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At least 739 records · Page 41Linked to original sources
PubMed2002

Evidence that RDX biodegradation by Rhodococcus strain DN22 is plasmid-borne and involves a cytochrome p-450.

AIMS: To investigate the biodegradation of the explosive compound RDX in Rhodococcus strain DN22, a bacterium previously isolated for its ability to grow on RDX as sole nitrogen source. METHODS AND RESULTS: Analysis of the rates of RDX degradation and nitrite production indicated that 2 mol nitrite were produced per mole RDX degraded. Cells of strain DN22 had the highest activity against RDX during the exponential phase and low activity in the stationary phase. Nitrite production from RDX was inhibited by metyrapone, menadione, piperonyl butoxide, n-octylamine and carbon monoxide and inducible by pyrrolidine, pyridine and atrazine. Acridine orange treatment yielded RDX-minus derivatives of strain DN22 at a curing rate of 1.5% and all of the cured derivatives had lost a large plasmid. CONCLUSIONS: RDX biodegradation in strain DN22 appears to involve a plasmid-encoded cytochrome p-450 enzyme. SIGNIFICANCE AND IMPACT OF THE STUDY: Plasmid-borne RDX degradation genes could potentially be transferred between bacteria. Our research into RDX metabolism in strain DN22 will facilitate future applications of this bacterium for bioremediation.

Acridine Orange↗
PubMed1982

Foods, and food and drug combinations, responsible for head and neck pain.

The literature has been reviewed to uncover the existence of head and neck pain syndromes caused by foods and food and drug combinations. Knowledge of the etiology of such syndromes may help in their treatment. At least twenty-five syndromes have been described. These include those induced by coloring and flavoring agents, alcoholic products, chocolate, coffee and tea, foods containing tyramine, vitamins, minerals, pesticides, and several others. Where possible, the active ingredients and the minimal amounts responsible for the induction of pain have been identified.

Adult↗
PubMed1995

[Repeated ingestion with suicidal intent of potentially lethal amounts of thallium].

30 minutes after drinking half a cup of rat poison a 16-year-old girl was admitted to hospital. In addition to various enteric detoxification measures forced dialysis was instituted and, after the urinary thallium level had become known (9 mg/l), haemodialysis was begun and ferric ferrocyanide (Prussian blue) administered (0.5 mg daily for six days). She had no symptoms at any time. After 10 days she was discharged. Five days after discharge she was again admitted, with colic-like abdominal pain, vomiting, paraesthesias of the hands and feet, and in a state of agitation. She had once again ingested rat poison, about one cup. Physical examination revealed little of consequence, except diffuse alopecia. Urinary thallium concentration was 37 mg/l. In the electrocardiogram the P-R interval was shortened to 0.11 s and T waves inverted in leads III and V1. Electronmicroscopy of cardiac and skeletal biopsies revealed lipid droplets, increased sarcoplasm and widening of some of the tubules. Treatment consisted of haemodialysis, forced diuresis (1 l urine/h), administration of ferric ferrocyanide, orthograde intestinal infusions and potassium substitution (serum level: 5 mmol/l). After 28 days the patient was discharged into psychiatric care.

Adolescent↗
PubMed1980

The neurotoxicity of the rat poison vacor. A clinical study of 12 cases.

Oral ingestion of a new rat poison that antagonizes nicotinamide metabolism, N-3-pyridylmethyl-N'-p-nitrophenyl urea (PNU, Vacor), is known to cause diabetes mellitus. I describe neurologic complications of PNU ingestion in 12 patients 19 to 50 years of age who swallowed between 0.39 and 7.02 g of PNU. One died within a day, and five died of chronic complications 40 to 182 days after taking the poison. Apart from the acute hyperglycemic ketoacidosis, the clinical presentation was variable, but orthostatic hypotension, gastrointestinal hypomotility, peripheral neuropathy, and encephalopathy were typical. The peripheral, autonomic, and central-nervous dysfunction could develop either acutely or other several days. It is possible that nicotinamide, given parenterally within minutes, prevents toxicity, but the cases discussed in this paper indicate that the neurologic deficits may progress despite later nicotinamide administration. Neurologic improvement took many months. Full recovery was uncommon, and the orthostatic, hypotension tended to persist.

