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PubMed2004

Carbonic anhydrase inhibitors. Inhibition of the zinc and cobalt gamma-class enzyme from the archaeon Methanosarcina thermophila with anions.

Anions represent the second class of inhibitors of the zinc enzyme carbonic anhydrase (CA, EC 4.2.1.1), in addition to sulfonamides, which possess clinical applications. The first inhibition study of the zinc and cobalt gamma-class enzyme from the archaeon Methanosarcina thermophila (Cam) with anions is reported here. Inhibition data of the alpha-class human isozymes hCA I and hCA II (cytosolic) as well as the membrane-bound isozyme hCA IV with a large number of anionic species such as halides, pseudohalides, bicarbonate, carbonate, nitrate, nitrite, hydrosulfide, bisulfite, and sulfate, etc., are also provided for comparison. The best Zn-Cam anion inhibitors were hydrogen sulfide and cyanate, with inhibition constants in the range of 50-90 microM, whereas thiocyanate, azide, carbonate, nitrite, and bisulfite were weaker inhibitors (K(I)s in the range of 5.8-11.7 mM). Fluoride, chloride, and sulfate do not inhibit this enzyme appreciably up to concentrations of 200 mM, whereas the substrate bicarbonate behaves as a weak inhibitor (K(I)s of 42 mM). The best Co-Cam inhibitor was carbonate, with an inhibition constant of 9 microM, followed by nitrate and bicarbonate (K(I)s in the range of 90-100 microM). The metal poisons were much more ineffective inhibitors of this enzyme, with cyanide possessing an inhibition constant of 51.5mM, whereas cyanate, thiocyanate, azide, iodide, and hydrogen sulfide showed K(I)s in the range of 2.0-6.1mM. As for Zn-Cam, fluoride, chloride, and sulfate are not inhibitors of Co-Cam. These major differences between the two gamma-CAs investigated here can be explained only in part by the different geometries of the metal ions present within their active sites.

Anions↗
PubMed1993

Phosphorylated nutrient uptake by Treponema denticola and other potential periodontopathogens.

Nutrient uptake may contribute to the survival of certain potential periodontopathogens in the competitive environment of the gingival sulcus. This study was conducted to assess the uptake of commercially available, key radiolabelled phosphorylated compounds by Treponema denticola. There was a linear relationship in the uptake of ATP and G-1-P with cell concentrations of 0.1-2.5 mg of cell dry weight. This uptake reached a steady state within 15 min, and at temperatures of 25-37 degrees C the uptake ranged between 13-21%. At 50 degrees C, or above 50 degrees C the assay cells took up 0-1% of the assay nutrients. The maximum uptake of ATP was 47.5, 38 and 47.6 pmoles for serovars a, b and c. G-1-P yielded maximum uptake values of 306, 304, and 306 pmoles respectively. Significant uptake of ATP, or G-1-P occurred at pH 4.8 for serovars a, or c, while serovar b showed a broad pH range for the uptake of G-1-P. Stannous fluoride at a concentration of 0.17 mM enhanced the uptake of ATP while chlorhexidine digluconate inhibited the uptake of ATP. At concentrations usually employed (0.05-0.5 mM) the metabolic poisons 2,4-dinitrophenol, sodium azide, sodium arsenite and the ATPase inhibitor N,N1-dicyclohexylcarbodiimide did not alter significantly the uptake of ATP. The uptake of ATP, by Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Fusobacterium nucleatum and T. denticola at pH 4.8 was 13.4, 1.5, 6.9, and 18-20.4%, respectively. At pH 6.5 the uptake for the microorganisms indicated above was 22, 1.3, 6.6 and 6.2%, respectively. G-1-P showed the same trend in its uptake by A. actinomycetemcomitans, P. gingivalis, F. nucleatum and T. denticola. This study provides for the first time specific examples of phosphorylated nutrient uptake by potential periodontopathogens, and that the uptake of phosphorylated nutrients can be suppressed by oral hygienic compounds.

