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At least 1,783 records · Page 99Linked to original sources
PubMed1976

Evaluation of redox state of isolated perfused rat lung.

The metabolic responsiveness of lung tissue to inhibition of oxidative metabolism was determined by measurement of the redox state of the isolated perfused and ventilated rat lung. Changes in redox state were evaluated by fluorescence from the lung surface at wavelengths suitable for reduced pyridine nucleotides and by measurement of the ratios of redox couples in rapidly frozen lung tissue. Maximal change of redox state was observed during ventilation with carbon monoxide; surface fluorescence increased 6.6%, lactate/pyruvate increased 5.8 times, glycerol 3-P/dihydroxyacetone-P increased fourfold and glutamate/alpha-ketoglutarate doubled. KCN infusion resulted in similar changes. Hypoxia produced with N2 ventilation resulted in less than maximal changes in redox couple ratios until alveolar PO2 was reduced below 0.1 mmHg. Redox changes observed during infusion of 0.5 mM aminoxyacetic acid suggested that maintenance of cytoplasmic redox state depended on functioning of a malate-aspartate "shuttle." The isolated perfused lung appears suitable to study factors controlling pulmonary parenchymal oxidative metabolism. The results emphasize the need for ventilation with CO to establish intracellular anoxia.

Amobarbital↗
PubMed1976

Oxygen delivery in perfused rat kidney: NADH fluorescence and renal functional state.

Changes in steady-state levels of reduced pyridine nucleotide (PN) recorded by continuous monitoring of surface fluorescence were correlated with changes in physiological function of perfused rat kidneys when subjected to anoxia, ischemia, hypothermia, variations in perfusion pressure, inhibition of Na-K ATPase, and uncoupling of oxidative phosphorylation. Biphasic responses of PN reduction and oxidation during ischemic cycles at varying temperatures and anoxic cycles at different perfusion pressures demonstrated the presence of two different cell populations in the kidney cortex, those with sufficient oxygen and those without. The magnitude of PN fluorescence change during ischemia increased with decreasing temperature demonstrating better tissue oxygenation during hypothermia. The measurement of mitochondrial NADH oxidation in the perfused kidney during transitions from CO anoxia to normoxia was made possible by flash photolytic activation of mitochondrial electron transport. The half time for NADH oxidation (125 ms) was independent of the rate of oxygen delivery while the initial rate and extent of reaction was faster and steeper, respectively, at higher perfusion pressure, due to a better tissue oxygenation and faster CO washout.

Adenosine Triphosphatases↗
PubMed1983

Fume inhalation chloracne.

Chloracne in a factory worker manufacturing sodium pentachlorophenate, triggered by inhalation of fumes, is reported.

Acne Vulgaris↗
PubMed1989

Metabolism of triiodothyronine in rat hepatocytes.

The metabolism of T3 by isolated rat hepatocytes was analyzed by Sephadex LH-20 chromatography, HPLC, and RIA for T3 sulfate (T3S) and 3,3'-diiodothyronine (3,3'-T2). Type I iodothyronine deiodinase activity was inhibited with propylthiouracil (PTU), and phenol sulfotransferase activity by SO4(2-) depletion or with competitive substrates or inhibitors. Under normal conditions, labeled T3 glucuronide and I- were the main products of [3'-125I]T3 metabolism. Iodide production was decreased by inhibition (PTU) or saturation (greater than 100 nM T3) of type I deiodinase, which was accompanied by the accumulation of T3S and 3,3'-T2S. Inhibition of phenol sulfotransferase resulted in decreased iodide production, which was associated with an accumulation of 3,3'-T2 and 3,3'-T2 glucuronide, independent of PTU. Formation of 3,3'-T2 and its conjugates was only observed at T3 substrate concentrations below 10 nM. Thus, T3 is metabolized in rat liver cells by three quantitatively important pathways: glucuronidation, sulfation, and direct inner ring deiodination. Whereas T3 glucuronide is not further metabolized in the cultures, T3S is rapidly deiodinated by the type I enzyme. As confirmed by incubations with isolated rat liver microsomes, direct inner ring deiodination of T3 is largely mediated by a low Km, PTU-insensitive, type III-like iodothyronine deiodinase, and production of 3,3'-T2 is only observed if its rapid sulfation is prevented.

