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At least 829 records · Page 46Linked to original sources
PubMed1990

Pulmonary toxicity of thioureas in the rat.

Administration of alpha-naphthylthiourea (ANTU) to rats causes damage to pulmonary endothelial cells and possibly mesothelial lining cells that together may account for the massive pleural effusion characteristic of thiourea toxicity. Using 35S-thiourea as a model compound, the extent of binding of 35S to lung proteins correlated well with the extent of edema, suggesting that the extent of binding of thiourea metabolites is a measure of lung toxicity. ANTU and phenylthiourea (PTU) compete for 35S binding to lung slices, suggesting that these toxins may act in a similar way. Binding of 35S in lung slices from resistant rats is much less than in controls, and resistance cannot be explained by differences in either whole body metabolism or redistribution of thiourea in vivo. Lung glutathione levels (in vitro and in vivo) in normal and resistant rats following thiourea administration were essentially the same. However, at doses of thiourea that cause pleural effusion, there was an increase in total lung glutathione.

Animals↗
PubMed1992

Diffuse alveolar hemorrhage secondary to superwarfarin ingestion.

A 27-year-old woman with severe vitamin K deficiency presented with hemoptysis and diffuse pulmonary infiltrates. She rapidly developed respiratory failure requiring ventilatory support. Surreptitious ingestion of brodifacoum, a long-acting warfarin derivative, was ultimately found to be the cause of her coagulopathy and DAH.

4-Hydroxycoumarins↗
PubMedDate not supplied

Biosynthesis of the bufadienolide ring of scillirosid in Scilla maritima.

Administration of sodium [1,2-14C2]oxaloacetate and sodium [1-14C]acetate to Scilla maritima plants yielded labelled scillirosid. A systematic degradation of scillirosid indicated that the alpha-pyrone ring of the bufadienolide is formed by the condensation of a pregnane derivative (derived from mevalonic acid via squalene) and one molecule of oxaloacetic acid.

Acetates↗
PubMed2004

Neurotoxic effects of alpha-fluoro-beta-alanine (FBAL) and fluoroacetic acid (FA) on dogs.

In order to clarify the mechanism of the neurotoxicity of 5-FU and/or its masked compounds, we studied the effects of alpha-fluoro-beta-alanine (FBAL) and fluoroacetic acid (FA) on the formation of vacuolar changes in the dog cerebrum, using the dosage of 3.0 mg/kg/day of FBAL-HCl (FBAL x HCl) and 0.03 mg/kg/day of FA-Na (FA x Na), respectively. These 2 compounds were selected because they are the metabolites of 5-FU claimed to be responsible for the neurotoxic effects of 5-FU and/or its masked compounds, and we wanted to confirm their effects. Tegafur-uracil mixture (UFT) was used as a positive control drug for the formation of vacuolar changes in the dog cerebrum. All compounds were orally administered daily for 3 months to beagle dogs. Each study group consisted of 3 males. Neurotoxic signs such as hyperesthesia and/or excitement, as well as convulsions, were observed in both FBAL x HCl and FA x Na groups; these toxic signs were also found in the UFT group. Slight loss of body weight gain and of food consumption was observed in the FBAL x HCl and UFT groups. Neuropathologically, vacuolar changes were detected in several areas of the dog cerebrum following administration of FBAL x HCl, FA x Na or UFT. In terms of morphology, the neuropathological effects of these 2 drugs were very similar to those induced by UFT. In conclusion, we clearly showed that FBAL is one of the main substances that cause neurotoxic signs and neuropathological changes in dogs intoxicated by 5-FU or its masked compounds. Moreover, FA might be considered to be a causative factor in addition to FBAL.

Administration, Oral↗
PubMedDate not supplied

RDX loss in a surface soil under saturated and well drained conditions.

On military training ranges, low-order, incomplete detonations deposit RDX (hexahydro-1,3,5-trinitro-1,3,5-triazine) into surface soils. In this study, we evaluated RDX biodegradation in surface soils obtained from a military training range in Alaska. Two factors were compared: (i) soil water potential during the incubations; and (ii) the use of acetonitrile (ACN) as an RDX carrier to spike samples. Organic solvents have been used in laboratory studies to dissolve slightly water-soluble contaminants before addition to soil. We added ACN to obtain final soil ACN concentrations of 0 mg kg(-1) (0%), 1000 mg kg(-1) (0.1%) and 10 000 mg kg(-1) (1%). We then compared RDX attenuation in the soil under saturated and unsaturated conditions. RDX fell below the limit of detection within 3 wk of study initiation under the saturated condition. A maximum degradation rate of 0.15 mg RDX L(-1) d(-1) was measured. Under the unsaturated condition, 42% of the original RDX was still present at study termination (5 wk). The addition of acetonitrile at 0.1 or 1.0% had no affect on RDX loss in the saturated soil. In the unsaturated soil, however, ACN at 1.0% inhibited RDX loss by as much as 25%. These findings indicate that soil water potential and carrier solvent concentrations can impact the rate and extent to which RDX is attenuated in a surface soil.

Acetonitriles↗
PubMedDate not supplied

Pilot-scale treatment of RDX-contaminated soil with zerovalent iron.

