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NTP Toxicology and Carcinogenesis Studies of Commercial Grade 2,4 (80%)- and 2,6 (20%)- Toluene Diisocyanate (CAS No. 26471-62-5) in F344/N Rats and B6C3F1 Mice (Gavage Studies).
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Toluene diisocyanate (TDI) is commercially produced as an approximate 80:20 mixture of the 2,4- and 2,6-isomers. In 1980, 580,000 pounds of this chemical were produced in the United States, primarily for use in the manufacture of flexible polyurethane foams. These foam elastomers are found in
Toluene exposure during brain growth spurt and adolescence produces differential effects on N-methyl-D-aspartate receptor-mediated currents in rat hippocampus.
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Toluene, an industrial organic solvent, is voluntarily inhaled as drug of abuse. Because inhibition of N-methyl-d-aspartate (NMDA) receptors is one of the possible mechanisms underlying developmental neurotoxicity of toluene, the purpose of the present study was to examine the effects of toluene
The role of physical activity and feeding schedule on the kinetics of inhaled and oral toluene in rats.
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Published studies of the kinetics of toluene in rats have shown that its concentration in the blood rises during inhalation and falls after exposure stops; a similar uptake profile and longer persistence in blood typify the kinetics after oral exposure. Because rats in these studies are typically
Dermal uptake and excretion of 14C-toluene diisocyante (TDI) and 14C-methylene diphenyl diisocyanate (MDI) in male rats. Clinical signs and histopathology following dermal exposure of male rats to TDI.
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Polyurethanes (PU) are polymers made with diisocyanates such as MDI (4,4'-methylene diphenyl diisocyanate) and TDI (2,4-toluene diisocyanate and 2,6-toluene diisocyanate). Investigations have been undertaken with MDI and TDI to assess dermal uptake and resulting systemic exposure. Absorption,
Toluene diisocyanate: an assessment of carcinogenic risk following oral and inhalation exposure.
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Although respiratory sensitization and pulmonary irritation have been the subject of particular studies with toluene diisocyanate (TDI), in recent years the potential carcinogenicity of TDI has been a reason for concern and speculation. This has arisen from the expectation that following exposure to
Toluene effects on the motor activity of adolescent, young-adult, middle-age and senescent male Brown Norway rats.
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Life stage is an important risk factor for toxicity. Children and aging adults, for example, are more susceptible to certain chemicals than are young adults. In comparison to children, relatively little is known about susceptibility in older adults. Additionally, few studies have compared toxicant
Neurobehavioral development of rats exposed to toluene through maternal milk.
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Organic solvents have been detected in the milk of workers in the rubber industry exposed during gestation to a mixture of solvents at average concentrations lower than the currently accepted occupational limit of exposure (100 ppm). The objective of the present study was to determine if exposure of
Adolescent toluene exposure produces enduring social and cognitive deficits in mice: an animal model of solvent-induced psychosis.
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OBJECTIVE
Abuse of toluene-containing volatile solvents by adolescents is a significant public health problem. The present study characterized the long-term behavioural and neurochemical consequences of toluene exposure during adolescence.
METHODS
Male NMRI mice received one injection per day of
Toluene exposure during the brain growth spurt reduced behavioral responses to nicotine in young adult rats: a potential role for nicotinic acetylcholine receptors in fetal solvent syndrome.
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Toluene, an industrial organic solvent, is voluntarily inhaled as drug of abuse. Toluene has been shown to inhibit the nicotinic acetylcholine receptors. Nicotinic receptors play an important role in brain development during brain growth spurt and early adolescence. The long-term effects of neonatal
Involvement of NO/cGMP pathway in toluene-induced locomotor hyperactivity in female rats.
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BACKGROUND
Nitric oxide (NO) is implicated in the acute locomotor activating effects of some addictive drugs such as amphetamine, caffeine, and PCP, but has not been investigated in the case of toluene.
OBJECTIVE
This study determined the contribution of the NO-cyclic GMP (cGMP) pathway to locomotor
NTP Toxicology and Carcinogenesis Studies of Toluene (CAS No.108-88-3) in F344/N Rats and B6C3F1 Mice (Inhalation Studies).
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Toluene is used to back-blend gasoline, as a chemical intermediate, and as a solvent; 920 million gallons were produced in the United States in 1988. Toxicology studies were conducted by administering toluene (greater than 99% pure) in corn oil by gavage to groups of F344/N rats and B6C3F1 mice of
Protective effects of caffeic acid phenethyl ester and thymoquinone on toluene induced liver toxicity.
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Toluene is an organic solvent that is toxic to humans. Caffeic acid phenethyl ester (CAPE) and thymoquinone (TQ) exhibit antioxidant and antitoxic effects. We investigated the protective effects of CAPE and TQ on toluene induced hepatotoxicity. Wistar albino rats were divided into seven groups of
Ototoxicity of toluene in rats.
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Toluene is a major industrial solvent and substance of abuse which is ototoxic in rats as shown by both behavioral testing and measurement of brainstem auditory evoked response (BAER) thresholds. The objective of this investigation was to examine the morphological (hair cell loss) and functional
The carcinogenic activity of commercial grade toluene diisocyanate in rats and mice in relation to the metabolism of the 2,4- and 2,6-TDI isomers.
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Groups of 50 F344/N rats of each sex and 50 B6C3F1 mice of each sex were gavaged with corn oil or a mixture of toluene diisocyanate (TDI) in corn oil for 5 days per week for 105 or 106 weeks. Female rats and mice were given doses of 60 or 120 mg/kg body weight, while male rats received 30 or 60
Pulmonary phospholipid changes induced by butylated hydroxy toluene, an antioxidant, in rats.
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Butylated hydroxy toluene (BHT), 800 mg/kg body weight, dissolved in corn oil and administered (ip) in a single injection to male rats, damaged the lung as indicated by an increase in lavage ACE, protein and LDH and caused a significant increase in phospholipid, particularly, phosphatidyl choline
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