Adult↗
PubMed2000

Natural selection mapping of the warfarin-resistance gene.

In theory, genes under natural selection can be revealed by unique patterns of linkage disequilibrium (LD) and polymorphism at physically linked loci. However, given the effects of recombination and mutation, the physical extent and persistence of LD patterns in natural populations is uncertain. To assess the LD signature of selection, we survey variation in 26 microsatellite loci spanning an approximately 32-cM region that includes the warfarin-resistance gene (Rw) in five wild rat populations having resistance levels between 0 and 95%. We find a high frequency of heterozygote deficiency at microsatellite loci in resistant populations, and a negative association between gene diversity (H) and resistance. Contrary to previous studies, these data suggest that directional rather than overdominant selection may predominate during periods of intense anticoagulant treatment. In highly resistant populations, extensive LD was observed over a chromosome segment spanning approximately 14% of rat chromosome 1. In contrast, LD in a moderately resistant population was more localized and, in conjunction with likelihood ratios, allowed assignment of Rw to a 2. 2-cM interval. Within this genomic window, a diagnostic marker, D1Rat219, assigned 91% of rats to the correct resistance category. These results further demonstrate that "natural selection mapping" in field populations can detect and map major fitness-related genes, and question overdominance as the predominant mode of selection in anticoagulant-resistant rat populations.

Animals↗
PubMedDate not supplied

Mortality in 1969 from pesticides, including aerosols.

Among the 87 deaths in the United States in 1969 for which a causal relationship to pesticides could not be excluded, there were 62 valid accidents, 20 intentionally inflicted deaths, and five deaths incorrectly attributed to pesticides. The reduction in the number of such deaths compared to the decade and a half prior to 1962 probably involves a trend. As in the past, a disproportionate fraction of the victims were children, boys and men, and nonwhites. Findings in four cases (three in 1969) were consistent with the conclusion that intensive inhalation of an aerosol can sensitize the heart to fatal arrhythmia, even though there is no intentional misuse of the aerosol and no attempt to seek a thrill. Medical examiners should be alert to the possibility of such deaths associated with both pesticide and non-pesticide aerosols.

Accidents↗
PubMed2006

Acceptance by stoats (Mustela erminea) of 1080 (sodium monofluoroacetate) in small-volume baits and its effect on behaviour and time to death.

AIMS: To assess whether stoats (Mustela erminea) would eat small baits containing 0.1% sodium monofluoroacetate (1080); whether they would die from it; how long it would take to kill them; and to document the behaviour of 1080-intoxicated stoats. METHODS: Stoats were offered 1-g baits of two semi-fluid formulations containing 0.1% 1080, presented in open dishes, and their subsequent behaviour was monitored by video and direct observation. Muscle samples from stoats that died were analysed for 1080 residues. RESULTS: There was no significant difference between two types of bait with regard to acceptance, mortality, and time to death, and behavioural effects were similar; consequently, results from the two types of bait were combined. Twelve of 14 stoats offered the baits ate them voluntarily, and a 13th licked bait off its fur; all 13 died between 1 h 15 min and 4 h 7 min (mean 2 h 38 min) later. At first (range 29 min - 2 h 7 min, mean 1 h 1 min), their behaviour appeared to be normal. Ataxia and hyperactivity were the first behavioural signs of poisoning, and lasted 2 min - 1 h 40 min (mean 26 min). This was followed by recumbency with convulsions and rapid breathing (range 16 min to 2 h, mean 58 min), then recumbency with limited activity and progressively shallow breathing prior to death (range 1-51 min, mean 33 min). Stoats became non-responsive to a light being turned on, or to touch once recumbency became sustained. Residues of 1080 were found in muscle tissue of all 13 dead stoats, at concentrations ranging from 0.075 microg/g in a 287-g male that died 4 h 7 min after eating only 0.74 g of bait, to 2.5 microg/g in a 254-g female that died 2 h 42 min after taking a whole 1-g bait. CONCLUSION: Stoats will voluntarily take small (1-g) baits containing a lethal dose of 1080 at 0.1%, and die from it comparatively rapidly for a mammalian carnivore.

Animals↗
PubMed1997

Cytogenetic observations following thallium poisoning.

