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Biomedical subjects

M Janssen

Publications and source records attributed to M Janssen.

At least 109 records · Page 6Linked to original sources
PubMed1993

In vitro and ex vivo xanthine oxidoreductase activity in rat and guinea-pig hearts using hypoxanthine or xanthine as substrate.

Through oxyradical formation xanthine oxidoreductase (XOD) could play a role in the etiology of cardiac damage. Its measurement poses problems, due to little substrate specificity, self-inactivation and endogenous inhibitors. Perfusion of guinea-pig hearts with hypoxanthine gave rise to only little xanthine release; in contrast rat hearts showed vivid xanthine production. Therefore, xanthine breakdown was hypothesized to exceed its formation in guinea-pig hearts. The kinetics of both substrates for XOD in cardiac homogenates were therefore compared with those obtained in perfused hearts. Oxypurine contents and effluent catabolites were determined by HPLC. Regardless of substrate, Vmax values in homogenates were about 38 and 13 mU/g for rat and guinea-pig heart, respectively. Km values were in the 3-5 microM range; therefore the hypothesis concerning the low xanthine release in guinea-pig hearts must be rejected. Activities in hearts perfused with hypoxanthine (50 microM) were 40 and 18 mU/g for rat and guinea pig, respectively; perfusion with xanthine produced < 50% of the activities observed with hypoxanthine (p < 0.002). Intracellular xanthine concentration, estimated from sorbitol distribution space and myocardial xanthine content was negative in both species, contrasting intracellular hypoxanthine levels, which approached extracellular concentrations. This disparate distribution indicates that hypoxanthine transport across the cell membrane far exceeds that of xanthine. Consequently, hypoxanthine is preferable to xanthine as substrate in perfused hearts to estimate XOD activity in situ.

Animals↗
PubMed1993

Formation and breakdown of uridine in ischemic hearts of rats and humans.

In contrast to cardiac purine metabolism, little is known about pyrimidine catabolism in heart. We therefore investigated uridine and uracil formation in ischemic rat and human hearts. Human donor hearts accumulated uridine 3 x (P < 0.05) before implantation. Hearts released this pyrimidine during implantation or correction of cardiac defects. During the former systemic blood uridine rose 38% (P < 0.05). In explanted human hearts, uridine was the only pyrimidine released during reperfusion; isolated, perfused rat hearts produced initially 3 x more uracil than uridine. Uridine phosphorylase activity in human heart homogenate was 3.4 mU/g wet weight, i.e. 60 x lower than that in rat myocardium (198 mU/g, P < 0.02); its purine counterpart, nucleoside phosphorylase, differed much less in activity (0.32 and 1.12 U/g, respectively; P < 0.001). Thus human heart is virtually devoid of uridine phosphorylase, contrasting rat heart. Consequently uridine accumulates in ischemic human heart while uracil production predominates in rat heart.

Animals↗
PubMed1993

Temperature dependence of glucocorticoid binding in sensitive and refractory murine leukaemia cells.

The validity of in vitro assays in predicting the susceptibility of leukaemic cells to glucocorticoid-mediated lysis was evaluated in a panel of six murine leukaemia cell lines. In this panel susceptibility to glucocorticoids ranged from highly sensitive to fully resistant. The panel was screened for specific 3H-dexamethasone binding in whole cells and for activation of cytosolic receptors in cell lysates. Specific binding of 3H-dexamethasone was strongly affected by the incubation temperature. In all cell lines, rapid and reversible changes were observed in the stability of agonist-receptor association with a transition temperature of 28 degrees C. Below this temperature, intracellular receptors were found to be in a stable-binding, high-affinity configuration, masking differences in receptor status among the various cell lines. When assayed at 37 degrees C, refractory and fully resistant cells revealed nonsaturating, low-affinity binding of steroid. Saturating, high-affinity binding was, however, restored in these cells by the drug meta-iodobenzylguanidine with concomitant sensitization to dexamethasone-induced lysis. Contrary to observations with intact cells, heat-induced agonist-receptor dissociation in cytosols caused irreversible loss of (re)binding capacity. Activation of cytosolic receptors only recognized fully resistant cell lines as being deficient in the transformation of liganded receptors into a DNA-binding configuration. The assay, however, could not discriminate between three cell lines with highest but varying degrees of sensitivity because of maximal activation. The results indicate that non-physiological temperature and cell disruption strongly and differentially affect steroid binding and receptor activation, respectively. The observations may account for the poor correlation between conventional predictive assays and steroid responsiveness in clinical leukaemia.

