Diethyl Lead Research Articles

Structural and Biochemical Characterization of Organotin and Organolead Compounds Binding to the Organomercurial Lyase MerB Provide New Insights into Its Mechanism of Carbon-Metal Bond Cleavage.

The organomercurial lyase MerB has the unique ability to cleave carbon-Hg bonds, and structural studies indicate that three residues in the active site (C96, D99, and C159 in E. coli MerB) play important roles in the carbon-Hg bond cleavage. However, the role of each residue in carbon-metal bond cleavage has not been well-defined. To do so, we have structurally and biophysically characterized the interaction of MerB with a series of organotin and organolead compounds. Studies with two known inhibitors of MerB, dimethyltin (DMT) and triethyltin (TET), reveal that they inhibit by different mechanisms. In both cases the initial binding is to D99, but DMT subsequently binds to C96, which induces a conformation change in the active site. In contrast, diethyltin (DET) is a substrate for MerB and the SnIV product remains bound in the active site in a coordination similar to that of HgII following cleavage of organomercurial compounds. The results with analogous organolead compounds are similar in that trimethyllead (TML) is not cleaved and binds only to D99, whereas diethyllead (DEL) is a substrate and the PbIV product remains bound in the active site. Binding and cleavage is an exothermic reaction, while binding to D99 has negligible net heat flow. These results show that initial binding of organometallic compounds to MerB occurs at D99 followed, in some cases, by cleavage and loss of the organic moieties and binding of the metal ion product to C96, D99, and C159. The N-terminus of MerA is able to extract the bound PbVI but not the bound SnIV. These results suggest that MerB could be utilized for bioremediation applications, but certain organolead and organotin compounds may present an obstacle by inhibiting the enzyme.

Feasibility study for the remediation of groundwater contaminated by organolead compounds

The aim of this research was to assess the effectiveness of chemical oxidation, Advanced Oxidation Processes (AOPs) and adsorption on granular activated carbon (GAC) for the ex situ remediation of a groundwater contaminated by organolead compounds, including tetraethyl lead (TEL), triethyl lead (TREL) and diethyl lead (DEL). The groundwater of concern was collected from the site of a former tetraalkyllead producing company in Trento (Italy), and showed an average total organic lead (TOL) content about 95.1 μg/L (TEL 0.5 μg/L, TREL 86.4 μg/L, DEL 8.3 μg/L). The main target of the study was to find out which method was more effective in reducing the pollutant content. For this purpose, several laboratory tests were performed, including chemical oxidation tests with different reactants (hydrogen peroxide, modified Fenton's reagent, potassium permanganate, activated potassium persulfate, oxygen and combinations of potassium permanganate and modified Fenton's reagent), AOPs with ozone, UV radiation and hydrogen peroxide and filtration on granular activated carbon. A combination of chemical and physical treatments was also tested, with GAC filtration followed by chemical oxidation. According to the results achieved, the treatments which showed the best remediation performances were: chemical oxidation with modified Fenton's reagent, AOPs with hydrogen peroxide and ozone (perozone), AOPs with hydrogen peroxide and UV radiation, and the combined treatment with activated carbon filtration followed by chemical oxidation with perozone. All these treatments showed a 90% TOL removal, with excellent removals of both TEL and TREL, and final DEL concentrations below 5 μg/L.

Effects of the metals on dihydropteridine reductase activity

Metals are the oldest toxins known to human. Particularly, occupational and environmental exposure to aluminium, lead, mercury, cadmium, and manganese cause serious health problems by interaction with biological systems. Cellular targets of these metals are mostly specific biochemical processes (enzymes) and/or membranes of cells and organelles. To prevent and/or reduce the untoward or irreversible toxic effects of the metals by using biomarkers are as important as to know and to understand of their toxicity mechanisms. Dihydropteridine reductase (DHPR), which possessed essential thiol groups at the activite site, plays a crucial role in the maintenance of tetrahydrobiopterin (BH 4). BH 4 is the cofactor in the synthesis and regulation of neurotransmitters. A limited number of the evidences have shown that DHPR may be a target for the metals. Therefore, the present study was designed to assess possible in vitro effects of the commonly exposed metals on the enzyme activity. It was found that aluminium, cadmium, mercury, di-phenyl mercury, lead, diethyl lead, in chloride forms, and manganese, in sulphate form, led to statistically significant decreases in DHPR activity, in a concentration-dependent manner, in vitro.

