Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ENDOTOXINS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,693 records · Page 94Linked to original sources
PubMed1998

Endotoxin reduces maximal oxygen consumption in hepatocytes independent of any hypoxic insult.

OBJECTIVE: The cause of the metabolic disturbances in sepsis remains uncertain, but there is increasing evidence suggesting that haemodynamic changes are not solely responsible. We addressed the question of whether endotoxin has a significant effect on cellular oxygen metabolism, independent of confounding haemodynamic defects. DESIGN: Prospective, controlled experimental study. SETTING: University Laboratory. MODEL: Human hepatocyte cell line. METHODS: The oxygen consumption rate (OCR) was calculated from the fall in oxygen tension in a sealed cuvette containing Hep G2 cells in suspension. The oxygen tension was measured by porphyrin phosphorescence half-life analysis. Resting OCR was measured in control cells and after 1, 6 and 24 h of endotoxin exposure. In a second series of experiments, resting and maximal OCR was measured after 6 and 24 h of endotoxin exposure and in control cells using the addition of a mitochondrial uncoupler (FCCP); this uncouples the respiratory chain from ATP synthesis, thereby removing negative feedback and allowing the respiratory chain to work at maximal rate. RESULTS: Endotoxin caused a rise in resting OCR at 1 h which was significant by 6 h but had returned to control values by 24 h. Maximal OCR also increased at 6 h, however exposure to endotoxin for 24 h significantly reduced maximal OCR compared to the control cells. CONCLUSIONS: Endotoxin has complex effects on cellular energy metabolism causing an initial rise in the oxygen consumption rate and a significant limitation in oxygen consumption capacity at 24 h. These complex effects would be in keeping with the varied responses seen in patients.

Cell Line↗
PubMed1999

Relationship of antibodies to endotoxin core to mortality in medical patients with sepsis syndrome.

OBJECTIVES: To assess the prognostic value of determining anti-endotoxin core antibodies (EndoCab) immunoglobulin (Ig)G and IgM in medical patients with sepsis syndrome in order to identify patient subgroups that may profit from endotoxin-neutralizing therapy. The findings were correlated with clinical outcome, endotoxin levels and sepsis score. DESIGN: Cohort study with a follow-up period of 30 days. SETTING: Medical intensive care units (2) of a university hospital. PATIENTS AND METHODS: Twenty-nine patients who fulfilled the criteria of sepsis syndrome and did not present with septic shock or had not been treated with antibiotics for more than 3 days were included in the study. Twenty-one intensive care patients without infections served as controls for antibody concentrations. INTERVENTIONS: Blood samples were obtained from indwelling arterial catheters or direct venipuncture on admission and daily thereafter until transfer to a regular unit. Sepsis scores were determined daily. RESULTS: The mortality rate at 30 days was 44.8% (13 out of 29). Sepsis patients had significantly lower initial EndoCab IgM and IgG concentrations than controls. Initial EndoCab IgG concentrations were significantly lower in non-survivors of sepsis syndrome but not in survivors compared to controls (median concentrations 51.5 vs 110.1 vs 245.4 MU/ml). EndoCab IgM and IgG were lower in non-survivors compared to survivors, though that difference failed to reach significance (p = 0.11 in both cases). Depletion of initial EndoCab IgM concentrations (defined as a value below the 10th percentile of a control population) was present in 15 patients, 9 of whom died, and depletion of IgG in five patients, four of whom died. EndoCab IgM and IgG concentrations rose concordantly in survivors and non-survivors in the course of the disease. Endotoxin levels were significantly higher in non-survivors compared to controls but not in survivors. A sepsis score of 21 and higher was associated with 90.9% mortality (specificity 93.8%, sensitivity 76.9%). CONCLUSIONS: Decreased EndoCab IgG concentrations are associated with increased mortality in medical patients with sepsis syndrome. The measurement of initial anti-endotoxin antibodies may provide a useful tool to identify septic patients who profit potentially from endotoxin neutralizing therapy, however considerable overlap of antibody concentrations warrants additional parameters. The sepsis score is easy to determine and useful in the evaluation of medical patients with sepsis.

Adult↗
PubMed2002

Effect of internal biliary drainage on plasma levels of endotoxin, cytokines, and C-reactive protein in patients with obstructive jaundice.