3-Iodobenzylguanidine↗
PubMed1993

Antioxidant defences in rat, pig, guinea pig, and human hearts: comparison with xanthine oxidoreductase activity.

OBJECTIVE: Cardiac injury, related to ischaemia and reperfusion, may be caused by the action of oxygen free radicals. Xanthine oxidoreductase activity may be an important free radical source. During cardiac ischaemia, the native dehydrogenase form may be converted to the oxidase form, which uses molecular oxygen to form superoxide radicals. Superoxide dismutase converts the radicals to H2O2, which is detoxified by catalase and glutathione peroxidase. In view of the large differences in xanthine oxidoreductase in various species, the activity of these antioxidant enzymes was investigated. METHODS: Normal rodent and porcine as well as explanted human hearts were perfused according to Langendorff. After a 30 minute stabilisation period, hypoxanthine was added to the perfusion buffer to estimate xanthine oxidoreductase. Hearts or biopsies were freeze clamped after 90 minutes. Effluent xanthine and urate were assayed with high performance liquid chromatography; tissue reduced glutathione content and the activity of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were determined spectrophotometrically. Apparent xanthine oxidoreductase was calculated as xanthine +2 x urate production. RESULTS: Xanthine oxidoreductase was (mU.g-1 protein, mean(SEM), n = 5-7): rat, 470(40); guinea pig, 270(41); pig < 1.5; and human, 5.4(1.0). Superoxide dismutase activities were (U.g-1 protein): rat, 13,370(1030); guinea pig, 10,100(1110); pig, 12,800(450); and human, 7400(450). Catalase activity (k < or = 10.g-1 protein) was low in all species studied. Glutathione peroxidase activity was 93(7) U.g-1 protein in rat heart, and 10 x lower in the other species. Glutathione reductase activity was (U.g-1 protein): rat, 15.0(1.6); guinea pig, 10.4(1.3); pig, 16.0(1.5); and human, 26.6(2.0). Tissue reduced glutathione concentrations were (mumol.g-1 protein): rat, 13.5(0.8); guinea pig, 18.5(0.9); pig, 11.1(2.9); and human 17.2(1.7). CONCLUSIONS: Considerable species differences in xanthine oxidoreductase activity exist, contrasting with the smaller variations in antioxidant enzyme activities. In the species examined catalase activities were very low. Rat hearts are far better protected against H2O2 than the other three species. Xanthine oxidoreductase induced free-radical damage probably plays a minor role in pig and human hearts. Human myocardium seems less protected against superoxide radicals.

Allopurinol↗
PubMed1993

The frequency of extremely low serum pepsinogen, indicative of corpus gastritis with severe atrophy, in rheumatoid arthritis, other chronic rheumatic diseases and non-rheumatic diseases.

The aim of this study was to assess the frequency of corpus gastritis with severe atrophy (CGA), pernicious anaemia and combined severe atrophy of antrum and corpus by non-invasive methods (i.e. determination of low serum pepsinogen A (PgA) and serum gastrin) in outpatients with RA (n = 249), compared to outpatients with other rheumatic diseases (n = 181) and outpatients with chronic non-rheumatic diseases (n = 429). In addition we investigated whether NSAIDs could cause or prevent CGA. A low serum PgA level (< 17 micrograms/l), indicating pentagastrin-refractory achlorhydria in patients without gastric resection, was found in 13 patients (5.2%; 95% Confidence Interval (CI) 2.4-8.0) with RA, in 11 (6.1%; 95% CI 2.6-9.5) with other rheumatic diseases and in 12 patients (2.8%; 95% CI 1.2-4.4) with chronic non-rheumatic diseases (NS). Low serum PgA values were more frequent in older patients (P < 0.005) and females (P < 0.05). Pernicious anaemia occurred in RA in 1.2% (95% CI 0-2.6) of the patients while for other rheumatic diseases the frequency was 1.7% (95% CI 0-3.5) and for chronic non-rheumatic diseases 0.2% (95% CI 0-3.6) (NS). In patients with a serum PgA below 17 micrograms/l, normal serum gastrin levels (< 90 ng/l) as an indication of combined severe atrophy of antrum and corpus, were found in 1/13 patients with RA, in 3/11 with other rheumatic diseases and 2/12 with chronic non-rheumatic diseases (NS). The frequency of low serum PgA levels was no different between patients on NSAIDs 17/355 (4.8%) and those without NSAIDs 19/502 (3.8%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Impact of innovative techniques on the waiting list and results in pediatric liver transplantation.