Determination of the speciation of organolead compounds in airborne particulate matter by gas chromatography–inductively coupled plasma mass spectrometry

The speciation of organolead compounds in airborne particulate matter was determined by gas chromatography–inductively coupled plasma mass spectrometry. The analytes were extracted from the sample using 0.5 M acetic acid in methanol. The ionic organolead compounds were extracted into hexane using diethydithiocarbamate at pH 9 in the presence of EDTA to complex inorganic Pb. Derivatisation of the organolead species was performed with butylmagnesium chloride. Separation and detection of the butylated trimethyllead (TML), dimethyllead (DML), triethyllead (TEL) and diethyllead (DEL) was achieved. Detection limits, as Pb, were 3.2 fg for TML, 2.4 fg for DML, 1.8 fg for TEL and 9 fg for DEL for a 1 μl sample injection. Typical precision of repetitive injections was 1.5–4% using tetraethyllead (TrEL) as internal standard. The method proposed was validated by the determination of TML in the reference material CRM 605 and was applied to the analysis of airborne particulate matter in the atmosphere of the city of Oviedo. DML, DEL and methylethyllead (MEL) were detected at pg m −3 levels.

Biological and chemical degradation of ionic ethyllead compounds in soil

AbstractDegradation rates and formation of organolead metabolites of ionic triethyllead (TREL) and diethyllead (DEL) in nonsterile and autoclaved surface and subsurface soil samples of Arredondo fine sand were determined using 14C‐labeled chemicals. Both [14C]TREL and [14C]DEL in nonsterile and autoclaved soils initially declined rapidly, and both chemicals initially disappeared more rapidly from the surface samples (0 to 15 cm depth) than from the subsurface samples (30 to 45 cm depth), with the exception of the surface sample treated with [14C]DEL. In this soil, [14C]DEL in the autoclaved sample disappeared more rapidly than that in the nonsterile sample. The [14C]DEL was briefly detected in [14C]TREL‐treated soil samples, and [14C]DEL remained in the autoclaved samples longer than in the nonsterile samples. Both [14C]TREL and [14C]DEL in nonsterile surface and subsurface samples were initially mineralized rapidly, and at the end of 31 and 28 d of incubation, 15 to 16% and 18 to 19% of the applied 14C was mineralized, respectively. Mineralization was not observed in autoclaved soil samples. It was concluded that both biological and chemical degradation of TREL and DEL in soil occurred, and chemical degradation was probably the major factor contributing to the disappearance of TREL and DEL in soil. The exact extent of chemical degradation is not known. Chemical and physical properties of soil could be altered significantly by autoclaving, and may account for the increase in chemical degradation rates.

Degradation and metabolism of tetraethyllead in soils

The objective of this study was to determine the disappearance of the leaded gasoline enhancer tetraethyllead (TEL), formation of degradation products, and mass balance in nonsterile and autoclaved Leon and Madison soils. Ethyl-1-14C-labeled TEL was used so that mineralization rates of TEL and mass balance could be determined.14C-TEL in nonsterile and autoclaved surface and subsurface samples of the two soils disappeared rapidly, and ionic ethyllead products, water soluble nonlead organic products and bound residues were rapidly formed. A small fraction (≤7.74%) of14C-TEL in nonsterile soil samples was mineralized to14CO2 in 28 days. Triethyllead (TREL) was the major ionic ethyllead product detected in both nonsterile and autoclaved soils; diethyllead (DEL) was occasionally detected. Recovery of14C from mass balance studies for all nonsterile and autoclaved soil samples after 28 days of incubation was poor, less than 50% of the14C applied. It appears that unknown volatile and/or gaseous organic products were the major degradation products of TEL in soils. Based on the observations of more rapid initial disappearance of14C-TEL, more rapid formation and more rapid disappearance of14C-DEL, and occurrence of14CO2 production in nonsterile soils, it was concluded that both biological and chemical degradation contributed to the degradation of TEL in soils, with chemical degradation being the major factor.

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.