Preoperative biliary drainage may improve the cytokine and acute-phase response derangements observed in patients with obstructive jaundice. We conducted a prospective longitudinal, before-after trial in our 600-bed teaching hospital. Twenty-four patients with obstructive jaundice were investigated, 11 with benign obstruction and 13 with malignant disease. Endoscopic internal biliary drainage was performed in all patients (7 by papillotomy and 17 by endoprostheses). Endotoxin, tumor necrosis factor alpha (TNF-a), interleukin-6 (IL-6), nitric oxide production, and C-reactive protein (CRP) were determined at admission and on days 2 and 7 after internal biliary drainage was accomplished. Bile cultures were obtained before and at the time of drainage. Endotoxin, IL-6, TNF-a, and CRP were significantly higher in patients with cancer. After internal drainage, endotoxin (11.4 vs. 2 EU/L; p <0.05), TNF-a (87.5 vs. 48 pg/ml; p = 0.03), and IL-6 (324 vs. 232 pg/ml; p <0.05) plasma levels decreased significantly in the early postdrainage period in patients with cancer. Endotoxin, cytokines, as well as the CRP plasma values, however, increased again on day 7 after drainage. This trend was less marked in patients with benign obstruction. Patients with positive bile cultures after drainage displayed higher levels of CRP (115 vs. 62 mg/L; p = 0.03), IL-6 (598 vs. 330 pg/ml; p = 0.04), and endotoxin (10.6 vs. 4.8 EU/L; p = 0.02) than those with negative bile cultures. Biliary tract obstruction is associated with an increase in endotoxin levels, a positive acute-phase response, and plasma cytokine elevation. After biliary drainage a transitory improvement of these alterations was observed, although values remained high 1 week postdrainage. These findings were associated with positive bile cultures.

Adenocarcinoma↗
PubMed1999

Clinical relevance of antibiotic-induced endotoxin release in patients undergoing hepatic resection.

It has been proved that antibiotics binding to penicillin-binding protein 3 (PBP3) are associated with the greater release of endotoxin than those that bind to PBP2 in both in vitro and animal models. The aim of this study is to evaluate the potential clinical implications of antibiotic-induced endotoxin release after hepatic resection. Forty-five patients who underwent hepatic resection in our clinic were enrolled. The patients were divided into two groups. Group A (n = 26): antibiotics that bind primarily to PBP3, including cefmetazole (CMZ), latamoxef (LMOX), flomoxef (FMOX), were used. Group B (n = 19); antibiotics that bind to both PBP2 and PBP3, including cefazolin (CEZ), cefoperazone (CPZ), cefotiam (CTM). Postoperative complications, liver functional tests, and chemical mediators [endotoxin, interleukins (IL-6, IL-8), tumor necrosis factor alpha (TNFalpha), granulocyte colony-stimulating factor (G-CSF), hepatotrophic growth factor (HGF) were examined after hepatic resection. There were no significant differences in the backgrounds of the two groups. Eight patients in each group developed postoperative complications; in particular, 9 of 13 patients with biliary tract carcinoma developed postoperative complications. No significant elevation of peripheral blood endotoxin was noted by the endospecy method, in any of the patients, although six died following sepsis. Pre- and postoperative levels of cytokines showed no significant difference between the two groups. Our data suggest that clinical antibiotic-induced endotoxin release would not occur after hepatic resection regardless of the antibiotic, probably owing to continuous scavenging of endotoxin from peripheral blood.

Analysis of Variance↗
PubMed1999

Structural changes in the rat middle ear mucosa due to endotoxin and eustachian tube obstruction.

The middle ears of 48 rats were used to examine the effects of endotoxin injection, eustachian tube obstruction or a combination of eustachian tube obstruction and endotoxin injection. Animals were killed after 1, 2, 4, or 12 weeks and the middle ears processed for light and scanning electron microscopy. Compared to the normal middle ear mucosa, the epithelial layer was more pseudostratified, cuboidal or cylindrical after endotoxin injection or obstruction of the eustachian tube. In the early phase, numerous ciliated cells occurred in areas originally almost devoid of these cells. At 3 months, degeneration of ciliated cells was observed. The combination of eustachian tube obstruction and endotoxin injection also induced a more pseudostratified, cuboidal or cylindrical epithelium with an increased number of goblet cells. However, an early decrease occurred in the number of ciliated cells in the tympanic orifice of the eustachian tube. Furthermore, inflammatory cells, mainly PMNs, macrophages and lymphocytes, invaded the subepithelial layer after eustachian tube obstruction and endotoxin injection. These structural changes resulted in an impairment of the mucociliary transport system for clearance of the middle ear cavity. For this reason we believe that both endotoxin and eustachian tube obstruction or dysfunction play an important role in inducing persistent mucosal changes in the middle ear cavity, thereby prolonging otitis media with effusion.

