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Query: UMLS:C0034067 (
emphysema
)
11,506
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Intraruminal doses of L-
tryptophan
cause acute pulmonary edema and
emphysema
in cattle. The D and L isomers of
tryptophan
and 22 related indolic compounds were incubated with ruminal microorganisms in vitro. Incubation of L-[U-benzene ring-(14)C]
tryptophan
with ruminal microorganisms for 24 h resulted in 39% of the added radioactivity being incorporated into skatole, 7% into indole, and 4% into indoleacetate (IAA). D-Tryptophan was not degraded to any of these metabolites. The major pathway of skatole formation from L-
tryptophan
appeared to be by the decarboxylation of IAA. Incubation of [2-(14)C]IAA with ruminal microorganisms for 24 h resulted in 38% incorporation into skatole. L-[5-Hydroxy]
tryptophan
was degraded to 5-hydroxyskatole and 5-hydroxyindole, whereas 5-hydroxyindoleacetate was degraded to only 5-hydroxyskatole. Incubation of indolepyruvate, indolelactate, and indolealdehyde with ruminal microorganisms resulted in the formation of both skatole and indole. Under similar conditions, indoleacetaldehyde was converted to IAA and tryptophol. The addition of increasing concentrations of glucose (0 to 110 mM) reduced the formation of both skatole and indole from L-
tryptophan
and resulted in the accumulation of IAA. Antibiotics reduced the degradation of L-
tryptophan
to skatole and indole, with kanamycin and neomycin particularly effective in reducing the decarboxylation of IAA to skatole.
...
PMID:Dissimilation of tryptophan and related indolic compounds by ruminal microorganisms in vitro. 454 42
Microorganisms from rumen converted L-
tryptophan
and indoleacetic acid to 3-methylindole in vitro. Oral doses of 3-methylindole caused interstitial pulmonary edema and
emphysema
in cattle and goats. Intravenous infusion of this metabolite also induced pulmonary disease in cattle. These results demonstrate than an end product of ruminal fermentation of
tryptophan
can induce acute pulmonary disease in cattle and goats.
...
PMID:Induction of pulmonary edema and emphysema in cattle and goats with 3-methylindole. 501 84
3-Methylindole (3MI), the main ruminal fermentation product of L-
tryptophan
, causes acute pulmonary edema and interstitial
emphysema
in ruminants. Intravenous infusion of 3MI in goats causes necrosis and sloughing of pneumocytes and bronchial epithelial cells. Previous studies indicate that a reactive metabolite or metabolites of 3MI bind covalently to tissue macromolecules in the lung and this binding is associated with the pneumotoxicity of 3MI. We undertook this autoradiographic study of 3MI covalent binding to test the hypothesis that reactive 3MI metabolite(s) bind to the lung cells susceptible to 3MI-induced injury. We infused goats with [3H]3MI and killed them either 0.5, 2 or 6 h after start of the infusion. Sections of fixed lung were extensively washed, alcohol dehydrated and embedded in plastic. Only covalently bound radioactivity remained. Silver grains were quantitated per area in the developed autoradiographs. There was a 2:1 ratio of binding to the small airway epithelium compared to the interalveolar septa in all the goats. Both ciliated and non-ciliated bronchiolar cells were labeled, as were both types I and II pneumocytes. Normal goat lung slices incubated in vitro with [3H]3MI were labeled in the same pattern. Inclusion of either of the inhibitors of cytochrome P-450, SKF-525-A or piperonyl butoxide significantly reduced this binding to both the pneumocytes and the bronchiolar cells. We consider these results supportive of our hypothesis that 3MI is metabolized to reactive intermediates by the epithelial cells of the lung, where they bind to macromolecules, which may cause cellular damage.
...
PMID:Autoradiographic evidence of 3-methylindole covalent binding to pulmonary epithelial cells in the goat. 620 22
Cattle with Pasteurella bronchopneumonia usually have a fever, abnormal respiratory sounds in the cranioventral lung fields, consolidation, pleuritis and abscesses. Lungworms primarily affect 4- to 6-month-old calves, which become febrile and dyspneic, with moist rales. Diagnosis is by fecal examination using the Baermann technic. Proliferative pneumonia usually affects stabled adults, which develop severe dyspnea and tachypnea. Diagnosis is by the history, clinical signs and lung biopsy. Acute bovine pulmonary
emphysema
is caused by ingestion of large amounts of L-
tryptophan
in lush pasture. Affected cattle have severe, acute dyspnea, an expiratory grunt and froth around the muzzle. Diagnosis is by the history and clinical signs. Bronchiolitis obliterans narrows the airways of older animals to cause dyspnea. A positive response to corticosteroids aids diagnosis. Anaphylaxis occurs in cattle of all types and ages and is precipitated by various antigens in a type-I hypersensitivity reaction. Use of atropine aids diagnosis. Allergic or hypersensitivity pneumonia is caused by an allergy to insecticides, dead ascarid larvae or the mold, Micropolyspora faeni. Diagnosis is by a history of insect fogger use, finding M faeni in the forage, and typical histologic lesions in lung samples. Cattle with caudal vena caval thrombosis have dyspnea, a fever, froth around the muzzle, an expiratory groan and hypergammaglobulinemia. Malignant catarrhal fever is diagnosed by a history of previous exposure to sheep and finding swollen lymph nodes, fever, neutropenia and arteritis.
