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Results for “Tetraethyl Lead”

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At least 19 recordsLinked to original sources
PubMed1984

Changes in endogenous monoamine levels of rat brain induced by tetraethyl lead.

Tetraethyl lead (TEL) was given to adult rats at single doses of 30, 90, or 180 mumol/kg in soya bean oil by gavage. 24 h later the concentrations of three monoamines were measured in the hypothalamus, occipital cortex and corpus striatum. Cortical noradrenaline (NA) decreased by 17-31% with increasing TEL dose and hypothalamic NA by 32% at the highest TEL dose. After administration of the cumulative total doses of 3, 10, or 30 mumol/kg TEL over 3 weeks, the corpus striatum was most severely affected: levels of NA and dopamine (DA) decreased by 12-22% while that of 5-HT increased by 11% at the highest TEL dose. The changes of 5-HT levels were opposite to those of catecholamines in other brain regions as well suggesting a reciprocal interaction between serotonergic and catecholaminergic neurones.

Animals↗
PubMed1985

[Effect of lead and tetraethyl lead poisoning on the microcirculatory bed of the conjunctiva of the eye].

The ultrastructure of the bulbar conjunctiva bioptates have been studied in 12 persons suffering from lead intoxication (saturnism), 2-from tetraethyl-lead (TEL) intoxication and 3-are practically healthy persons; they make the control group. In all the patients manifested disturbances in the microcirculatory bed of the bulbar conjunctiva are revealed, the general character being identical at saturnism and TEL-intoxication. The main changes are observed in the wall of the blood microvessels: destruction of the endothelial lining up to revealing the basal membrane with adhesion of the blood formed elements and their diapedesis. This results in disorders of vascular permeability, in edema of the perivascular space and in appearance of cells and cellular detritus in it. An essential role in morphogenesis of the vascular disturbances produced by intoxication play certain rheological imparements: sludge-syndrome and microthrombosis. They produce certain distrophic changes.

Adult↗
PubMed2002

Differential ototoxicities induced by lead acetate and tetraethyl lead.

Lead poisoning disrupts many biological structures and functions, including those of the auditory system. This study examined the ototoxic effects of lead acetate (LA) and tetraethyl lead (TEL) of equal lead content on cochlear function and the ability of alpha-phenyl-tert-butyl-nitrone (PBN) to attenuate such effects. Baseline 1.0 microV cochlear microphonic (CM) and compound action potential (CAP) responses were recorded and animals administered either PBN (100 mg/kg, i.p.) or an equal volume of 0.9% saline, followed by an i.p. injection of LA (50 mg/kg) in an ethanol vehicle, TEL (42.7 mg/kg) in a corn oil vehicle, corn oil or ethanol vehicle alone. Two hours after administration, post-exposure CM and CAP responses were recorded. CAP threshold shifts in the saline-LA group were elevated by 5-10 dB at mid to high frequencies relative to controls (20-24 kHz, P<0.05). Mean CAP threshold shifts in the saline-TEL were significantly greater than those of both control groups at all tested frequencies except 2 kHz (P<0.001). However, threshold shifts in the group receiving PBN prior to TEL were significantly smaller than shifts in the group receiving saline prior to TEL (P<0.01). These data suggest that TEL is more ototoxic than is LA and that free radicals partially mediate TEL-induced CAP disruption.

Acoustic Stimulation↗
PubMed1985

Metabolism of tetraorganolead compounds by rat-liver microsomal mono-oxygenase. III. Enzymic dealkylation of tetramethyl lead compared with tetraethyl lead.

The enzymic transformation of tetramethyl lead (PbMe4) to the trimethyl lead cation is very rapid with sp. activities of 40-50 nmol/min per mg protein. The reaction has an apparent Km of 1.28 X 10(-5) M. PbMe4 binds to cytochrome P-450 with a type 1 difference spectrum, Ks is 6.65 X 10(-6) M. Comparison of the data with results previously obtained for lead tetraethyl (PbEt4) shows that the 20 times higher metabolic rates observed with PbMe4 are related to an intrinsic higher O2 activation as well as to a more effective O2 utilization by that substrate.

Animals↗
PubMed1983

[Biliary excretion of diethyl lead after administration of tetraethyl lead in rabbits].