Animals↗
PubMed1998

Longitudinal changes in inflammatory markers in nasal lavage of cotton workers. Relation to endotoxin exposure and lung function changes.

OBJECTIVES: The aim of this study was to evaluate time-related changes in inflammatory markers in nasal lavage (NAL) in relation to endotoxin exposure and lung function changes. METHODS: Endotoxin in cotton dust is well known to elicit proinflammatory mediators involved in acute or chronic respiratory inflammation due to cotton dust. We applied nasal lavage as well as lung function and exposure measurements in a small group (n = 11) of cotton workers during 6 weeks of observation (after 2 weeks free of exposure). Several inflammatory markers in NAL, such as interleukin 8 (IL-8), IL-6, and down-stream mediators, including soluble tumor necrosis factor receptor 75 (sTNF-R75) and soluble intercellular adhesion molecule 1 (ICAM-1), cell counts, marker of epithelial response (uric acid), and marker of plasma exudation (albumin) were measured. RESULTS: At the exposure levels examined in this study [cotton dust, geometric mean (GM) = 1.10 mg/m3; endotoxin, GM = 2,869 EU/m3], several inflammatory markers in NAL such as IL-8, sTNF-R75, and albumin tended to increase through the measurement period with increasing airborne endotoxin concentration (in six workers who had paired measurements in weeks 1 and 6). Although no statistical significance was reached, airborne endotoxin exposure and all inflammatory markers in NAL were relatively higher in cotton workers with a 6-week lung function decrease. CONCLUSION: The data suggest that inflammatory markers in NAL are associated with repeated airborne endotoxin exposure.

Adult↗
PubMed1986

Endotoxin: routes of transport in experimental peritonitis.

A quantitative endotoxin assay was applied in this study of endotoxin transport from the infected abdomen. In rats with fecal peritonitis, extremely high concentrations were found in thoracic duct lymph (approximately 400 times higher than those found in arterial and portal vein plasma). Taking flow rates into account, the thoracic duct carries 34 ng/hour and the protal vein 49 ng/hour after 2 hours of peritonitis. Endotoxin quantities transported by the portal vein never exceed the proposed endotoxin filtrating capacity of the liver. Furthermore, the onset of systemic endotoxemia parallels the appearance of endotoxin in the thoracic duct. The hypothesis put forward is that the development of systemic endotoxemia is mainly mediated by lymphatic transport. The results also indicate that endotoxin is normally absorbed from the intestine and transported by portal blood.

Animals↗
PubMed1992

Endotoxin release and tumor necrosis factor formation during cardiopulmonary bypass.

Endotoxin, when released into the systemic circulation during cardiopulmonary bypass (CPB), might induce activation of plasmatic systems and blood cells during CPB, in addition to a material-dependent blood activation during CPB. However, the role of endotoxin in the development of this so-called whole-body inflammatory reaction in CPB is still unclear. We investigated the release of endotoxin into the systemic circulation in relation with the activation of the complement system and in particular the formation of tumor necrosis factor in 10 patients undergoing CPB. Immediately after the start of CPB the endotoxin concentrations increased significantly (p less than 0.01), accompanied by increases in C3a concentration (p less than 0.05). After release of the aortic cross-clamp, there was a second increase in endotoxin followed by a continuous increase in tumor necrosis factor, reaching a peak concentration 1 hour after the end of CPB (p less than 0.01). These observations demonstrate a release of endotoxin into the systemic circulation associated with tumor necrosis factor formation, which contributes to the whole-body inflammatory reaction associated with CPB.

Aged↗
PubMed1996

The role of endotoxin and cytokines in the pathogenesis of odontogenic cysts.