...
PMID:Diagnosis of causes of respiratory diseases in cattle. 623 84
Ruminal bacteria can perform biochemical transformations on plant constituents that may affect the health of ruminant animals. Reactions carried out by ruminal bacteria on oxalates and some pyrrolizidine alkaloids include decarboxylation, hydrolysis and reduction steps. Prior exposure of ruminal bacteria to these substances increases the rate of detoxification, indicating an adaptive response by the bacteria to these substrates. The formation of toxic substances by ruminal bacteria also occurs and may involve similar reactions. Hydrolysis of cyanogenic glycosides and miserotoxins , reduction of nitrate and S-methylcysteine sulfoxide to nitrite and dimethyl disulfide can result in toxicity in ruminants. Similarly, the deamination and decarboxylation reactions associated with the degradation of
tryptophan
and tryosine result in the formation of 3-methylindole and p-cresol, which are toxic. Formation of 3-methylindole results from fermentation of
tryptophan
to indoleacetic acid, with subsequent decarboxylation of indoleacetic acid to 3-methylindole by a Lactobacillus sp. The 3-methylindole causes acute pulmonary edema and
emphysema
in ruminants as a result of mixed function oxidase metabolism in tissues. The 3-methylindole is also the cause of naturally-occurring acute bovine pulmonary edema and
emphysema
after abrupt pasture change. Inhibition of ruminal 3-methylindole formation by monensin and other antibiotics lowers ruminal 3-methylindole concentrations and prevents acute lung injury in experimental animals.
...
PMID:Ruminal metabolism of plant toxins with emphasis on indolic compounds. 637 6
Ozone decreased the trypsin, chymotrypsin, and elastase inhibitory activities of human alpha 1-proteinase inhibitor (alpha 1-PI) both in plasma and in solutions of the pure inhibitor. The total loss of porcine elastase inhibitory activity required 18 mol of ozone/mol of pure alpha 1-PI and approximately 850 mol of ozone/mol of alpha 1-PI in plasma. A corresponding loss of the ability to inhibit human leukocyte elastase was observed. Inactivated alpha 1-PI contains four residues of methionine sulfoxide, in addition to oxidized tyrosine and
tryptophan
. Electrophoretic analysis demonstrated that the ozone-inactivated alpha 1-PI did not form normal complexes witrh serine proteinases. These findings suggest that the inhalation of ozone could inactivate alpha 1-PI on the airspace side of the lung to create a localized alpha 1-PI deficiency, which might contribute to the development of
emphysema
.
...
PMID:Ozone inactivation of human alpha 1-proteinase inhibitor. 690 14
Indole and 3-methylindole (3MI) are ruminal metabolites of L-
tryptophan
(
TRP
) and have similar physical and chemical properties. 3-Methylindole causes acute bovine pulmonary
emphysema
(ABPE). The effects of indole when administered orally to cows were determined. Four mature Holstein cows were given increasing doses of 0.05, 0.1 and 0.2 g indole per kg body-weight orally at two-week intervals. The animals were killed one week after the last dose. Plasma indole concentrations peaked three house after administration at 4.5, 8.8 and 19.8 microgram per ml after the 0.05, 0.1 and 0.2 doses, respectively. Detectable concentrations of indole (more than 0.02 microgram per ml) persisted in the plasma from three to 25 hours after dosing. Packed cell volume was decreased (P less than 0.01) at 48 and 72 hours after the 0.2 g per kg dose and at 72 hours after the 0.1 g per kg dose. Plasma haemoglobin was increased (P less than 0.05) at 48 hours after the 0.2 and 0.1 g per kg doses. By 72 hours after the 0.2 g per kg dose, all cows had mild diarrhoea and haemolysis and two of the cows had haemoglobinuria. At necropsy, microscopic lesions of haemoglobinuric nephrosis were seen in all four cows. No lesions of ABPE were found in any of the animals.
...