Adenosine Triphosphate↗
PubMedDate not supplied

[Drug poisonings in childhood at a regional poisons unit].

BACKGROUND: Drug poisonings in childhood account with about one fourth for the most important group of poisonings in this age group. METHOD: From 1995 to 2004 the inquiries to a poison centre regarding drug poisonings of children < or = 6 years of age were analyzed. Additionally, a standardized questionnaire was sent for follow-up information. RESULTS: During the study period a total number of 17 553 cases of drug poisonings in childhood was determined and follow-up information was obtained for 8 590 cases (48.9 %). Boys were more likely to be affected (53.4 %) and most children were between 2 and 4 years of age (57.5 %). Mostly oral contraceptives, homeopathic drugs, nonsteroidal anti-inflammatory drugs, sodium fluoride and paracetamol were ingested. In 97.8 % of the reported cases none or minor symptoms and in 1.5 % medium or major symptoms (1 death) were observed. In the latter group of patients mostly neuroleptics, antihistaminics, nonsteroidal anti-inflammatory drugs, beta2-sympathomimetics and paracetamol were ingested. In most cases the application of fluids (47.3 %) or activated charcoal (32.0 %) was sufficient. CONCLUSIONS: Severe symptoms have rarely been observed in drug poisonings and in most children a treatment by non-professionals was sufficient. Most frequently activated charcoal was currently used for primary poison elimination. We suggest an early involvement of a poison centre in drug intoxications.

Child↗
PubMed1994

[Effect of quercetin on the course of chronic poisoning with fluorine compounds in rats].

Biochemical examinations in serum, homogenates and microsomal fraction of the liver, as well as biochemical and morphological examinations of liver tissue were performed in rats of Wistar strain exposed chronically for 6 months to ammonium fluoride vapours. A part of animals was protected with a mixture of sodium salts of quercetin synthetized in Inorganic Chemistry Department of the Technical University at Rzeszów, and added to the standard feed in a dose of 5 and 20 mg/kg body weight. It has been disclosed that NH4F causes disturbances in the activities of enzymes (cholinesterases, transaminases, alkaline and acid phosphatase), a rise of bilirubin concentration in serum, as well as disturbances in lipid metabolism, an increase in the content of total lipids, and disorders of lipid metabolism--increase in the content of total lipids, cholesterol and triglycerides, with phospholipids being decreased. The biochemical changes are accompanied by the hepatic tissue lesion. The use of quercetin alleviates, to a considerable degree, the biochemical and morphological disturbances due to protracted exposure to ammonium fluoride vapours.

Administration, Oral↗
PubMed1995

Ethyl octylphosphonofluoridate and analogs: optimized inhibitors of neuropathy target esterase.

The relation between organophosphorus-induced delayed neuropathy (OPIDN) and brain neuropathy target esterase (NTE) inhibition is further examined in hens by structure-activity studies leading to the most potent in vitro NTE inhibitors known, which are then examined for their neuropathic effects in vivo in hens. The principal compounds studied are alkyl alkylphosphonofluoridates and dialkyl phosphorofluoridates. Potencies that exceed those of any previous inhibitors under the standard in vitro NTE assay condition are achieved with alkyl octylphosphonofluoridates (ethyl, isopropyl, 2-chloroethyl, 2-bromoethyl, 2-iodoethyl, and 3-iodopropyl), 2-iodoethyl hexylphosphonofluoridate, and dialkyl phosphorofluoridates [ethyl, nonyl; di(2-iodoethyl); di(3-iodopropyl); dipentyl]. The concentration for 50% NTE inhibition (I50) of these compounds is 0.04-0.14 nM. Thirty-eight less active analogs including aryl phosphonates and aryl phosphates give I50s of 0.27-4730 nM. For highest potency the summation of length of the alkyl and alkoxy groups on phosphorus should be 12-16 atoms (carbons, oxygens, and phosphorus) (a terminal iodo substituent in this relationship is equivalent to a propyl group). In general, the phosphonofluoridates and phosphorofluoridates are more active than analogs with leaving groups other than fluorine, i.e., phenoxy, 4-nitrophenoxy, 4-cyanophenoxy, 3,4-dichlorophenoxy, and 4H-1,3,2-benzodioxaphosphorin. Considering the exceptional potencies of ethyl and 2-iodoethyl octylphosphonofluoridates (I50s of 0.04 and 0.09 nM, respectively), it is not surprising that at ip doses of 10-30 mg/kg they inhibit brain NTE by 82-97% 48 h after treatment. However, unexpectedly, only the ethyl but not the 2-iodoethyl compound induces OPIDN, possibly associated with the greater ease of aging for NTE inhibited with the ethyl than the 2-iodoethyl compound (as observed in vitro both spontaneously and on induction by potassium fluoride). The high potency of ethyl octylphosphonofluoridate and several analogs as NTE inhibitors suggests that they are useful probes in determining the toxicological features of this secondary lesion for organophosphorus poisoning.