Animals↗
PubMed1990

Effects of sulfur-containing metabolites of hexachlorobenzene on the heme metabolic enzymes in rat liver.

Effects of hexachlorobenzene (HCB) and its sulfur-containing metabolites on the heme metabolic enzymes in rat liver were investigated. A single injection of HCB caused the increase in activities of delta-aminolevulinic acid (ALA) synthetase and heme oxygenase, and contents of cytochrome P-450 and total heme. After a single injection of pentachlorothioanisol (PCTA) or pentachlorophenyl methyl sulfore (PCPSO2Me), ALA synthetase activity was enhanced. Heme oxygenase activity was increased by PCPSO2Me treatment. Cytochrome P-450 and total heme contents were increased by PCPSO2Me or 1,4-bis(methylthio)tetrachlorobenzene (MTTCB). When HCB was injected once daily for 5 weeks, a marked increase in ALA synthetase activity, a significant decrease in ALA dehydratase, almost complete inhibition of uroporphyrinogen decarboxylase activity, and an increased excretion of total porphyrin in the urine were shown. After chronic treatment with its sulfur-containing compounds, PCPSO2Me and MTTCB produced a significant increase in ALA synthetase activity. However, activities of ALA dehydratase and uroporphyrinogen decarboxylase, and excretion of total porphyrin in the urine were unaltered. At this time, the concentrations of the corresponding sulfur-containing compound and related metabolite(s) in blood, liver and kidney were nearly the same as those observed in HCB-treated rats. It is suggested that PCPSO2Me and MTTCB could induce the hepatic ALA synthetase, but, these metabolites, and also PCTA, were not able to induce the porphyria in female rats, and the induction of porphyria by HCB is not attributable to the action of its sulfur-containing compound.

5-Aminolevulinate Synthetase↗
PubMed2004

Activities of UDP-glucuronyltransferase, beta-glucuronidase and deiodinase types I and II in hyper- and hypothyroid rats.

We have investigated the hypothesis that uridine 5'-diphosphate (UDP)-glucuronyltransferases (UGTs) and beta-glucuronidase are jointly involved in a mechanism for the storage and mobilization of iodothyronine metabolites in liver, kidney, heart and brain. Specifically, we predicted UGT activities to decrease and increase respectively, and beta-glucuronidase activity to increase and decrease respectively in hypo- and hyperthyroidism. To this end we have studied the effects of thyroid status on the activities of different enzymes involved in thyroid hormone metabolism in liver, kidney, heart and brain from adult rats with experimentally induced hypo- and hyperthyroidism. We used whole organ homogenates to determine the specific enzyme activities of phenol- and androsteron-UGT, beta-glucuronidase, as well as iodothyronine deiodinase types I and II. Deiodinase type I activities in liver and kidney were decreased in hypothyroid animals and, in liver only, increased in hyperthyroidism. Deiodinase type II activity was increased in hyperthyroid rat kidney only. Interestingly, in the heart, deiodinase type I-specific activity was increased fourfold, although the increase was not statistically significant. Cardiac deiodinase type I activity was detectable but not sensitive to thyroid status. Hepatic phenol-UGT as well as androsteron-UGT activities were decreased in hypothyroid rats, with specific androsteron-UGT activities two to three orders of magnitude lower than phenol-UGT activities. Both UGT isozymes were well above detection limits in heart, but appeared to be insensitive to thyroid status. In contrast, cardiac beta-glucuronidase activity decreased in hypothyroid tissue, whereas the activity of this enzyme in the other organs investigated did not change significantly. In summary, cardiac beta-glucuronidase, albeit in low levels, and hepatic phenol-UGT activities were responsive only to experimental hypothyroidism. Although a high basal activity of the pleiotropic beta-glucuronidase masking subtle activity changes in response to thyroid status cannot be ruled out, we conclude that hepatic, renal and cardiac UGT and beta-glucuronidase activities are not regulated reciprocally with thyroid status.