The wide application of liver transplantation in children is hampered by the shortage of size-matched pediatric donors; this results in high mortality rate on the waiting list, a long waiting time, worsening of the clinical condition of the waiting patient, deterioration of the overall results, and an increase in the cost. Reduced-size liver transplants have been shown to be a safe way to alleviate the shortage of size-matched organs. We have retrospectively analyzed the impact of the reduced-size liver transplants on the waiting list and the results in a consecutive series of 314 transplants performed in 261 children over an 8-year period (1984-1991). Among these 314 grafts, 160 (51%) were innovative techniques including 86 reduced livers (stricto senso), 66 partial livers (with preservation of the recipient vena cava), and 8 split livers. Such an extensive use of these technical variants allowed a sharp decrease in the waiting list mortality: from 14.9% between 1984 and 1989 to 6.6% in 1990 and 5% in 1991; the corresponding figures for infants registered under the age of 1 year were 25%, 13.3%, and 8.3%, respectively. Results obtained with a full-size graft or a technical variant were similar regarding surgical complications (with a significantly lower incidence of arterial thrombosis for the reduced transplants), graft loss, and patient survival. The 5-year survival of the whole group was 78.1% without any significant difference regarding type of transplant, indications (with the best results: 89.4% 5-year survival obtained in 41 children grafted for metabolic diseases), or age (the 5-year survival was 82.2% for the 41 infants transplanted under the age of 1 year, 78.9% for the 124 children transplanted between 1 and 3 years, and 81.3% for the 96 children transplanted between 6 and 15 years). This series of reduced-size liver transplants, which is the largest worldwide single institutional experience, confirms that the extensive use of reduced transplants in children is safe; this study also shows that innovative techniques, including the split liver, allow a drastic decrease of the waiting list mortality of candidates in the pediatric age range without alterations of the results.

Adolescent↗
PubMed1993

Effects of indomethacin on intragastric pH and meal-stimulated serum gastrin secretion in rheumatoid arthritis patients.

The effects of oral indomethacin on intragastric pH and serum gastrin were investigated in rheumatoid arthritis patients. Nine patients (1 male, 8 female) without a history of peptic ulcer disease and 6 patients with a history of peptic ulcer disease (5 male, 1 female) were studied. To obviate Helicobacter pylori infection as a confounding factor, only patients with positive H. pylori serology were included. After a 5-day period of placebo treatment and after a 5-day period of indomethacin (50 mg t.d.s.; total dose 750 mg), 24-h intragastric pH and basal and meal-stimulated serum gastrin levels were measured in a double-blind placebo controlled cross-over study. There were no differences in the median 24-h pH values between placebo and indomethacin users irrespective of peptic ulcer disease history. Indomethacin resulted in a higher basal and stimulated gastrin response than placebo in patients with a history of peptic ulcer disease. The basal and incremental responses were lower in patients with a history of peptic ulcer disease than in patients without a history of peptic ulcer disease, both during indomethacin and placebo. The same basal and stimulated incremental serum gastrin responses were found during placebo and indomethacin treatment in patients without a history of peptic ulcer disease. No correlation was established between median 2-h post-prandial intragastric pH and post-prandial incremental serum gastrin concentration. We conclude that indomethacin does not influence the intragastric pH of rheumatoid arthritis patients irrespective of history of peptic ulcer disease.

Administration, Oral↗
PubMed1993

Malondialdehyde and glutathione production in isolated perfused human and rat hearts.

