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At least 1,621 records · Page 90Linked to original sources
PubMed1999

Methylprednisolone therapy for retinal laser injury.

OBJECTIVE: Laser photocoagulation treatment of the posterior pole of the retina is often complicated by immediate visual impairment, which is caused by the unavoidable laser-induced destruction of the normal tissue adjacent to the lesion. A neuroprotective therapy aimed at salvaging this normal tissue might enhance the benefit obtained from treatment and permit safe perifoveal photocoagulation. To determine whether corticosteroids can provide neuroprotection during photocoagulation, we examined the effect of methylprednisolone on laser-induced retinal injury in a rat model. METHODS: Argon laser lesions were inflicted on the retinas of 36 rats and were followed immediately by intraperitoneal injections of high-dose methylprednisolone or saline. The animals were sacrificed after 3, 20, or 60 days, and their retinal lesions were evaluated histologically and morphometrically. RESULTS: No histopathologic differences were observed between the treated and control animals. Methylprednisolone treatment was demonstrated to posses some neuroprotective effect for a short time after laser exposure, but was ineffective in ameliorating the long-term results of retinal laser injury. CONCLUSIONS: On the basis of our results, we suggest that high-dose methylprednisolone treatment is ineffective in ameliorating laser-induced retinal injury. Other drugs should be investigated for their potential role as neuroprotective agents to prevent the spread of retinal laser damage.

Animals↗
PubMed2003

Bothrops lanceolatus (Fer de lance) venom stimulates leukocyte migration into the peritoneal cavity of mice.

The ability of Bothrops lanceolatus venom to induce neutrophil migration into the peritoneal cavity of mice was investigated. Intraperitoneal injection of venom caused dose- and time-dependent neutrophil migration, which peaked with 750 ng of venom/cavity 4h after venom injection. The neutrophil migration was significantly reduced by pretreatment with dexamethasone (0.5 mg/kg, s.c.), an indirect inhibitor of phospholipase A(2) (PLA(2)), and AA861 (0.01 mg/kg, s.c.), a 5-lipoxygenase inhibitor, but in contrast, was not modified by pretreatment with indomethacin (2 mg/kg, s.c.), an inhibitor of the cyclooxygenase pathway, meloxicam (5 mg/kg, s.c.), an inhibitor of the cyclooxygenase-2 pathway, or the PAF inhibitor WEB2086 (40 mg/kg, s.c.). Dexamethasone and AA861 also inhibited the neutrophil migration by 60% when administered immediately after venom injection, and the coadministration of these two drugs caused a 75% reduction in migration. BLV-induced neutrophil migration was not due to contamination by endotoxin since polymyxin B-treated venom retained its activity. Heating the venom (97 degrees C, 2 min) reduced the PLA(2) activity by 64% and this was accompanied by a corresponding reduction (68%) in neutrophil migration. These results suggest that arachidonate-derived lipoxygenase metabolites (possibly leukotriene B(4)) are involved in the chemotaxis observed. Macrophages may be an important source of these metabolites since the migratory response to venom was potentiated in mice pretreated with thioglycollate, but reduced when the peritoneal cavity was washed with sterile saline.

Animals↗
PubMed2003

Simultaneous production of homoanatoxin-a, anatoxin-a, and a new non-toxic 4-hydroxyhomoanatoxin-a by the cyanobacterium Raphidiopsis mediterranea Skuja.

A neurotoxin, homoanatoxin-a, was identified from a toxic strain of the cyanobacterium Raphidiopsis mediterranea Skuja (strain LBRI 48) isolated from Lake Biwa, Japan, as the major toxin component (0.57% of dry cell-weight). This cyanobacterium produced anatoxin-a and a new homoanatoxin-a derivative as minor components (0.04 and 0.06%, respectively). The structure of a new compound was assigned based on the spectral data as 4-hydroxyhomoanatoxin-a, which was not toxic to mice up to 2.0 mg/kg by intraperitoneal injection. The isolation of minor components was accomplished by improved extraction and separation procedures: (1) extraction with methanol-water (4:1) from dried cells, (2) adsorption of aqueous residue on ODS column (or cartridge) after evaporation of methanol, (3) cleaning up of the column by successive elution with water and 50% methanol/water, (4) elution of a toxic fraction by 20% methanol/water containing 0.1% TFA and (5) HPLC (ODS) purification with methanol/water containing 0.05% TFA. The procedures were effective in removing impurities and concentrating alkaloidal neurotoxins. It should be noted that this is the first report demonstrating the simultaneous production of anatoxin-a and homoanatoxin-a by the same strain of cyanobacterium.