Organic and total lead in selected fresh and canned seafood products

Various fresh and canned seafood products were examined for ionic alkyl lead, tetraalkyl lead and total lead. Dimethyl lead, diethyl lead, trimethyl lead and triethyl lead were extracted with diphenylthiocarbazone (dithizone) at pH 8 and 9 from enzymically hydrolysed samples. Butyl derivatives were formed by Grignard reaction prior to analysis by gas chromatography-atomic absorption spectrometry (GC-AAS). Tetraalkyl lead was extracted from the hydrolysates with hexane. Total lead was determined by reductive coprecipitation with palladium in the presence of ascorbic acid after nitric-perchloric digestion. Many of the samples contained low (less than 0.09-0.7 ng g-1) levels of trimethyl- and dimethyl lead. Triethyl lead was found at similar levels in several samples. Total lead levels were higher with values ranging from less than 5 ng g-1 to 2.9 micrograms g-1. Detection limits for the organolead and total lead methods were 0.07-0.2 and 3-19 ng Pb g-1 respectively.

Subchronic oral toxicity of triethyl lead in the male weanling rat. Clinical, biochemical, hematological, and histopathological effects

This study was designed to ascertain the effects of low level exposure of triethyl lead (3EL) to the male weanling rat. Groups of 20 animals were administered by gavage 3EL at 0.05, 0.10, 0.20, 0.50, and 1.00 mg/kg body wt for 91 days, 5 days/week. Lead acetate (PbHOAC) at 200 mg/kg body wt/day was given as a positive control. Weight gain was reduced in those animals receiving 1.0 3EL. Spleen and kidney weights were elevated in the PbHOAC group. Residues of 3EL and its metabolites diethyl lead (2EL) and lead (Pb) accumulated in a dose-dependent manner in blood, liver, kidney, and brain; 3EL accumulated preferentially in the liver while inorganic lead accumulated in the kidney. Dose-dependent changes occurred in serum calcium which was decreased and in phosphorus which was elevated for all dose groups. Serum cholesterol was elevated in the three highest 3EL groups as was alkaline phosphatase. LDH was lowered in the PbHOAC-treated group but microsomal aniline hydroxylase was elevated. Hematological changes consisted of elevated platelet ccunts in the 1.0 3EL group and decreased mean corpuscular hemoglobin content and mean corpuscular volume in the PbHOAC-treated group. Treatment related histopathological changes were seen in thyroid, liver, kidney, and bone marrow. Based on these data a no observed adverse effect level for 3EL was set at 0.10 mg/kg/body wt.

Subchronic Oral Toxicity of Triethyl Lead in the Male Weanling Rat. Clinical, Biochemical, Hematological, and Histopathological Effects

Subchronic Oral Toxicity of Triethyl Lead in the Male Weanling Rat. Clinical, Biochemical, Hematological, and Histopathological Effects. YAGMINAS, A. P., FRANKLIN, C. A., VILLENEUVE, D. C, GILMAN, A. P., LITTLE, P. B., AND VALLI, V. E. O. (1990). Fundam. Appl. Toxicol. 15, 580–596. This study was designed to ascertain the effects of low level exposure of triethyl lead (3EL) to the male weanling rat. Groups of 20 animals were administered by gavage 3EL at 0.05, 0.10, 0.20, 0.50, and 1.00 mg/kg body wt for 91 days, 5 days/week. Lead acetate (PbHOAC) at 200 mg/kg body wt/day was given as a positive control. Weight gain was reduced in those animals receiving 1.0 3EL. Spleen and kidney weights were elevated in the PbHOAC group. Residues of 3EL and its metabolites diethyl lead (2EL) and lead (Pb) accumulated in a dose-dependent manner in blood, liver, kidney, and brain; 3EL accumulated preferentially in the liver while inorganic lead accumulated in the kidney. Dose-dependent changes occurred in serum calcium which was decreased and in phosphorus which was elevated for all dose groups. Serum cholesterol was elevated in the three highest 3EL groups as was alkaline phosphatase. LDH was lowered in the PbHOAC-treated group but microsomal aniline hydroxylase was elevated. Hematological changes consisted of elevated platelet counts in the 1.0 3EL group and decreased mean corpuscular hemoglobin content and mean corpuscular volume in the PbHOAC-treated group. Treatment related histopathological changes were seen in thyroid, liver, kidney, and bone marrow. Based on these data a no observed adverse effect level for 3EL was at 0.10 mg/kg/body wt.