A number of studies show the relation between oxygen-derived free radicals and cardiac ischemia/reperfusion injury. However, little is known about oxidative stress in the human heart, which can be measured by oxidized glutathione (GSSG) and malondialdehyde (MDA) formation. Furthermore, data on MDA production by rat hearts are controversial, possibly because of the use of the aspecific thiobarbituric acid assay. Therefore, GSSG and MDA were measured, with colorimetric and high-performance liquid chromatographic assays, respectively, in buffer-perfused explanted human hearts and normal rat hearts made temporarily ischemic. Human hearts received cardioplegia; rat hearts were studied in a control and an ischemic group with or without cardioplegia. Baseline GSSG release was < 0.01 nmol.min-1.g wet wt-1 in both species. During reperfusion, GSSG release from human hearts and from ischemic and cardioplegic/ischemic rat hearts peaked at 0.24 +/- 0.12, 1.1 +/- 0.4, and 0.19 +/- 0.04 nmol.min-1.g-1, respectively. MDA was undetectable (< 0.02 nmol.min-1.g-1) in the effluent of both species and in human hearts (< 4 nmol/g protein). Rat heart reduced glutathione levels decreased 32% as a consequence of cardioplegia and ischemia. Cardioplegia induced a 41% (P = .08) decrease in rat heart MDA content, whereas cumene hydroperoxide increased it 3.6 times (P < .01). Thus, after ischemia human and rat hearts release GSSG, indicating that oxidative stress has occurred. Apparently, lipid peroxidation takes place in normal rat hearts, decreases after cardioplegia, but does not increase after ischemia/reperfusion. Human hearts lack MDA under normoxic and ischemic conditions. This novel finding seems to reflect a low MDA-forming potential in both situations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Myocardial xanthine oxidoreductase activity in hypertensive and hypercholesterolemic rats.

In several species, xanthine oxidoreductase activity seems to be a major source of free radicals in myocardial tissue. Its activity changes during development and aging, at least in the rat heart. Hardly any data are available about its activity in two important diseases, hypertension and hypercholesterolemia, in which the production of free radicals induced by xanthine oxidoreductase activity could play a role. Therefore we measured the activity of xanthine oxidase and dehydrogenase in myocardial tissue of spontaneously hypertensive. Wistar (control hypertensive), Yoshida (hypercholesterolemic) and Brown Norway (control hypercholesterolemic) rats of various ages. Cytosolic fractions were incubated at 30 degrees C, pH 8.3, with 60 microM xanthine, and the formation of urate was measured with high performance liquid chromatography. In the Wistar group, xanthine oxidoreductase activity was relatively constant during aging (about 1.8 U/g protein). In the hypertensive group, the activity increased gradually from 1.7 to 2.3 U/g at 18 months (p < 0.05 compared with Wistar at 18 months). Xanthine oxidase was about twice as high in both groups at 18 months (p < 0.001 compared with 2 and 6 months). The ratio of xanthine dehydrogenase to xanthine oxidase had decreased 42% at this age (p < 0.001). In the Yoshida and Brown Norway groups, xanthine oxidoreductase activity was similar, with a peak at 6 months. These data suggest that the hypercholesterolemic state does not influence xanthine oxidoreductase activity. In contrast, in hypertrophied myocardium, xanthine oxidoreductase activity was higher than in the control, suggesting a different potential for free-radical generation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1992

Virus-induced airway hyperresponsiveness in guinea pigs in vivo: study of broncho-alveolar cell number and activity.

Recently, we demonstrated that an increased airway responsiveness in vitro can be measured 4, 8, and 16 days, but not 2 days, after intratracheal inoculation of parainfluenza-3 (PI-3) virus to guinea pigs. In the present study airway responsiveness was measured in vivo, and the number, types and activity of broncho-alveolar cells was determined. A significant increase in airflow resistance was measured in spontaneously breathing anesthetized guinea pigs in response to histamine and methacholine, 4 and 8 days after PI-3 virus inoculation. 2 days after inoculation with control solution or PI-3 virus, no difference in the total number of inflammatory cells was observed in the broncho-alveolar lavage fluid. In contrast, on days 4, 8, and 16 after infection a significant increase in the number of alveolar macrophages (102%, 76%, 68%, respectively), monocytes (552%, 374%, 360%, respectively), and lymphocytes (253%, 675%, 396%, respectively) was found. The number of eosinophils was increased as well, but faded with time (378%, 312%, 63%, respectively). PI-3 virus was found to be a very potent activator of broncho-alveolar cells as measured by chemiluminescence. The increase in chemiluminescence production in response to PI-3 virus was reduced in cells obtained from PI-3 virus pretreated animals (day 2, 42%; day 4, 65%; day 8, 22%; and day 16, 30%). In conclusion, PI-3 virus can stimulate broncho-alveolar cells and the virus-induced airway hyperresponsiveness is associated with an influx of inflammatory cells in the respiratory tract.