Animals↗
PubMed1997

Isolation and toxicity of Cylindrospermopsis raciborskii from an ornamental lake.

In Australia, the tropical/subtropical cyanobacterium Cylindrospermopsis raciborskii forms substantial blooms in some drinking water supply reservoirs, rivers and recreational water bodies during the warmer months of the year. This paper describes the isolation, culture and toxicity characterisation of Cylindrospermopsis from a water bloom in a small lake in NSW, Australia. The cyanobacterium grew as straight trichomes terminating with a characteristic heterocyst. The toxic alkaloid cylindrospermopsin was separated and identified by high-performance liquid chromatography at a concentration of 5.5 mg/g dry cells, 0.026 pg/cell. Intraperitoneal injection of sonicated cells caused liver, kidney, intestinal and lung damage, with an LD50 of 52 mg cells/kg mouse body weight at 24 hr, and 32 mg/kg at 7 days. The 24 hr mouse toxicity is not consistent with previous studies using pure cylindrospermopsin, and is suggestive of other toxic compounds in this isolate.

Alkaloids↗
PubMed2003

Indomethacin-induced morphologic changes in the rat urinary bladder epithelium.

OBJECTIVES: To evaluate the morphologic changes in rat urothelium induced by indomethacin. Nonsteroidal anti-inflammatory drug-induced cystitis is a poorly recognized and under-reported condition. In addition to tiaprofenic acid, indomethacin has been reported to be associated with this condition. METHODS: Three groups were established: a control group (n = 10), a high-dose group (n = 10), treated with one intraperitoneal injection of indomethacin 20 mg/kg, and a therapeutic dose group (n = 10) in which oral indomethacin was administered 3.25 mg/kg body weight daily for 3 weeks. The animals were then killed and the bladders removed for light and electron microscopic studies. RESULTS: The light microscopic findings showed some focal epithelial degeneration that was more prominent in the high-dose group. When compared with the control group, both indomethacin groups revealed statistically increased numbers of mast cells in the mucosa (P <0.0001) and penetration of lanthanum nitrate through intercellular areas of the epithelium. Furthermore, the difference in mast cell counts between the high and therapeutic dose groups was also statistically significant (P <0.0001). CONCLUSIONS: Indomethacin resulted in histopathologic findings typical of interstitial cystitis, such as leaky bladder epithelium and mucosal mastocytosis. The true incidence of nonsteroidal anti-inflammatory drug-induced cystitis in humans must be clarified by prospective clinical trials.

Animals↗
PubMed2000

The effects of pyridostigmine bromide and permethrin, alone or in combination, on response acquisition in male and female rats.

It has been hypothesized that concurrent exposure to pyridostigmine bromide and permethrin may have contributed to the development of neurocognitive symptoms in Gulf War veterans. The present experiment was designed to investigate the effects of pyridostigmine bromide and permethrin alone, or in combination, on the acquisition of a novel response, one measure of normal cognitive functioning. Male and female Sprague-Dawley rats were treated with pyridostigmine bromide (1.5 mg/kg/day, by gavage in a volume of 5 ml/kg) or its vehicle for 7 consecutive days. They then also received an intraperitoneal injection of permethrin (0, 15, or 60 mg/kg) before they were exposed to an experimental session during which they could earn food by pressing a lever in an operant chamber. Serum permethrin levels increased as a function of its dose, and were higher in rats treated with pyridostigmine bromide. Sex differences were observed as permethrin levels were higher in female rats than in male rats following the highest dose. Pyridostigmine bromide delayed response acquisition in male and female rats, and resulted in higher response rates on the inactive lever in female rats than in male rats. Although permethrin levels were higher in subjects treated with pyridostigmine bromide than in those treated with vehicle, there were no differences in the behavioral effects of permethrin. Whether or not these behavioral effects of pyridostigmine bromide are of central or peripheral origin will need to be determined in future studies, as its effects on motor activity and/or gastro-intestinal motility may have affected response acquisition.