Animals↗
PubMed1989

Biochemical and clinical tests of the delayed neuropathic potential of some O-alkyl O-dichlorophenyl phosphoramidate analogues of methamidophos (O,S-dimethyl phosphorothioamidate).

The interaction in vivo of four O-alkyl O-2,5-dichlorophenyl phosphoramidates with neural neuropathy target esterase (NTE) and acetylcholinesterase (AChE) and their ability to cause delayed polyneuropathy in hens has been examined. Previous studies in vitro (Vilanova, Johnson & Vicedo, Pestic. Biochem. Physiol., 28 (1987) 224) had led to the prediction that these compounds would not be neuropathic but, rather, would be prophylactic agents against organophosphorus-induced delayed polyneuropathy. In vivo the effects of these esters on the enzymes differ in 2 respects from effects in vitro: (i) Relative sensitivity of the enzymes was different: thus greater than 50% of brain NTE remained 24 h after an oral dose of 15 mg/kg of the n-hexyl ester while only 10-30% of AChE remained although NTE was the more sensitive enzyme in vitro; (ii) In no case could the inhibited NTE or AChE in autopsy samples from birds dosed with any of the 4 esters be reactivated by treatment with potassium fluoride in vitro: the inhibited enzymes produced by incubation of tissue with the esters in vitro had been reactivatable. Prophylaxis, with therapy in some cases, was required to prevent acute anticholinesterase poisoning when doses were sufficient to cause high inhibition of neural NTE. Inhibition in brain was typically 5-10% more than in spinal cord and 10-15% more than in sciatic nerve. Unambiguous signs of polyneuropathy (Grade 3 or more on an 8-point scale) were not seen in birds observed up to 3 weeks after doses which caused less than 70% inhibition of NTE in brain and spinal cord or less than 60% inhibition in sciatic nerve of pair-dosed birds assayed 24 h after dosing. Doses of 300, 10, 100 and 65 mg/kg, respectively, of the methyl, ethyl, n-butyl and n-hexyl esters caused greater than 70% inhibition of NTE in all 3 neural tissues and neuropathy in the majority of observed birds. Analysis of consolidated dose/response data from 36 assayed and 51 observed birds showed that effects of Grade 3 or more were produced in about 90% of birds when inhibition of NTE was greater than 90% in brain, greater than 85% in spinal cord or greater than 75% in sciatic nerve.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

An electrophysiologic and ultrastructural study of the phenylmethanesulfonyl fluoride protection against a delayed organophosphorus neuropathy.