Airway Resistance↗
PubMed1992

Purification and characterization of an antithrombin III inactivating enzyme from the venom of the African night adder (Causus rhombeatus).

A serine proteinase was isolated from the venom of the night adder (Causus rhombeatus) by fast protein liquid chromatography (anion-exchange, gel filtration and hydrophobic interaction). The protein (termed CR-serpinase) had an estimated mol. wt of 45,500 as determined by SDS-PAGE, pI of 4.7 and a carbohydrate content of 18.9%. Incubation of CR-serpinase with purified human antithrombin III at a molar ratio of 1:66 resulted in a loss of more than 90% of the initial AT III activity within 10 min. The reaction was dependent on heparin. In SDS-PAGE inactivation of human antithrombin III was correlated with the occurrence of two cleavage products. The cleavage site in the antithrombin III molecule was determined to be Arg 393-Ser 394 by amino-terminal sequencing. CR-Serpinase had no thrombin-like activity since no fibrinogen conversion was induced and had no procoagulant activity. CR-Serpinase activity was not inhibited by antithrombin III-heparin and was not decreased by a 10-min preincubation in normal human plasma. Inactivation of antithrombin III by CR-serpinase appeared to be very specific.

Amino Acid Sequence↗
PubMed1992

Virus-induced airway hyperresponsiveness in the guinea pig can be transferred by bronchoalveolar cells.

For the investigation of whether inflammatory cells were responsible for virus-induced airway hyperresponsiveness, tracheal spirals from healthy guinea pigs were incubated in organ baths with different numbers of bronchoalveolar cells obtained from guinea pigs 4 days after their inoculation with parainfluenza-3 (P-3) virus or control solution. Airway responsiveness was measured by performance of histamine concentration/response (C/R) curves on the tissues. Preparations incubated with 5 x 10(5) cells/ml obtained from guinea pigs treated with P-3 virus demonstrated a significant upward shift of the histamine C/R curve. The maximal contraction was increased by 26% as compared with the tissues incubated with the same number of cells from animals inoculated with control solution. When the number of cells was increased further to 5 x 10(6) cells/ml, no additional upward shift of the C/R curve was seen; the increase in maximal contraction was 24%. Tracheal spirals incubated with 5 x 10(4) cells/ml did not affect the histamine C/R curves. Addition of P-3 virus to the organ bath during the incubation period with the cells did not affect the histamine C/R curve either, irrespective of the inoculation solution or the number of bronchoalveolar cells used. The relative number of alveolar macrophages in bronchoalveolar lavage fluid decreased significantly from 86.3% +/- 2.6% in the control group to 71.8% +/- 3.3% in the P-3 virus group as a consequence of a significant increase in the percentage of monocytes, lymphocytes, and eosinophils. These results suggest that bronchoalveolar cells are causally involved in the virus-induced airway hyperresponsiveness.

Animals↗
PubMed1992

Upper gastrointestinal complaints and complications in chronic rheumatic patients in comparison with other chronic diseases.

The aim of this study was to compare the frequency of upper gastrointestinal (GI) complaints and complications between chronic rheumatic patients who are most often non-steroidal anti-inflammatory drugs (NSAIDs) users and patients with other chronic conditions. In this comparison we took into account known risk factors for upper GI disease. To achieve the study aims we performed a combined cross-sectional and retrospective study. We therefore interviewed by means of a standard questionnaire, an index and a reference group, about current upper GI complaints and previous complications. The former group comprises 578 outpatients of the Department of Rheumatology, the latter of 531 outpatients of the Departments of Internal Medicine, Pulmonology, and Cardiology. Although the number of patients in the index group being chronically treated with NSAIDs was very high (62% versus 9% in the reference group: P < 0.00001), no between-group differences were found for the frequency of several current upper gastrointestinal complaints or for the number of upper gastrointestinal investigations ever performed (35% and 37%: NS) or for the use of gastric drugs (14% and 10%: NS). Risk factors for upper GI complaints were not related to NSAID use but with the use of prednisolone, history of duodenal ulcer disease, family history of peptic ulcer disease and female sex. For peptic ulcer disease, bleeding, and gastric surgery, the only difference between the index and reference groups concerned the frequency of gastric ulcers (6.7% and 2.8%: P < 0.005), which was highest in patients with rheumatoid arthritis. Upper GI bleeding had more often been present in male seropositive rheumatoid arthritis patients (13.2% [corrected] and 4.5%: P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Intra-articular rheumatoid nodules and triggering of the knee joint.

