Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four groups of young adult male Brown-Norway rats (strain: BN/RijHsd) were either exposed whole-body (WB) to filtered air (negative control) or to respirable aerosols of monomeric diphenylmethane-4,4'-diisocyanate (MDI) at actual breathing zone concentrations of 9.2 +/- 1.5 and 118 +/- 8.6 mg/m3. One additional group was exposed to 11,0 +/- 14.4 mg/m3 MDI using a nose-only (NO) mode. Exposure was 1 h/day, one exposure per week on 3 consecutive weeks. MDI aerosols were generated using either a condensation (WB) or a dispersion-condensation (NO) principle with resultant MMADs of 2.4-3.1 microm and 1.2 microm (GSD approximately l.5), respectively. Humidity ranged from approximately 40% (WB) to approximately 5% (NO). Positive controls received cyclophosphamide and colcemid. Micronuclei in polychromatic erythrocytes (MN-PCE) were counted in bone marrow smears prepared after the final exposure on post-exposure days 1, 2 and 7 and stained with acridine orange or Wright-Giemsa. Both the WB-exposure regimen and the 7-day sampling time point were based upon a previous study in which a significant increase in MN-PCE was reported to occur. Rats exposed to 118 (WB) and 110 mg/m3 MDI (NO) exhibited signs of respiratory distress, including hypothermia, and increased lung weights when compared to WB-exposed rats. The intensity of changes appeared to be slightly more pronounced in NO-exposed rats. At no time point did this study provide any evidence of an MDI-induced effect on the frequency of MN-PCE. No differences in outcome existed following staining with acridine orange or Wright-Giemsa. There was an absence of any effect on the frequency of mast cells and their frequency was low enough not to interfere with the outcome of study. Positive control groups exhibited significant increases in MN-PCE. In summary, monomeric MDI aerosol did not induce cytogenetic damage in Brown-Norway rats when investigated according to current testing guidelines.
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PMID:Bone marrow micronucleus assay in Brown-Norway rats exposed to diphenyl-methane-4,4'-diisocyanate. 1148 22

Leukocyte dynamics were evaluatyed in vivo in rat retinal microcirculation following exposure to lipid hydroperoxide (LHP) in the vitreous.Various amounts (1, 5, 10 or 100 microg) of LHP (18:2) dissolved in 5 microl of sodium borate buffer (SBB, 0.02M) were injected into the vitreous of Brown-Norway rats. As a comparative study, 10 microg of linoleic acid (LA) dissolved in 5 microl of SBB was injected in the same way. Rats that did not undergo injection were evaluated as un-treated. At 2 to 48 hr after LHP exposure, the following were examined: (1) the flux of rolling leukocytes along the major retinal veins, (2) the number of leukocytes that accumulated in the retinal microvasculature using acridine orange digital fluorography and (3) the diameter of major retinal vessels. In the LHP-treated eyes, leukocyte rolling along the major retinal veins was observed and the number increased in a dose-dependent manner ( 1 to 10 microg). The flux of rolling leukocytes peaked at 6 hr after LHP (10-100 microg) injection. No rolling leukocytes were observed in LA-treated or un-treated eyes. The number of accumulated leukocytes started to increase at 4 hr and peaked at 24 hr after LHP (10 microg) injection. This number was significantly higher than that in LA-treated and un-treated eyes. Venous dilation was seen from 4 hr after LHP (10 microg) injection and became significant at 6 and 24 hr as compared with LA-treated and un-treated eyes. The results indicate that increased LHP levels in the vitreous due to oxidative stress enhance leukocyte-enothelium interaction in the retinal microcirculation.
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PMID:Lipid hydroperoxide stimulates leukocyte-endothelium interaction in the retinal microcirculation. 1212 38

The purpose of this study was to evaluate the effects of insulin on leukocyte-endothelial cell adhesion in the retinal microcirculation in vitro and in vivo. Human retinal endothelial cells (HRECs) were cultured in medium with or without insulin, and neutrophils allowed to adhere. Adherent neutrophils were quantified by measuring myeloperoxidase activity. Surface expression of endothelial adhesion molecules were studied with the use of an enzyme immunoassay. Insulin at concentrations of 50 and 100 microU/ml significantly increased neutrophil adhesion to HRECs compared with the control cells (P < 0.01, respectively). Surface expression of intercellular adhesion molecule-1 (ICAM-1) significantly increased when HRECs were exposed to 100 microU/ml insulin, as compared with the control cells (P < 0.05). Anti-ICAM-1 antibody significantly inhibited neutrophils adhesion to HRECs (P < 0.0001). Brown-Norway rats received subcutaneous injection of 0.2 U per 100 g body weight insulin three times. Control rats received the same amount of phosphate-buffered saline. Leukocyte entrapment in the retina was evaluated using acridine orange leukocyte fluorography. The number of leukocytes trapped in the retina of insulin-treated rats was significantly elevated compared with that in the control animals (P < 0.0001). These results suggested that insulin enhances leukostasis in retinal microcirculation. Hyperinsulinemia may be a risk factor of retinal microcirculatory disturbances.
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PMID:Insulin enhances leukocyte-endothelial cell adhesion in the retinal microcirculation through surface expression of intercellular adhesion molecule-1. 1589 55

The levels of lipid hydroperoxide (LHPs) in vitreous are elevated in a variety of retinal disorders. Recently, we have shown that increased levels of LHPs in the vitreous enhanced leukocyte-endothelium interaction in the retina, which should contribute to the initial disturbance of the retinal microcirculation. Based upon the previous work, the purpose of the present study was to investigate the effect of polyethylene glycol-superoxide dismutase (PEG-SOD), one of the important enzyme antioxidants, on leukocyte-endothelial interaction in the retinal microcirculation under LHP-induced oxidative stress. Male Brown-Norway rats weighing approximately 250 g were used. LHP(18:2) was made from linoleic acid (LA) with lipoxygenase and 10 microg of LHP dissolved in 5 microl of sodium borate buffer (SBB, 0.02 m) was slowly injected into the vitreous using a 33-gauge needle. PEG-SOD (5000 units/kg) was given intravenously 5 min before LHP injection. At 2, 4, 6, 12, 24 and 48 hr after the vitreous injections, we evaluated the number of rolling leukocytes along the major retinal veins and the number of leukocytes that accumulated in the retinal microvasculature with acridine orange digital fluorography. In LHP-treated rats, leukocyte rolling along the major retinal veins was maximal at 6 hr after LHP injection. The number of rolling leukocytes in the PEG-SOD-treated rats was decreased to 5.5% of those in the LHP-treated rats at 6 hr after LHP injection (P<0.01). No rolling leukocytes were observed in either control or vehicle-treated eyes. The number of accumulated leukocytes in LHP-treated eyes started to increase at 12 hr, and peaked at 24 hr which was significantly higher than in both control and vehicle-treated eyes (P<0.01). The number of accumulated leukocytes in the PEG-SOD-treated rats was reduced by 88.0% at 24 hr (P<0.01). Intravenous injection of PEG-SOD significantly inhibited the leukocyte rolling and its accumulation under LHP-induced oxidative stress. These results suggest that PEG-SOD might attenuate various retinal microcirculatory disorders associated with LHP.
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PMID:Protective effect of polyethylene glycol-superoxide dismutase on leukocyte dynamics in rat retinal microcirculation under lipid hydroperoxide-induced oxidative stress. 1608 Sep 13