On the toxic effects of tetraethyl lead and its derivatives on the chrysophyte Poterioochromonas malhamensis: VI. Effects on lorica formation, mitosis, and cytokinesis

Effects of tetraethyl lead (TEL) and derivatives triethyl lead (TriEL), diethyl lead (DiEL), and inorganic lead (Pb) on lorica formation of the unicellular alga Poterioochromonas malhamensis were investigated by light and electron microscopy. Lorica formation is microtubule (MT)--mediated and disturbed by agents interfering with MTs. TEL, largely ineffective as such, inhibited lorica formation of P. malhamensis when the lead compound was illuminated during or before the experiment. TriEL inhibited most; DiEL produced qualitatively effects similar to those of TriEL at about 10 times higher concentrations. Inorganic lead was even less toxic and did not selectively inhibit lorica formation of the algae. Low concentrations of TriEL (5 to 7.5 microM) selectively disturbed lorica formation, causing formation of numerous stalk-less loricae which exhibited gross and ultrastructural alterations like those induced by the antimitotic drug colchicine. The effects of TriEL on mitosis and cytokinesis of P. malhamensis were also investigated. The most sensitive mitotic phase was metaphase, which, however, accumulated only up to 5% after treatment of the cells with toxic concentrations (10 microM) of TriEL for 24 hr (control, 2%). On the other hand, up to 15% telophases (including binucleated cells) and even multinucleated cells with up to eight nuclei per cell were found, indicating that cytokinesis was considerably more effectively disturbed by TriEL than mitosis. In giant multinucleated algae, mitoses normally proceeded synchronously; some asynchronous mitoses were found. Beside normal-looking mitotic spindles in giant algae, multipolar spindles, disoriented spindles, and metaphase-like chromosome arrays completely lacking MTs were observed by electron microscopy. The effects of TriEL on cytokinesis of the algae were largely reversible. Giant cells spontaneously recovered and underwent cytokinesis after transferred into TriEL-free growth medium. Colchicine acted qualitatively identical to TriEL (accumulation of metaphases and telophases: 5 and 19%, respectively), but TriEL was about 600 times more toxic than colchicine. Unlike colchicine, its derivative, colchicine, which is known not to interfere with MTs, remained without any selective inhibitory influence on mitosis and cytokinesis of the algae, although much more toxic than the parent compound. From the inhibitory effects of TriEL and the close qualitative similarities to the effects of colchicine, it is concluded that TriEL selectively interferes with cytoplasmic and mitotic MTs of the algae, thereby causing the observed inhibitory effects on lorica formation, mitosis, and cytokinesis.

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.

On the toxic effects of tetraethyl lead and its derivatives on the chrysophyte Poterioochromonas malhamensis. III. Chemical analyses

Abstract The photolytic decomposition of tetraethyl lead (TEL) into the derivatives triethyl lead (TriEL), diethyl lead (DiEL) and into inorganic lead (Pb) in aqueous environment has been examined by using a single‐step dithizone extraction method. In cell‐free medium, TEL decomposes rapidly upon illumination to form TriEL, which accumulates in the medium. DiEL is formed in very small quantities only and without any significant accumulation, whereas the concentration of Pb increases slightly but continuously. In darkness the formation of TriEL amounts, as compared to light, to a maximum of 10 %, and DiEL as well as Pb are below the analytical threshold. There is a considerable loss of the initially added TEL: after 98 hr of incubation 96 % of the total lead are eliminated from the illuminated medium and 99.5 % from the non‐illuminated one. In illuminated tap water, where the creation of TriEL takes place much faster than in cultivation medium, the loss of total lead amounts to only 84 %. The formation kinetics for TriEL during the first 72 hr of incubation were determined as follows: tap water/ light: y = 0.18 x; cultivation medium/light: y = ln(l + 0.924 x); cultivation medium/darkness: y = ln(l + 0.006 x), with y being TriEL as ppm Pb and x the hours of incubation. Compared to previous biological experiments, these data conclusively indicate that TriEL is the toxic derivative of TEL which is created upon illumination and causes the severe inhibitory effects in cultures of Poterioochromonas malhamensis poisoned by TEL. The significance of these findings for polluted natural environments and for the metabolic pathway of organolead in intoxicated mammalia is discussed briefly, and a diagrammatical model is presented describing the presumed fate of TEL and its derivatives under experimental conditions.