Odontogenic cysts arise from tooth-forming epithelial residues. The stimulus for the formation of radicular cysts is thought to be endotoxin released from the infected necrotic tooth pulp. However, in keratocysts and follicular cysts, such a stimulus is not present. In order to investigate what drives the cyst epithelium to proliferate, explant media and fluids from 16 radicular cysts, eight keratocysts and seven follicular cysts and explant media from four specimens of non-inflamed gingival tissue were examined for the presence of endotoxin and cytokines. Cyst fluids were also cultured for 72 h in anaerobic and aerobic conditions to detect micro-organisms. Endotoxin from three different bacteria, cytokines [interleukin-(IL) 1 alpha, IL-1 beta and IL-6] as well as prostaglandin E2 (PGE2) were tested in an epithelial cell-proliferation assay. As the cyst epithelium is supported by a connective tissue capsule, the effect of fibroblast culture media on epithelial cell proliferation was also investigated. The results showed significantly higher concentrations of endotoxin in radicular cyst fluid than in the keratocyst or the follicular cyst. None of the cyst fluids contained micro-organisms. Immunoassays demonstrated the presence of IL-1 alpha and -6 in all fluids and explants tested; IL-1 beta was only found in the inflammatory radicular cysts. However, reverse transcriptase-polymerase chain reaction showed that mRNAs for IL-1 alpha, -1 beta and -6 were present in all cyst types. Proliferation studies indicated that endotoxin and the cytokines had a mitogenic effect on epithelia at low concentrations; PGE2 had very little effect at low concentrations, and had an inhibitory effect at high concentrations. Cyst fibroblast culture media had a mitogenic effect on the epithelia that was enhanced by the presence of endotoxin.

Aggregatibacter actinomycetemcomitans↗
PubMed1989

Endotoxin stimulates endothelin-release in vivo and in vitro as determined by radioimmunoassay.

A marked increase in immunoreactive endothelin was observed in rat serum collected within 10-15 min after infusion of endotoxin. Endothelin level was 117 +/- 11.5 pg/ml (mean +/- S.E., N = 4) in rats exposed to endotoxin as compared with undetectable levels (less than 2 pg/ml, N = 4) in controls. We have also observed a significant stimulation of endothelin-release by endotoxin from cultured bovine transformed thoractic aortic endothelial cells at concentrations of endotoxin ranging between 0.1 and 10.0 micrograms/ml. Serum was indispensable for the stimulating effect of endotoxin, although serum itself did not show any effect at the concentration used (1%). These results suggest that endothelin plays an important role in mediation of pathophysiological responses caused by endotoxin. The levels of endothelin were measured by radioimmunoassay with high sensitivity.

Animals↗
PubMed1993

A simple assay for ecto-5'-nucleotidase using intact pulmonary artery endothelial cells. Effect of endotoxin-induced cell injury.

Adenosine may be protective in acute vascular injury by inhibiting platelet aggregation and neutrophil oxidant release. In contrast, adenine nucleotides, which may be released with acute vascular injury, stimulate platelet aggregation and neutrophil oxidant release. Ectonucleotidases, membrane enzymes that catabolize extracellular nucleotides, are the primary mechanism for degrading circulating nucleotides to adenosine. Ecto-5'-nucleotidase converts extracellular AMP to adenosine. We hypothesized that endothelial cell injury alters ecto-5'-nucleotidase activity. Using a novel assay first reported by Jamal et al. (Biochem J 250: 369-373, 1988) with rat adipocytes, we studied the properties of ecto-5'-nucleotidase in intact monolayers of cultured bovine pulmonary artery endothelial cells (BPAEC) and examined the effect of endotoxin on enzyme activity. The assay uses a fluorescent analog of AMP, 1,N6-etheno-AMP (E-AMP), as the substrate for ecto-5'-nucleotidase, and measures ethenoadenosine (E-Ado) formation. Etheno-AMP in Hepes buffer, pH 7.4, at 22 degrees, was added to confluent monolayers of BPAEC; samples of supernatant were collected after various intervals, and E-AMP and E-Ado were quantitated by HPLC. Using these methods we found a Km of 15 +/- 6 microM, a pH optimum of 7.48, minimal effect of MgCl2 or CaCl2 at physiologic pH, and inhibition by alpha,beta-methylene ADP, a known 5'-nucleotidase inhibitor. We established that the monolayer assay was indeed measuring cell surface associated 5'-nucleotidase. To determine the effect of endotoxin, we incubated confluent monolayers with endotoxin in Minimal Essential Medium plus 10% fetal bovine serum for 24 hr, washed them, and assessed the conversion of E-AMP to E-Ado by the endotoxin-injured cells. Endotoxin stimulated endothelial ecto-5'-nucleotidase activity. This increase in 5'-nucleotidase activity in response to endotoxin injury may represent an important clearance mechanism for circulating adenine nucleotides and may be protective in acute vascular injury by increasing adenosine production.