Animals↗
PubMed1998

Effects of propranolol, buspirone, pCPA, reserpine, and chlordiazepoxide on open-field behavior.

The study examined the possibility that propranolol, buspirone, pCPA, and reserpine have antianxiety effects by comparing their effects with those of chlordiazepoxide on an open-field test of emotionality in rats. The effects of intraperitoneal injections of d,l, propranolol (5, 10, 20 mg/kg), buspirone (1.25, 2.5, 5 mg/kg), reserpine (0.5 mg/kg), parachlorophenylalanine (pCPA) (100 mg/kg), and chlordiazepoxide (CDP) (2.5, 5, 10 mg/kg) were compared with performance of rats under saline or water using an open-field test on 5 successive days. Significant effects were found on peripheral movements, rearing, grooming, immobility, and defecation. The patterns of effects of high doses of propranolol and buspirone resembled those of CDP, while pCPA had some of the effects of CDP, and reserpine produced few effects. With propranolol, buspirone, and CDP, there was evidence of dose sensitivity. The effects of repeated testing across 5 days were different from these of CDP or other drugs. The results are consistent with the hypothesis that the effects of propranolol and buspirone on open-field behavior are anxiolytic, and may be mediated by action on the same brain systems.

Animals↗
PubMed1987

Diesel-exhaust particulates inoculated by the intranasal route have an adjuvant activity for IgE production in mice.

Our previous study indicated that the IgE antibody responses in mice immunized with intraperitoneal injection of the antigens mixed with diesel-exhaust particulates (DEP) were higher than those in the animals immunized with the antigens alone. We examined the adjuvant activity of DEP inoculated by the intranasal route, i.e., the natural entrance of DEP. In 3-week interval immunization, the IgE antibody responses in mice immunized with intranasal inoculation of ovalbumin (OA) mixed with DEP were higher than responses in the animals immunized with OA alone. DEP had an adjuvant activity for anti-OA IgE antibody production, even in a small dose such as 1 micrograms administered with a 3-week interval. Also in 1-week interval immunization, the enhancing effect of DEP on anti-OA IgE antibody production was demonstrated when mice were immunized with intranasal inoculation of OA and DEP. The possibility cannot be excluded that DEP, which are kept buoyant in the environmental atmosphere of urban districts, may exert an adjuvant activity for IgE antibody production after being inhaled into the human body and have some relation to the mechanism of the outbreak of allergic rhinitis caused by pollens in Japan.

Adjuvants, Immunologic↗
PubMedDate not supplied

Slow releasing of ara-C from poly(2-hydroxyethyl methacrylate) and poly(2-hydroxyethyl methacrylate-co-N-vinyl-2-pyrrolidone) hydrogels implanted subcutaneously in the back of rats.

The release of cytarabine (ara-C) from poly(2-hydroxyethyl methacrylate) and poly(2-hydroxyethyl methacrylate-co-N-vinyl-2pyrrolidone) hydrogels cross-linked with different amounts of ethyleneglycol dimethacrylate (EGDMA) 'in vivo' has been studied. Two ara-C loaded hydrogel discs, each with 25 mg of the drug, were subcutaneously implanted in the back of male Wistar rats. Total ara-C dose was 230 mg kg(-1). Ara-C and ara-U plasmatic concentration were determined by HPLC. Periods of constant drug concentration are observed from all gels. Ara-C concentrations in the steady-state are between 19.0 +/- 2.0 and 2.2 +/- 0.8 micromol l(-1). The release time of ara-C was between 3 days from pH EMA 0.5% and 16 days from H80/VP20/E15 gels. These results are very different of that obtained when ara-C is administered by intraperitoneal injection, in this case peaks of maximum concentration (between 24 +/- 1 and 3.9 +/- 0.4 microg ml(-1)) 30 min after the injection are originated, and no drug is detected 4 h after the injection.

Animals↗
PubMed1998

Diurnal variations of opioid peptides and synenkephalin in vitro release in the amygdala of kindled rats.