Rheumatoid nodules are a common extra-articular manifestation in rheumatoid arthritis. Intra-articular localisation of these nodules is rare and may produce clinical symptoms. Seven patients with walking problems due to an intra-articular rheumatoid nodule, which became entrapped on the ridge of the tibial plateau of the knee joint resulting in a phenomenon referred to as trigger knee, are described. After excision of the nodules all symptoms completely disappeared.

Adult↗
PubMed1992

Decreased level of antibodies against Helicobacter pylori in patients with rheumatoid arthritis receiving intramuscular gold.

BACKGROUND: Sodium aurothiomalate has been reported to have in vitro activity against Helicobacter pylori. Intramuscular gold, as given to patients with rheumatoid arthritis (RA), may therefore influence the colonisation of the gastric mucosa with H pylori. METHODS: Two groups were compared. One group of 42 patients was treated with intramuscular gold; the other group of 58 patients was treated with antimalarial drugs. Antibodies to H pylori (IgA and IgG) were assessed by an enzyme linked immunosorbent assay (ELISA) and total IgA and IgG were measured by nephelometry. RESULTS: IgA and IgG antibody titres against H pylori and total IgA and IgG levels were lower in the patients treated with gold than in the group treated with antimalarial drugs. The ratio of IgA antibodies to H pylori to total IgA antibodies and the ratio of IgG antibodies to H pylori to total IgG antibodies were lower in the group treated with gold. The percentage of seropositivity to H pylori was significantly lower in the group treated with gold than in the group treated with antimalarial drugs for the two IgA antibodies (35 and 55% respectively) and IgG antibodies to H pylori (40 and 65% respectively). CONCLUSIONS: Although this study cannot completely exclude the possibility that a suppressive effect of intramuscular gold on total immunoglobulin production plays a part in the decrease in the titres of IgA antibodies to H pylori and IgG antibodies to H pylori, the lower ratios of antibodies to H pylori to total immunoglobulin antibodies and the lower percentages of seropositivity to H pylori in the group treated with gold suggests that treatment with intramuscular gold decreases H pylori colonisation.

Adolescent↗
PubMed1991

Pharmacokinetics and intracellular distribution of the tumor-targeted radiopharmaceutical m-iodo-benzylguanidine in SK-N-SH neuroblastoma and PC-12 pheochromocytoma cells.

Radiodinated meta-iodobenzylguandine (MIBG) is increasingly used for the diagnosis and targeted radiotherapy of neuro-adrenergic tumors. We have investigated various conditions for specific tumor loading and prolonged retention of this radiopharmaceutical in poorly differentiated SK-N-SH neuroblastoma and highly differentiated PC-12 pheochromocytoma cells. At a constant value of drug concentration x incubation time, short incubations were superior to protracted incubations for maximal cell loading. This effect was most pronounced in the SH-N-SH neuroblastoma cells. In highly differentiated pheochromocytoma cells, the levels of MIBG storage remained high and unchanged during incubations up to 46 hr in label-free medium, while primitive SK-N-SH cells lost 40-50% of accumulated drug by diffusion. In PC-12 cells, susceptibility of stored MIBG to exocytotic release induced by acetylcholine or K+ was similar to that of natural norepinephrine (NE) and prevented by the Ca(++)-channel blockers verapamil and nifedipine. Conversely, granule-poor SK-N-SH cells were insensitive to exocytotic release of MIBG. Uptake and retention capacities were minimally impaired by an externally delivered radiation dose of 5 Gy to mimic the radiobiological effect of 131I-MIBG in tumors. In pre-irradiated cultures, drug uptake was even stimulated, probably due to enrichment in non-proliferating cells. An autoradiographic comparison of the (sub)cellular distributions of 3H-norepinephrine and 125I-MIBG showed that routine conditions of cell fixation and sample processing do not yield reliable results regarding localization of MIBG.

3-Iodobenzylguanidine↗