On the toxic effects of tetraethyl lead and its derivatives on the chrysophyte Poterioochromonas malhamensis: II. Triethyl lead, diethyl lead, and inorganic lead

The toxic effects of the tetraethyl lead (TEL) derivatives triethyl lead (TriEL), diethyl lead (DiEL), and of inorganic lead (Pb 2+) on the Chrysophyte Poterioochromonas malhamensis were studied. The algae's parameters of interest were cell growth, and the formation of giant cells and of polyploid nuclei. (1) Based on their zero-growth-inducing concentrations, the tested lead compounds reveal the following relative toxicities to the algae: Pb 2+, light/darkness = 1 1 ; DiEL, light/darkness = 11 10 ; TriEL, light/darkness = 55 33 ; TEL, light/darkness = 7 0 . (2) The lead compounds differ greatly in the concentration ranges which cause slight inhibitory to lethal effects. The ranges are: Pb 2+ = 5 to >1000 μ m (>200×); DiEL = 5 to 100 μ m (20×); TriEL = 5 to 25 μ m (5×). (3) Pb 2+ is the least toxic TEL derivative. Its growth-inhibiting effect is remarkably high at very low concentrations (10μ m) but it increases only slightly with rising concentrations. Even 3-day treatment with 1000 μ m Pb 2+ is not lethal to the whole culture. Between 10 to 500 μ m Pb 2+, the nuclear indices of the cultures stay nearly unaffected, whereas there is a moderate but distinct increase in the percentage of polyploids, with maxima of 10% in the light and 6% in darkness. (4) DiEL is about ten times more toxic to Poterioochromonas than Pb 2+. It inhibits cellular growth and leads to the formation of giant cells and of polyploid nuclei under light and dark conditions. DiEL is much less stable to light than TriEL. In the course of the experiments it obviously tends to decompose upon illumination to a less active and less water-soluble compound. (5) Among the tested TEL derivatives, TriEL is the most toxic. In light as well as in darkness it inhibits algal growth and leads to the formation of giant multinucleated cells and of polyploid nuclei. The effects of TriEL are identical to those which were observed in TEL-treated illuminated cultures of Poterioochromonas. (6) Although DiEL has TriEL-like activity, there is evidence suggesting that in these experiments DiEL is not formed from TEL in critical amounts. The present studies further support the idea that TriEL is the primary derivative of TEL in illuminated algal cultures and that TriEL is the agent which causes the severe inhibitory effects in TEL toxicity to Poterioochromonas malhamensis.

Excretion of triethyl lead, diethyl lead and inorganic lead after injection of tetraethyl lead in rabbits (author's transl)

Rabbits were dosed with tetraethyl lead at 12 mg/kg; their organs, bloods, urines and feces were then assayed for tetraehyl lead, triethyl lead, diethyl lead, inorganic lead and total lead, and the chemical species of the lead excreted in the urines and feces were also studied. 1) One day after the dosing, the total lead in the urine was made up of about 69% diethyl lead, about 27% inorganic lead and about 4% triethyl lead. This ratio of the chemical species of lead to total lead remained unchanged even 7 days after the dosing. 2) Two days after the dosing, the total lead in the feces consisted of about 85% inorganic lead, about 9% diethyl lead and about 6% triethyl lead. Seven days after the dosing, the total lead in the feces comprised about 95% inorganic lead, about 4% triethyl lead and about 1% diethyl lead. 3) Intravisceral levels of lead were also measured 24 hours after the dosing. Triethyl lead accounted for about 84% of the total lead in the liver, about 68% in the kidneys, and about 59% in the blood. 4) Lead levels in B bile and intestinal contents were determined 24 hours after the dosing. Diethyl lead accounted for about 93% of total lead in B bile, while inorganic lead made up about 90% of the total lead in the cecal, the colonic and the rectal contents. 5) Conversion of diethyl lead by intestinal contents was studied in vitro by adding diethyl lead to the intestinal contents of normal rabbits. Incubation of the mixtures in the presence of N2 at 38°C for 180 minutes resulted in the conversion of 16% of the diethyl lead into inorganic lead in the cecal, the colonic and the rectal contents. The conversion of diethyl lead into inorganic lead in the cencal contents was followed up and it was found that the inorganic lead output increased with the passage of time. Diethyl lead proved to be the principal chemical species of lead that is eliminated into the urine and bile after dosing rabbits with tetraethyl lead. However, inorganic lead accounted for the major portion of the lead excreted into the feces. This finding suggested that the diethyl lead eliminated into the bile could be converted into inorganic lead in the intestines.

