-naphthylamine to 2-naphthylamine in the Sprague-Dawley rat.

The metabolism of a widely used plastic and rubber antioxidant, N-Phenyl-2-Naphthylamine, was investigated in Sprague-Dawley rats. After repeated oral administration of this compound, urine and feces were collected for several days and analyzed for the presence of metabolites. Identification techniques included a preliminary clean-up followed by thin-layer chromatography of amines and gas chromatography-mass spectrometry of their hexafluoroacyl derivatives (HFBA). The compounds identified in both urine and feces were characterized as N-Phenyl-2-Naphthylamine (PBNA) and 2-Naphthylamine (BNA). Data obtained on urinary excretion of BNA seem to indicate that repeated administration of PBNA enhances its own metabolism.

2-Naphthylamine↗

PubMed1983

Effects of tri-n-butyl phosphate on the peripheral nervous system of the Sprague-Dawley rat.

Tri-n-butyl phosphate, a widely used plasticizer and solvent, was orally administered to male and female Sprague-Dawley rats for 14 consecutive days (low dose: 0.28 mL/kg; high dose: 0.42 mL/kg). Effects of this industrial chemical were investigated on the peripheral nervous system of these animals. A significant (P less than 0.05) reduction in conduction velocity of caudal nerve was observed in high dose male rats. Electron microscopic examination of sciatic nerve showed morphological changes such as retraction of Schwann cell processes surrounding unmyelinated fibres in both sexes of high dose groups.

Animals↗

PubMed1980

Acidic metabolites of pseudocumene in rabbit urine.

In order to identify biological indicators of exposure to trimethylbenzenes, the metabolism of pseudocumene (1,2,4-trimethylbenzene) was investigated in rabbits. After oral administration of this compound, urine was collected for several days and analyzed for the presence of acidic metabolites. Isolation techniques included steam-distillation, direct extraction of urine by ethyl acetate, preparative thin-layer and column chromatography of the extract. The metabolites were identified by microanalysis, followed by TLC, gas chromatography-mass spectrometry, infrared and ultraviolet spectroscopy. Two major urinary metabolites were identified namely 2,4-dimethylbenzoic acid and 3,4-dimethylhippuric acid. The presence of these acidic metabolites in urine is a good indication of exposure to pseudocumene.

Animals↗

PubMed1980

Studies on inhalation toxicity of 2-propanol.

Biological effects of a single exposure to moderate or high concentrations of 2-propanol were investigated in Sprague-Dawley rats. Acute toxicity (LC50, t:8 hours) of this widely used solvent was determined and found to be 19000 ppm (17380-20760 ppm) for females and 22500 ppm (19200-26400 ppm) for males. Determination of blood levels of 2-propanol and its metabolite, acetone, was carried out during and after a single 4-hour exposure (Concentration range: 500 to 8000 ppm). The amount of acetone and 2-propanol was directly related to the various air concentrations of alcohol inhaled. Increase of exposure time to 8 hours enhanced considerably the amount of blood acetone which could be determined even 20 hours after exposure. These findings indicate a slow conversion of this alcohol to acetone which can be used as biochemical indicator to exposure. Histopathological examination of rats exposed to high levels of 2-propanol shows typical lesions of chemical pneumonitis and pulmonary edema accompanied by foamy vacuolization of liver cells and severe focal cytoplasmic degradation.

1-Propanol↗

PubMed1978

Continuous monitoring of temperature in laboratory animals during inhalation exposure.

An automatic system was developed to monitor continuously the colonic temperature of laboratory animals during inhalation exposure to toxic chemicals. It includes: an automatic switchbox, a control circuit, a recorder and a digital voltmeter. The system was calibrated for different temperature ranges and used for a year to assess the effects of household solvents on temperature of Sprague-Dawley rats. Reliable monitoring of temperature in 16 rats was carried out in a sequential manner in the manual mode or in the automatic mode for several consecutive days. Very slight changes (.01 - .02 degrees C) in temperature can be measured with this system.

Animals↗

PubMed1978

[Toxicological studies on dichloromethane, a solvent simulating carbon monoxide poisoning (author's transl)].

Acute oral and inhalation toxicity of dichloromethane was investigated in both male and female Sprague-Dawley rats. Oral LD50 was found to be 1.72 ml/kg for males and 1.06 ml/kg for females. LC50 was found to be 18 100 PPM (1 X 6 hours) for both male and female rats. Acute oral intoxication is characterized by severe vascular changes and depression of the central nervous system accompanied by gastro-intestinal hemorrhagy. A similar CNS depression is also found in acute intoxication by inhalation. The nature of the symptoms as well as the sequence of physiological (hypotension, hypothermia) and biochemical events observed (high COHb level, etc.) indicate that the combined action of dichloromethane and its metabolite, carbon monoxide, are responsible for the development of vascular and CNS disturbances and subsequently the sudden death of the animals.

Administration, Oral↗

PubMed1974