5'-Nucleotidase↗
PubMed1991

Endotoxin impairs the response of rat anococcygeus muscle to electrical field stimulation.

Rat anococcygeus muscles were isolated 4 h after treatment with either E. coli endotoxin (20 mg kg-1 i.p.) or saline. The contractile responses of the muscle to electrical field stimulation, and to the alpha 1-adrenoceptor agonist cirazoline were impaired by endotoxin treatment. Inhibition of the L-arginine pathway with L-NG-nitro arginine methylester (3 x 10(-5) M) failed to restore responsiveness to either electrical field stimulation or to cirazoline. Endotoxin impaired inhibitory responses to electrical field stimulation in preparations precontracted with cirazoline. Responsiveness to sodium nitroprusside was also impaired by endotoxin under these conditions. These results show an impairment by endotoxin of both contractile and inhibitory responses of the rat anococcygeus muscle to electrical field stimulation. The impairment appears to be post-junctional. In contrast to the findings in vascular smooth muscle, the endotoxin-induced impairment of contractile responses does not appear to involve the L-arginine pathway.

Adrenergic alpha-Agonists↗
PubMed1992

The role of nitric oxide and platelet-activating factor in the inhibition by endotoxin of pentagastrin-stimulated gastric acid secretion.

Administration of E. coli endotoxin (1 mg/kg i.v.) abolished the acid secretory response induced by a bolus injection of pentagastrin (100 micrograms/kg i.v.) in the continuously perfused stomach of the anaesthetized rat. Endotoxin administration did not modify mean systemic arterial blood pressure. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME; 5-20 mg/kg i.v.), but not dexamethasone (5 mg/kg s.c. twice) or indomethacin (5 mg/kg i.m.), substantially restored the secretory responses to pentagastrin. The actions of L-NAME were reversed by the prior administration of L-arginine (100 mg/kg i.v.), but not by its enantiomer D-arginine (100 mg/kg i.v.). L-NAME (10 mg/kg i.v.) increased blood pressure but this does not seem to be the mechanism by which endotoxin-induced acid inhibition was prevented, since similar systemic pressor responses induced by noradrenaline (15 micrograms/kg per min i.v.) had no such effect. The platelet-activating factor (PAF) receptor antagonist, WEB 2086 (2 mg/kg), induced a partial reversal of the inhibition by endotoxin of acid responses to pentagastrin. In endotoxin-treated rats, the combined administration of L-NAME (10 mg/kg) and WEB 2086 (2 mg/kg) completely restored the degree of H+ output induced by pentagastrin to levels similar to those of control, vehicle-treated animals. These findings suggest that endotoxin-induced acute inhibition of acid responses to pentagastrin involves NO synthesis and the release of PAF.

Amino Acid Oxidoreductases↗
PubMed1995

Involvement of bradykinin in endotoxin-induced vascular permeability increase in the skin of rats.

The aim of the present study was to investigate the role of bradykinin as well as that of platelet-activating factor in the endotoxin-induced acute vascular permeability increase in the dorsal skin of rats by use of kininogen-deficient and normal Brown-Norway rats. In the kininogen-deficient rats, the dose-dependent dye exudation induced by endotoxin was about one half of that in the normal rats at any doses of endotoxin tested (0.1-1.0 mg per site), whereas the dose-response curves obtained by bradykinin (1-100 nmol per site), platelet-activating factor (0.1-1 nmol per site) or histamine (50-500 nmol per site) were the same in both rats. This effect induced by endotoxin in the kininogen-deficient rats was not changed by pretreatment with a bradykinin B2 receptor antagonist, HOE140 (D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin, 1 mg kg-1 i.v.), whereas the endotoxin-induced response in the normal rats was attenuated by the receptor antagonist. These responses in both kininogen-deficient and normal rats were significantly inhibited by a selective platelet-activating factor antagonist, TCV309 (3-bromo-5-[N-phenyl-N-[2-[[2-(1,2,3,4,-tetrahydro-2- isoquinolylcarbonyl-oxy)-ethyl]-carbamoyl]-ethyl]carbamoyl]-1-prop yl- pyridinium nitrate, 0.1 mg kg-1 i.v.). These results suggest that bradykinin could be one of the major mediators in the endotoxin-induced vascular permeability increase in rat skin in addition to platelet-activating factor.