Animals↗
PubMed1983

Sources of uncertainty in pharmacokinetic prediction.

Assessment of the hazard associated with residues in food animals must be based on an accurate estimate of the residue levels present in the final food product, as well as animal toxicology studies to determine the potential untoward effects of these residues. Extrapolation of residue levels or toxic effects produced by the administration of a chemical in one species to predict residue levels or toxicology that may be produced by lower doses in the same species or by equivalent or lower doses in another species is associated inextricably with knowledge of the pharmacokinetics of the chemical. There are several factors that may influence the pharmacokinetics of xenobiotics which, if left unconsidered, may introduce uncertainty in the predictions of toxicity following any chemical exposure. Two of these factors are dose level and species differences. Because initial toxicity studies are designed to characterize the type of toxicity and to elucidate target organ effects the use of high doses is the accepted practice. However, because biotransformation and excretion of many chemicals are capacity-limited processes, extrapolation of toxicity to lower doses, without adequate pharmacokinetic information at those lower dose levels may result in overestimation of predicted toxicity. Furthermore, determination of tissue residue levels following administration of doses that saturate these processes may result in an overestimation of residues remaining following lower doses. Finally extrapolation of toxicity results across species may result in an over or underestimation of hazard without adequate information on the pharmacokinetics of the chemical in both species.

Animals↗
PubMed1992

Conjugation of polychlorinated agrochemical sulphoxides and sulphones by glutathione.

1. Pentachlorophenyl methyl sulphoxide and pentachlorophenyl methyl sulphone were found to be substrates for microsomal and cytosolic glutathione-S-transferase of rabbit, monkey, chicken and human liver, covalently immobilized on beaded sepharose. 2. Protein was immobilized with greater than 95% transferase activity, measured by dinitrochlorobenzene. Immobilized rabbit liver microsomal transferase activity was more stable than immobilized cytosolic activity. 3. The sulphoxide moiety was displayed by glutathione in the presence of chicken liver microsomal protein. The sulphone moiety was displayed by glutathione in the formation of a diglutathione under catalysis by rhesus monkey liver cytosolic and microsomal protein. 4. Chlorine was displaced by transferases from all species to form regioisomeric monoglutathiones. 5. Qualitative and quantitative differences were observed in product distributions between species and between microsomal and cytosolic protein.

Agriculture↗
PubMed1981

Raman spectroscopic investigations on conformational changes induced by some phenol derivatives on phospholipid membranes.

Some phenol derivatives which uncouple oxidative phosphorylation in mitochondria alter the dipalmitoylphosphatidylcholine membrane structure in the same way that elevating the temperature does. Below the transition temperature, they disorder the membrane gel-phase by inducing the pretransition situation at concentrations within significant biological limits. When the temperature is higher than Tm, their effect on the membrane structure is negligible. The comparison of these phenol derivatives having uncoupling activity with a phenol derivative which does not have such activity demonstrates that the latter does not induce a similar physical effect.

2,4-Dinitrophenol↗
PubMed1982

Chemicals in marine and coastal environments: the need for toxicological information.

The tremendous increase in the number and amount of chemicals produced and transported in past years has resulted in increasing problems with accidental spills and uncontrolled waste sites involving these chemicals. The United States government has accordingly developed a mechanism for responding to such incidents. As part of that mechanism, the Hazardous Materials Response Project serves to coordinate scientific activities and facilitate in the gathering of scientific information needed for response to chemical spill or waste site emergencies involving coastal waters. Inevitably, much information of a toxicological nature is required to adequately evaluate potential hazards and appropriate responses. The Hazardous Materials Response Project is also able to provide a framework for significant progress in scientific understanding because it can bring together and encourage collaboration among experts in the various disciplines which are relevant to the environmental toxicological problems encountered.

Accidents↗