Observations have been performed on peripheral blood lymphocytes from a patient having ingested 200 mg thallium sulfate, in order to evaluate the ability of the compound to produce cytogenetic damage in vivo in humans. Our results demonstrate that neither the yield of structural chromosome aberrations nor sister chromatid exchanges were significantly modified. The drastic increase of binucleated cells with micronuclei indicates that thallium sulfate has in common with many metallic compounds the ability to interfere with chromosome distribution.

Cell Nucleus↗
PubMed2002

Prevention of alpha-naphthylthiourea-induced pulmonary edema with fructose-1,6-diphosphate.

Neutrophil-derived oxygen free radicals have been implicated in the pathogenesis of noncardiogenic pulmonary edema. Fructose-1,6-diphosphate (FDP) has been shown to inhibit oxygen free radicals production by activated neutrophils. Thus, we investigated whether FDP would attenuate formation of pulmonary edema in anesthetized dogs injected with alpha-naphthylthiourea (ANTU). Hemodynamic studies involved measurements of left ventricular systolic and end-diasystolic pressures (LVSP and LVEDP), pulmonary artery pressure (PaP), heart rate (HR), and cardiac output (CO). Mean wet weight to dry weight ratios of lung tissue samples were calculated. Following baseline measurements, dogs were injected intravenously (IV) with ANTU 5 mg / kg (n = 16) and 10 mg / kg (n = 8) and half of the dogs were randomly selected to receive 75 mg / kg FDP (10%) and subsequent infusion of 7 mg / kg / min. The rest were given 0.9% NaCl in the same manner. Four hours after ANTU administration, the animals were euthanatized. Except for decline in the CO (nonsignificant), no significant changes in systemic hemodynamics within and between the groups were noted. In the FDP group, PaP and pulmonary arteriolar resistance (PaR) remained unchanged. In the saline group, PaP increased from 12.5 +/- 2.44 to 21.8 +/- 3.14 mm Hg (P < .001) and PaR from 166 +/- 29 to 468 +/- 74 dynes. cm / sec(5) (P < .005). During the study LVDEP, PaO(2), PaCO(2), and hematocrit did not change significantly within and between the groups. The lungs mean wet weight to dry weight ratios for the sham-operated dogs were 4.20 +/- 0.41, for the FDP group 4.32 +/- 0.59 and 6.22 +/- 1.37 for the saline group (P < .0005). These data indicate that FDP protected the lung from ANTU-induced injury.

Animals↗
PubMed1992

Mutagenicity of trinitrotoluene and its metabolites formed during composting.

TNT was mutagenic for Salmonella typhimurium without the need of a rat liver metabolic activation system (S9). The mutagenic potency of TNT decreased in proportion to the number of nitro groups that were reduced to the amino form. The presence of a nitro group on the 4 position of the diamino congener is necessary for mutagenicity. Among the active congeners, mutagenicity was generally greater for TA100 than TA98, except that for the 4-amino congener the reverse was true. In cases when S9 was included in the assay, there was always a decrease in the number of mutants induced as compared with those without S9. Tetryl behaved like TNT, except that it was approximately three times more potent. RDX and HMX were not mutagenic under the conditions of the assay. When TNT was composed, the major metabolites identified in organic extracts of compost samples were the 2-amino and 4-amino congeners. An acetonitrile extract of compost was tested and found to be more mutagenic for TA98 than TA100, much like the authentic 4-amino congener, but the amount of this congener in the extract did not account for the degree of mutagenicity.

Aniline Compounds↗
PubMed1990

Poisoning by some insecticides, herbicides and fungicides.

To avoid accidental poisoning, pesticides must be handled according to prescribed rules. Furthermore, the exact composition of the pesticide formulation should be known. Cases of acute poisoning usually occur by ingestion and less frequently by the other routes. Symptoms may appear immediately but sometimes they can appear later and/or be more prolonged giving rise to delayed death and/or delayed morbidity. Acute poisoning by raticides and by organophosphate insecticides should deserve all our attention. Poisoning by herbicides containing chlorate salts, oxidative phosphorylation uncouplers or bipyridilium derivatives may be particularly dangerous. The ingestion of Paraquat, in particular, which is a veritable lesional poison, could be beyond all therapeutic resources.

Fungicides, Industrial↗