Pentylenetetrazol (PTZ) kindling was induced in male Wistar rats (250-300 g) by daily intraperitoneal injections of 35 mg/kg of the convulsant agent. Immunoreactive (IR)-Met-enkephalin (IR-ME), IR-Leu-enkephalin (IR-LE), IR-heptapeptide (IR-HE), IR-octapeptide (IR-OC) and IR-synenkephalin (IR-Syn) in vitro release was measured from amygdala slices 24 h after the last stimulus, in groups of eight rats, every 4 h beginning at 08:00 h. Opioid peptides in vitro release displayed diurnal variations. IR-ME and IR-Syn showed maximal levels before the onset of darkness (16:00 h). IR-LE and IR-OC release was enhanced 4 h later (20:00 h), no changes were detected for IR-HE. These results show that endogenous opioid system (EOS) release displays diurnal variations. The peak for the analysed peptides was reached before and during the dark phase. It is suggested that EOS release enhancement in PTZ-kindled rats, seems to be due to a compensatory mechanism against the excitation induced by the blockade of the GABAergic transmission.

Amygdala↗
PubMed1997

Induction and duration of long-term potentiation in the hippocampus of the freely moving mouse.

We describe a simple method, using readily available minaturised components, for inducing and monitoring long-term potentiation (LTP) at perforant path-granule cell synapses in the dentate gyrus of the freely moving mouse. Tetanic stimulation induced LTP of the field EPSP and the population spike which persisted for more than 24 h but was not present 10 days after the tetanus. The potentiation of the population spike was proportionately greater than the potentiation of the EPSP (E-S potentiation). Induction of LTP was blocked by intraperitoneal injections of the N-methyl-D-aspartate (NMDA) receptor antagonist, 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP).

Animals↗
PubMed1999

Catecholamines in paraganglia associated with the hepatic branch of the vagus nerve: effects of 6-hydroxydopamine and reserpine.

Paraganglia are clusters of cells containing catecholamines (CA), mainly norepinephrine (NE) and dopamine (DA). The presence of epinephrine (E), on the other hand, has only been determined by indirect methods in retroperitoneal paraganglia of newborn and aged rats. Because their location, paraganglia associated with the hepatic branch of the vagus nerve may be a possible source of CA for the liver. The main purposes of the present study were to determine CA levels and whether E can be found in the omentum minus which includes paraganglia associated with the hepatic branch of the vagus nerve, and then to study the effects of 6-hydroxydopamine and reserpine on their CA content. Twenty-four female Wistar rats were randomly ascribed to three groups receiving two intraperitoneal injections of either 6-hydroxydopamine, reserpine or saline. Twenty-four hours after the last administration the rats were anesthetized and a portion of the omentum minus was obtained. Left adrenal medulla and a liver fragment were also collected as controls. The samples were processed to be analyzed by high performance liquid chromatography and catecholamine histofluorescence. The results confirm previous reports about the presence of considerable amounts of norepinephrine and dopamine in paraganglia. Norepinephrine and dopamine in the omentum like the adrenal medulla were significantly depleted by reserpine but not by 6-hydroxydopamine treatment, suggesting that some other sources in addition to sympathetic terminals are responsible for CA in the omentum. On the contrary, both drugs reduced liver NE, consistent with the localization of this amine mainly to hepatic sympathetic terminals. Histofluorescence of the omentum revealed 2-4 paraganglia per tissue fragment. Paraganglia associated with the hepatic branch of the vagus nerve contain also E. The presence of perihepatic sources of extra-adrenal CA, and more specifically E, could be of physiological significance.

Adrenal Medulla↗
PubMed2000

Induction of active systemic anaphylaxis by oral sensitization with ovalbumin in mast-cell-deficient mice.

Mast-cell-deficient W/W(v) mice were sensitized by oral administration of 0.1 and 1.0 mg ovalbumin (OVA) by gavage every day for 9 weeks, and active systemic anaphylaxis (ASA) was induced by intraperitoneal injection of OVA. The production of OVA-specific IgE and IgG1 by oral immunization of the W/W(v) mice was high, and the production of IL-4 by splenocytes re-stimulated with OVA in vitro was increased. In contrast, production of OVA-specific IgG2a and IgG2b was low, and production of IFN-gamma by splenocytes after re-stimulation with OVA in vitro was rather decreased. These findings suggest that Th2-dominant helper T-cell activation had occurred. No increase in serum histamine level was observed following ASA induction. However, the plasma platelet-activating factor (PAF) levels of the mice sensitized with 0.1 and 1.0 mg OVA by gavage increased significantly. The increases in plasma PAF correlated well with the ASA-associated decreases in body temperature, suggesting that PAF plays an important role in ASA in W/W(v) mice. Taken together the above findings indicate that W/W(v) mice are a good model not only for studying induction of food allergy but also for examining the role of PAF in food-induced hypersensitivity.