The delayed organophosphorus neuropathy caused by diisopropylfluorophosphate (DFP) can be prevented by pretreatment with phenylmethanesulfonyl fluoride (PMSF). A single injection of DFP (2 mg/kg) into a cat femoral artery produced a delayed neuropathy in the injected leg. Clinical neurotoxic signs in the DFP treated leg were most prominent at 21 to 28 days after DFP administration: a high-step gait with some tip-toe walking. During that time the capacity of the cat soleus alpha-motor nerve terminals to generate a stimulus-evoked repetitive discharge, known as SBR, was greatly attenuated. At that time, the ultrastructure of the motor nerve terminals demonstrated prominent alterations that correlated well with the motor nerve terminal SBR deficit. These alterations included the presence of extensive whorls in nerve terminals and axoplasms, the retraction and disruption of nerve terminals from the synaptic cleft, and a widening of secondary junctional folds. From the sampled population, the incidence of normal terminals in soleus muscles of the DFP-treated leg was only 2%. Cats which received PMSF (30 mg/kg ip) 24 hr before DFP administration did not develop any neurotoxic signs. Motor movements were normal. The SBR function of the soleus alpha-motor nerve terminals was not lost and its incidence approached normal values. Moreover, the ultrastructure was normal in 86% of examined neuromuscular junctions in the PMSF pretreated DFP cats. Thus, in this model, pretreatment with PMSF protected cats against the delayed neurotoxic effects of organophosphorus poisoning.

Animals↗
PubMedDate not supplied

Can we protect everybody from drinking water contaminants?

Dozens of chemicals, both natural and manmade, are often found in drinking water. Some, such as the natural contaminants uranium and arsenic, are well-known toxicants with a large toxicology database. Other chemicals, such as methyl tertiary-butyl ether (MTBE) from leaking fuel tanks, we learn about as we go along. For still others, such as the alkyl benzenes, there are very little available data, and few prospects of obtaining more. In some cases, chemicals are purposely added to drinking water for beneficial purposes (e.g., chlorine, fluoride, alum), which may cause a countervailing hazard. Removing all potentially toxic chemicals from the water is virtually impossible and is precluded for beneficial uses and for economic reasons. Determination of safe levels of chemicals in drinking water merges the available toxicity data with exposure and human effect assumptions into detailed hazard assessments. This process should incorporate as much conservatism as is needed to allow for uncertainty in the toxicity and exposure estimates. Possible sensitive subpopulations such as unborn children, infants, the elderly, and those with common diseases such as impaired kidney function must also be considered. However, the range of sensitivity and the variability of toxicity and exposure parameters can never be fully documented. In addition, the validity of the low-dose extrapolations, and whether the toxic effect found in animals occurs at all in humans, is never clear. This publication discusses how these competing needs and uncertainties intersect in the development of Public Health Goals for uranium, fluoride, arsenic, perchlorate, and other highly debated chemicals.

Animals↗
PubMed1986

Induction of a heat shock puff by hypoxia in polytene foot pad chromosomes of Sarcophaga bullata.

The single large heat-responsive puff (hs puff) in polytene foot pad cells of fly pupae (Sarcophaga bullata) is shown to be inducible by oxygen deprivation but not, as in other systems, by reoxygenation following an hypoxic treatment. The ambient oxygen concentration must drop below 2% for the hs puff to be maximally induced but the puff is fully inducible and transcriptionally active even in the complete absence of oxygen. Lack of oxygen is also compatible with continued transport of puff materials (formation and dissipation of puff droplets at the hs locus). Hypoxia-induced hs puffs persist indefinitely (greater than 2 days) at maximal or intermediate size and only regress completely after oxygen is resupplied. The induction of the hs puff during hypoxia is highly specific and does not seem to involve activation of any other chromosomal loci, yet the reaction is not confined to the giant foot pad cells or to specific developmental stages. Azide poisoning of cultured foot pads simulates the in vivo effects of hypoxia. The induction of the hs puff by azide, heat, or other means is inhibited by sulfhydryl reagents (iodoacetamide, arsenite) and fluoride, but not by an inhibitor of substrate-linked phosphorylation (arsenate). Instead, arsenate, like other uncouplers (2,4-dinitrophenol) is an inducer of the hs locus. The hs puff can be fully induced by hypoxia at any temperature between 2 degrees and 45 degrees C. The rate of puff expansion is strictly temperature dependent and the temperature characteristics of this process are remarkably similar to those of a promoter RNA polymerase association.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

A fatality due to ingestion of hydrofluoric acid.