Animals↗
PubMed1990

Correlation between endotoxin-neutralizing capacity of human plasma as tested by the limulus-amebocyte-lysate-test and plasma protein levels.

In the present study the endotoxin-neutralizing capacity of human plasma obtained from healthy volunteers was determined by use of the limulus-amebocyte-lysate test. The extent of the endotoxin-neutralizing capacity which showed a very broad variation was correlated to the plasma levels of some proteins which are believed to contribute to endotoxin transport and detoxification. The plasma levels of alpha 2-macroglobulin and transferrin, the major transport proteins, as well as the levels of IgG, IgA and IgM and apoprotein A were not significantly correlated to the neutralizing capacity. Only the apoprotein B, the major apoprotein of the low density lipoprotein fraction shows a significant correlation. Together with previously published results it should be concluded that low density lipoproteins are involved in the endogenous endotoxin-neutralizing reaction occurring in human plasma, at least when high doses of endotoxin are administered. Nevertheless the endotoxin-neutralizing reaction seems to be a very complex multistep process.

Apolipoproteins A↗
PubMed1992

Hemodynamic effects of endotoxin and platelet activating factor in cirrhotic rats.

Acute infections may influence the hemodynamic alterations of liver disease. Therefore, the hemodynamic effects of endotoxin (LPS E. coli 0111:B4) in conscious, normal, and cirrhotic rats were compared. Endotoxin decreased cardiac index in cirrhotic but not in normal rats. Although the effect of endotoxin on portal tributary blood flow was minor in all animals, a reduction in portal pressure was found in cirrhotic rats. Because the most marked hemodynamic effects were observed in cirrhotic rats, the second part of our study investigated whether platelet activating factor played a role in endotoxin-induced hemodynamic alterations in the cirrhotic model. Platelet activating factor reduced cardiac index and kidney blood flow but did not influence portal tributary blood flow. Two antagonists to platelet activating factor reduced the adverse renal blood flow lowering effects of endotoxin in cirrhotic rats. Thus, it is suggested that the hemodynamic changes observed in cirrhosis may be aggravated during acute infections. Under this condition, antagonists to platelet activating factor may be of benefit in the prevention of hemodynamic complications induced by endotoxin.

Animals↗
PubMed1987

Effect of repeated endotoxin treatment and hypercholesterolemia on preatherosclerotic lesions in weaned pigs. Part 1. Scanning and transmission electron microscopic study.

Endothelial cell damage is considered to be the primary event in atherogenesis. In this study we compared the effects of mild hypercholesterolemia and repeated E. coli endotoxin infusions on the endothelial cells of the coronary arteries of the pig. We divided 24 pigs into 4 groups: I: controls on normal diet; II: normal diet and endotoxin treatment; III: fat-supplemented diet; IV: fat-supplemented diet and endotoxin treatment. The animals on a fat-supplemented diet showed the most frequent and most severe endothelial cell damage. The damage was less when this diet was combined with endotoxin treatment. Endotoxin reduced the serum total cholesterol level (P less than 0.01). The cholesterol level correlated very significantly (P less than 0.001) with endothelial damage of the coronary arteries. Mild hypercholesterolemia (s-cholesterol 5.68 mmol/l, controls 2.28 mmol/l) was thus associated with toxic effects in the endothelial cells. The E. coli endotoxin infusions did not have any cumulative effect on the lesions.

Animals↗
PubMed1992

Specific assay for endotoxin using immobilized histidine, Limulus amoebocyte lysate and a chromogenic substrate.

The Limulus amoebocyte lysate (LAL) test is inhibited or enhanced by many substances. In order to overcome this problem, a specific endotoxin assay method using a membrane filter unit, a chromogenic LAL reagent, and immobilized histidine (which is a specific adsorbent for endotoxins) was developed. Endotoxins are quantitatively adsorbed on immobilized histidine. The adsorbed endotoxins are separated from LAL-inhibiting or -enhancing substances by the membrane filter unit, and their activities are directly assayed with the LAL reagent in a filter cup without any inhibition or enhancement. The reproducibility and the accuracy of this method are high. This new endotoxin assay method using immobilized histidine can be used for the determination of endotoxins in a solution containing LAL-inhibiting or -enhancing substances such as amino acids and antibiotics, as an alternative to the more common gel-clot technique.

Adsorption↗