Soils in Technical Area 16 at Los Alamos National Laboratory (LANL) are severely contaminated from past explosives testing and research. Our objective was to conduct laboratory and pilot-scale experiments to determine if zerovalent iron (Fe(0)) could effectively transform RDX (hexahydro-1,3,5-trinitro-1,3,5-triazine) in two LANL soils that differed in physicochemical properties (Soils A and B). Laboratory tests indicated that Soil A was highly alkaline and needed to be acidified [with H2SO4, Al2(SO4)3, or CH3COOH] before Fe(0) could transform RDX. Pilot-scale experiments were performed by mixing Fe(0) and contaminated soil (70 kg), and acidifying amendments with a high-speed mixer that was a one-sixth replica of a field-scale unit. Soils were kept unsaturated (soil water content = 0.30-0.34 kg kg(-1)) and sampled with time (0-120 d). While adding CH3COOH improved the effectiveness of Fe(0) to remove RDX in Soil A (98% destruction), CH3COOH had a negative effect in Soil B. We believe that this difference is a result of high concentrations of organic matter and Ba. Adding CH3COOH to Soil B lowered pH and facilitated Ba release from BaSO4 or BaCO3, which decreased Fe(0) performance by promoting flocculation of humic material on the iron. Despite problems encountered with CH3COOH, pilot-scale treatment of Soil B (12 100 mg RDX kg(-1)) with Fe(0) or Fe(0) + Al2(SO4)3 showed high RDX destruction (96-98%). This indicates that RDX-contaminated soil can be remediated at the field scale with Fe(0) and soil-specific problems (i.e., alkalinity, high organic matter or Ba) can be overcome by adjustments to the Fe(0) treatment.

Environmental Pollution↗
PubMedDate not supplied

Remediating munitions-contaminated soil with zerovalent iron and cationic surfactants.

Soils contaminated from military operations often contain mixtures of HMX (octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine), RDX (hexahydro-1,3,5-trinitro-1,3,5-triazine), and TNT (2,4,6-trinitrotoluene) rather than a single explosive. Differences among explosives in solubility and reactivity make developing a single remediation treatment difficult. When Fe(0) was used to treat a munitions-contaminated soil, we observed high rates of destruction for RDX and TNT (98%) but not HMX. Our objective was to determine if HMX destruction by Fe(0) could be enhanced by increasing HMX solubility by physical (temperature) or chemical (surfactants) means. To determine electron acceptor preference, we treated RDX and HMX with Fe(0) in homogeneous solutions and binary mixtures. Increasing aqueous temperature (20 to 55 degrees C) increased HMX solubility (2 to 22 mg L(-1)) but did not increase destruction by Fe(0) in a contaminated soil slurry that also contained RDX and TNT. Batch experiments using equal molar concentrations of RDX and HMX demonstrated that RDX was preferentially reduced over HMX by Fe(0). By testing various surfactants, we found that the cationic surfactants (HDTMA [hexadecyltrimethylammonium bromide], didecyl, and didodecyl) were most effective in increasing HMX concentration in solution. Didecyl and HDTMA were also found to be highly effective in facilitating the transformation of HMX by Fe(0). Using HDTMA or didecyl solutions (3%, w/v) containing solid-phase HMX, we observed that 100% of the added HMX was transformed by Fe(0) in the didecyl matrix and 60% in the HDTMA matrix. These results indicate that cationic surfactants can increase HMX solubility and facilitate Fe(0)-mediated transformation kinetics but HMX destruction rates will be slowed when RDX is present.

Azocines↗
PubMed1999

Inhibition of mitochondrial oxidative phosphorylation induces hyper-expression of glutamic acid decarboxylase in pancreatic islet cells.

It has been hypothesised that mitochondrial dysfunction in pancreatic beta cells could produce hyper-expression of glutamic acid decarboxylase (GAD), a major autoantigen in insulin-dependent diabetes mellitus (IDDM) (Degli Esposti, M. and Mackay, I.R. Diabetologia 40: 352-356, 1997). Here we report that specific inhibition of mitochondrial respiration enhances the expression of GAD in both foetal mouse pancreatic tissue and hamster HIT-T15 cells. Inhibitors of NADH-ubiquinone oxidoreductase (complex I) seem to be particularly effective in increasing the expression of GAD in both foetal mouse pancreas and HIT-T15 hamster beta cells, especially in the presence of nutrients such as arginine and glucose. These results represent the first evidence that GAD expression is enhanced under conditions that are toxic to pancreatic beta cells, and establish a link between mitochondrial dysfunction and expression of IDDM autoantigens.

Animals↗
PubMed1981

Acute yellow phosphorus poisoning from pesticide pastes.

Ten cases of ingestion of yellow phosphorus rat poison, including four cases that occurred during the past 3 years, are reported. Comparison of these cases with 82 others from the literature showed that ingestion of yellow phosphorus paste often results in clinical findings that are different from those described for acute yellow phosphorus poisoning in current toxicology texts. The time lag between swallowing of the poison and onset of symptoms varied from a few minutes to 24 h. Garlic odor, mucosal burns, and phosphorescent vomitus or feces occurred in only a small percentage of cases. Diarrhea was not a presenting complaint. Initial symptoms were referable to the gastrointestinal tract, central nervous system, or both. Mortality rates were 23% for patients who had early symptoms of vomiting or abdominal pain; 73% for those where the first manifestation of intoxication was restlessness, irritability, drowsiness, stupor, or coma; and 47% for patients who had a combination of these GI and CNS symptoms initially. Applying standard diagnostic criteria for yellow phosphorus poisoning to patients who have consumed yellow phosphorus pastes may result in serious diagnostic errors.

Adolescent↗