We report a fatal case of hydrofluoric acid (HF) ingestion with suicidal intent. Quantitation using an ion-selective electrode for fluoride in fresh bile, gastric contents, kidney, liver, skeletal muscle, urine, and vitreous humor yielded 6.5, 39.0, 10.0, 6.0, 4.5, 5.0, and 4.5 ppm, respectively. In addition to the unfixed specimens, fluoride ion was measured in the following fixed tissue: brain, heart, kidney, liver, pancreas, stomach, and heart. Tissues were measured directly and/or by using the technique of standard addition. Fluoride concentrations using either method were found to be comparable. Fluoride concentration in fresh tissue was consistent with toxicity, although the urine fluoride concentration was in the range observed for asymptomatic workers exposed to fluoride in air. Fixed tissue preparations revealed fluoride concentrations consistent with nonexposure, whereas examination of the formalin fixative revealed fluoride concentrations only slightly higher than negative control formalin. We conclude that fixed tissues are inappropriate for fluoride determination. This is the first case we are aware of that provides fluoride concentrations in skeletal muscle in a fatality involving HF ingestion.

Adult↗
PubMedDate not supplied

[Toxicological evaluation of the outgassing of tetrafluoroethylene-based thermostable polymeric materials during heating].

The purpose of this study was to investigate the composition and toxicity of fluoroplastic F-40 thermodestruction products at 300-500 degrees C and to identify the maximally allowable temperature for their safe use. When heated over 400 degrees C, the products of luoroplastic F-40 evolution included such compounds as hydrogen fluoride, fluro-organic compounds, carbon monoxide, formaldehyde. When heated at 500 degrees C, the thermodestruction products caused the highest mortality rate of mice. The pathogenesis and clinical development of fluoroplastic F-40 poisoning are primarily associated with fluoro-compounds. It is concluded that the temperature 300 degrees C is the maximum temperature at which tetrafluroethylene-based polymers can be used.

Animals↗
PubMed2000

Carbon monoxide stability in stored postmortem blood samples.

Carbon monoxide (CO) poisoning remains a common cause of both suicidal and accidental deaths in the United States. As a consequence, determination of the percent carboxyhemoglobin (%COHb) level in postmortem blood is a common analysis performed in toxicology laboratories. The blood specimens analyzed are generally preserved with either EDTA or sodium fluoride. Potentially problematic scenarios that may arise in conjunction with CO analysis are a first analysis or a reanalysis requested months or years after the initial toxicology testing is completed; both raise the issue of the stability of carboxyhemoglobin in stored postmortem blood specimens. A study was conducted at the Bexar County Medical Examiner's Office to evaluate the stability of CO in blood samples collected in red-, gray-, and purple-top tubes by comparing results obtained at the time of the autopsy and after two years of storage at 3 degrees C using either an IL 282 or 682 CO-Oximeter. The results from this study suggest that carboxyhemoglobin is stable in blood specimens collected in vacutainer tubes, with or without preservative, and stored refrigerated for up to two years.

Carbon Monoxide↗
PubMed1993

Age and disease-related changes in the mineral of bone.

Bone mineralization changes with age and disease. The distribution of mineral particles in a given bone (mineralization profile) has been studied using density fractionation as well as microradiography and electron backscattering imaging. The biological determinant of mineralization is the rate of turnover. During rapid growth and periods of high remodeling, mineralization is shifted towards lower mineral density (hypomineralization). During aging and periods of low remodeling, mineralization is shifted towards higher mineral densities (hypermineralization). Chemicals can also influence the mineralization profile of bone. Fluoride induces hypermineralization by stabilizing the apatite lattice and reducing bone mineral solubility, whereas strontium induces hypomineralization by loosening the apatite lattice and increasing bone mineral solubility. Drugs such as bisphosphonates induce hypermineralization by inhibiting resorption and acting as crystal poison. Finally, mineralization can be impaired by defects as in rickets and osteomalacia or made excessive by continuous accretion of mineral without resorption as in osteopetrosis.

Absorptiometry, Photon↗