PMID:Indole toxicity in cattle. 721 Apr 36
Available evidence supports the view that acute bovine pulmonary edema and
emphysema
(ABPE) is related to ruminal production of 3-methylindole (3MI) from L-
tryptophan
(
TRP
). Ruminal production of 3MI is a two-step process involving the conversion of
TRP
to indoleacetic acid (IAA) followed by decarboxylation of IAA and 3MI. Reduction in ruminal 2MI production by the inhibition of either of these processes may prevent the onset of ABPE. A closed-system, in vitro ruminal fermentation technique was used to screen 27 compounds for their ability to reduce the conversion of
TRP
to 3MI. Several compounds tended to reduce 3MI production at both 25 and 5 micrograms/ml. Desoxysalinomycin, X-206, chloral hydrate, nigericin, lasalocid, monensin, narasin and salinomycin all reduced 3MI production by more than 80% at 5 micrograms/ml without reducing total VFA production. All of these compounds, except chloral hydrate, are polyether antibiotics. At least part of the inhibition due to monensin and narasin occurs at the level of
TRP
conversion to IAA.
...
PMID:Inhibition of ruminal degradation of L-tryptophan to 3-methylindole, in vitro. 741 Feb 74
The pathogenesis of acute bovine pulmonary oedema and
emphysema
(ABPE) is related to the ruminal formation of 3-methylindole (3MI) from L-
tryptophan
(
TRP
), a naturally occurring amino acid and constituent of forage. The objectives of the present study were to determine whether monensin and lasalocid, both polyether antibiotics, were effective in reducing ruminal conversion of
TRP
to 3MI in vivo and to confirm that reduction in ruminal conversion of
TRP
to 3MI prevented
tryptophan
induced ABPE. Sixteen mature Hereford cows were assigned to one of four groups and given
TRP
to induce ABPE. Group 1 was given 100 mg monensin orally twice daily starting one day before and ending four days after
TRP
dosing. Group 2 was given 200 mg monensin once daily and group 3 was given 100 mg lasalocid twice daily. Group 4, the control, was given only
TRP
without further treatment. All control cows developed clinical signs of respiratory disease and lesions of ABPE; one control cow died of ABPE. Mean ruminal 3MI concentrations in control cows reached a peak of 36.4 micrograms per ml. Clinical signs of pulmonary disease appeared in two cows treated with lasalocid and one died. Mean ruminal 3MI in these animals peaked at 38.8 micrograms per ml. No clinical signs of respiratory disease were observed in any of the monensin treated cows and at necropsy there were no pulmonary lesions of ABPE. Mean ruminal 3MI concentrations in monensin treated cows did not exceed 8.9 micrograms per ml. In all groups plasma 3MI concentrations generally reflected ruminal 3MI concentrations but at lower concentrations. The results of this experiment demonstrate that reduction in ruminal 3MI formation by monensin prevents
tryptophan
induced ABPE.
...
PMID:Prevention of tryptophan-induced acute bovine pulmonary oedema and emphysema (fog fever). 746 89
3-Methylindole (3-MI) is a metabolite of
tryptophan
that causes acute pulmonary edema and
emphysema
in ruminants when administered orally or intravenously. Electron paramagnetic resonance (EPR) spin-trapping techniques have been used to investigate the in vitro and in vivo formation of free radicals during 3-MI metabolism by goat lung. Utilizing C-phenyl-N-tert-butyl nitrone (PBN), a nitrogen-centered free radical has been detected from 3-MI in goat lung microsomal incubation. The EPR spectrum of the spin adduct is identical to that observed when 3-MI is irradiated with ultraviolet light. The formation of a nitrogen-centered 3-MI free radical is followed by the appearance of a carbon-centered radical in microsomal preparations. The objective of the present study is to prove that the nitrogen-centered radical generated from the 3-MI incubation system is a 3-MI radical utilizing [14C]-3 MI and the EPR-HPLC technique. The HPLC chromatogram includes three peaks that give EPR signals. These peaks are assigned to nitrogen-, oxygen- and carbon-centered radical adducts. The polarity of the three peaks follows the order: carbon-centered radical adduct > oxygen-centered radical adduct > nitrogen-centered radical adduct. The last has a polarity that is weaker than 3-MI. Only the nitrogen-centered peak and the 3-MI peak possessed radioactivity. The retention time of the nitrogen centered radical is the same as the spin adduct generated by 3-MI irradiation with ultraviolet light. These results demonstrate that the nitrogen-centered radical is a 3-MI-PBN spin adduct, and supports the hypothesis that 3-MI-induced lung damage results from activation of 3-MI to a free radical. Also, in this study the stability of the radical spin adducts and the best conditions to produce the radicals in the incubation system was investigated.
...
PMID:Identification of 3-MI-derived N-centered radicals obtained from incubation of 3-MI with microsomal-NADPH system by EPR-HPLC spin trapping. 795 63
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