In order to investigate into whether the large amount of inorganic lead excreted into the feces following intravenous injection of tetraethyl lead to rabbits is derived from the diethyl lead excreted into the bile, we administered 12 mg/kg of tetraethyl lead to rabbits which had been fistulated into the bile duct for taking the bile out of the body. The total lead excreted into the bile during the first 24 hours after the injection of tetraethyl lead amounted to about 8% of the injected amount of lead (with 97% of the excreted lead made up of diethyl lead). The amount of total lead contained in the cecal contents of unfistulated rabbits 24 hours after the injection of tetraethyl lead was equivalent to about 12% of the injected amount of lead (with inorganic lead accounting for about 90% of the excreted lead), but the counterpart of the fistulated rabbits was equivalent only to about 0.6%. The amount of lead excreted into the bile, when measured in terms of the total lead content of the liver, was slightly less in the fistulated rabbits than in the unfistulated ones. These findings indicated that the amount of total lead excreted into the bile of the fistulated rabbits was almost the same as that contained in the cecal contents of unfistulated rabbits, and that the major portion of the lead contained in the cecal contents or feces was composed of inorganic lead. From these results, we came to the conclusion that the large amount of inorganic lead detected in the feces after the injection of tetraethyl lead is derived from the diethyl lead excreted into the bile.

Animals↗
PubMed1997

Leaded gasoline abuse: the role of tetraethyl lead.

Volatile substance abuse is practised worldwide however reports of the abuse of leaded gasoline have been limited to northern Canada, southwestern USA and the Australian Outback. Chronic, heavy abuse of leaded gasoline results in an encephalopathy, cerebellar and corticospinal symptoms and signs, dementia, mental status alterations, and persistent organic psychosis. Much of this is due to the hydrocarbons of gasoline while the tetraethyl lead contributes to the altered mental status and is responsible for the persistent psychosis. Lead chelation therapy is not rational and has not been shown to benefit these patients.

Administration, Inhalation↗
PubMed1994

Early health effects and biological monitoring in persons occupationally exposed to tetraethyl lead.

Dependent on the level of occupational exposure to tetraethyl lead, the occurrence of early signs of toxicity and the urinary excretion of triethyl lead, diethyl lead and total lead compounds were investigated. This was done in the following cohorts in the province of Hubei, China: 277 workers at gasoline depots exposed to gasoline, 36 traffic policemen exposed to automobile exhaust and 342 public office workers (virtually non-exposed controls). Mean external tetraethyl lead exposure concentrations were 84.8 micrograms/m3 (as Pb) for the gasoline depot workers, 5.2 micrograms/m3 for traffic police and 1.1 microgram/m3 for the controls. No significant subclinical indications of organic lead toxicity were found in the group of traffic policemen compared with the controls. In the cohort of gasoline workers, however, there was a statistical increase (vs controls) in the frequency of appearance of tremor and of sinus bradycardia. When the cohort of gasoline workers was divided into subgroups of different ranges of exposure, dose-dependence was noted. In general, the urinary excretion of triethyl lead was very low compared to that of diethyl lead, which appears to be a sensitive and specific indicator of exposure to tetraethyl lead; total lead excretion did not correlate well with actual external tetraethyl lead exposure. On the basis of these data it seems that current occupational exposure limits for tetraethyl lead are inadequate and need to be revised. In addition, a biological limit, based on urinary diethyl lead excretion, may be proposed.

Adult↗
PubMed1983

Metabolism of tetraorganolead compounds by rat-liver microsomal mono-oxygenase. II. Enzymic dealkylation of tetraethyl lead.

The biological degradation of tetraethyl lead to the triethyl lead cation by rat-liver microsomes from untreated, phenobarbital-pretreated and methylcholanthrene-pretreated rats has been studied; NADPH and oxygen are essential. The reaction is inhibited by CO and can be reactivated in the presence of O2 by irradiation with u.v. light with a max. at 450 nm. Substrate binding to cytochrome P-450 is of type 1. Apparent Km values for triethyl lead formation in microsomes were determined. The highest activities (i.e. about 2 nmol triethyl lead per nmol cytochrome P-450 per min) and the lowest apparent Km values (i.e. 7 X 10(-6) M) are found in microsomes from methylcholanthrene-pretreated rats. In microsomes from control and phenobarbital-pretreated rats Ks values from substrate-binding studies (about 2 X 10(-6) M) are one order of magnitude lower than the apparent Km values (3 X 10(-5) M).

Animals↗