Urinary excretion pattern of triethyllead, diethyllead and inorganic lead in the tetraethyllead poisoning.

The fractional determination of triethyl lead, diethyl lead, inorganic lead and total lead in the urines of a patient with tetraethyl lead poisoning was performed by means of hydride generation-flameless atomic absorption spectrometry.The chemical species of lead in the urine 21 days after the exposure comprised about 50% diethyl lead, about 48% inorganic lead and about 2% triethyl lead.The fractional determination of triethyl lead, diethyl lead and inorganic lead in the urines of the patient after intravenous drip of 1000 mg of calcium ethylene-diaminetetraacetic acid (Ca-EDTA) only once (30 days after the exposure) was also performed. Compared with the lead output 2 days before the treatment (28 days after the exposure), the total lead output in the urine during the 12 hours after the intravenous drip of Ca-EDTA was increased to about 4 times, with inorganic lead accouting for about 98% of the increased output but with no increase in triethyl lead or diethyl lead output.

Diethyl lead dinitrate

The reaction, at 0 °C, between tetra-ethyl lead and dinitrogen tetroxide in both nitromethane and diethyl ether as solvents has been studied. The product in both solvents is always diethyl lead dinitrate, the properties of which have been investigated and compared with both dimethyl tin dinitrate and triethyl lead nitrate. The infrared spectrum is consistent with covalent unidentate nitrate groups, while molecular weight and conductivity measurements indicate that the compound behaves essentially as a 1:2 electrolyte in water and dimethyl sulfoxide. Decomposition of diethyl lead dinitrate in solution and in the solid state is discussed with the aid of ultraviolet spectroscopy and thermogravimetric analysis.

Thermal stabilities of the methyl ethyl lead alkyls

A single pulse shock tube has been used to study the thermal stabilities of the methyl ethyl lead alkyls in the temperature range 731° to 931°K. The stabilities are, in decreasing order, tetramethyl lead; ethyl trimethyl lead; and then, as a group, dimethyl diethyl lead, triethyl methyl lead, and tetraethyl lead. First-order kinetics over the entire temperature range were confirmed only for dimethyl diethyl lead. The stabilities parallel the engine performances of these anti-knocks.

Thermal stabilities of the methyl ethyl lead alkyls

A single pulse shock tube has been used to study the thermal stabilities of the methyl ethyl lead alkyls in the temperature range 731° to 931°K. The stabilities are, in decreasing order, tetramethyl lead; ethyl trimethyl lead; and then, as a group, dimethyl diethyl lead, triethyl methyl lead, and tetraethyl lead. First-order kinetics over the entire temperature range were confirmed only for dimethyl diethyl lead. The stabilities parallel the engine performances of these anti-knocks.

Biochemical Studies on the Toxicity of Tetraethyl Lead and Other Organo-Lead Compounds

The actions of purified tetra-, tri-, and di-ethyl lead on rats and rat brain slices and brain brei have been examined. A method based on a reaction with dithizone and capable of estimating tri- and di-ethyl tin in rat tissues has been developed. After injection into rats tetraethyl lead is converted into triethyl lead and this is responsible for the toxic effects. Diethyl lead is much less toxic and the effects are different. The utilization of lactate and the oxidation of glucose by brain brei and slices respectively are inhibited by triethyl lead. A similar effect is seen in slices taken from rats poisoned with tetra- or tri-ethyl lead. Rat liver cell microsomes readily convert tetraethyl to triethyl lead and the latter is stable and remains in the animal tissues for several days. The concentration of triethyl lead in the brain is not high in comparison with other tissues but brain tissue appears to be unduly sensitive to its toxic action. Neither tetra- nor tri-ethyl lead reacts with B.A.L. or ethylene-diamine-tetra-acetic acid (E.D.T.A.). Diethyl lead reacts with B.A.L. but not with E.D.T.A.