Administration, Oral↗
PubMed2002

Deficiency of neuronal nitric oxide synthase (nNOS) worsens alcohol-induced microencephaly and neuronal loss in developing mice.

Previous work conducted in vitro suggests that nitric oxide (NO) protects developing neurons against the toxic effects of alcohol. We tested the hypothesis that neonatal mice carrying a null mutation for neuronal nitric oxide synthase (nNOS), the enzyme which synthesizes NO in neurons, have increased vulnerability to alcohol-induced microencephaly and neuronal loss. Wild-type mice and mutant (nNOS(-/-)) mice received a single intraperitoneal injection of ethanol (0.0, 2.2, 3.3, or 4.4 g/kg) daily over postnatal days (PD) 4-9 and were sacrificed on PD 10. Peak blood alcohol concentrations were approximately 170, 280, and 385 mg/dl for the 2.2, 3.3 and 4.4 g/kg/day treatment groups, respectively, and did not differ significantly between wild-type and nNOS(-/-) strains. Exposure to alcohol induced dose-dependent reductions in total brain weight, forebrain weight and cerebellum weight in both strains of mice. However, the reductions in brain weight were significantly more severe in the nNOS(-/-) mice than in wild type. Quantification of cerebellar neurons revealed that alcohol-induced losses of Purkinje cells and granule cells were both significantly greater in the nNOS(-/-) mice than in wild type. The increased vulnerability of nNOS-deficient neurons to alcohol-induced cell death was confirmed in vitro. Cerebellar granule cell cultures derived from nNOS(-/-) and wild-type mice were exposed for 24 h to 0, 100, 200 or 400 mg/dl ethanol. At each alcohol concentration, the nNOS(-/-) neurons had a significantly greater cell loss than did the wild-type neurons. The results demonstrate that deficiency of nNOS decreases the ability of developing neurons to survive the toxic effects of alcohol. Because NO upregulates intracellular cGMP, which can activate cGMP-dependent protein kinase (PKG), we hypothesize that the NO-cGMP-PKG pathway has a neuroprotective role against alcohol toxicity within the developing brain.

Animals↗
PubMed1997

Induction of anti-GM1 ganglioside antibodies by Campylobacter jejuni lipopolysaccharides.

A frequent association exists between acute motor neuropathy, antecedent Campylobacter jejuni (CJ) and anti-GM ganglioside antibodies. Despite the chemical and immunological similarity between CJ lipopolysaccharides (LPS) and GM1, the mechanism of induction of anti-GM1 antibodies is still unclear. We used CJ LPS to immunize rats, mice and immunodeficient mice lacking in NK, CD8+ or T-cell populations. None of these animals developed significant anti-GM1 titers. However, rats immunized with keyhole limpet hemocyanin which contains the cross-reactive sugar epitope Gal(beta1-3)GalNAc developed high titers of IgM anti-GM1 antibodies. This occurred only after these rats were given an intraperitoneal injection of CJ LPS. These results suggest that a glycoprotein antigenic stimulus can induce B-cells which are autoreactive to ganglioside but which remain anergic. A second stimulus with a cross-reactive LPS can then overcome the anergy to induce autoantibody production. A similar mechanism may explain the occurrence of GM1 antibodies in patients after CJ enteritis.

Adjuvants, Immunologic↗
PubMed1999

Peritoneal antigen-presenting cells pulsed in vivo with myelin basic protein induce the suppression of experimental autoimmune encephalomyelitis (EAE) in Wistar rats.

Suppression of Experimental Autoimmune Encephalomyelitis (EAE) can be achieved by i.p. administration of soluble myelin basic protein (MBP) in adult Wistar rats before the immunization. In the present work, we analyze the role of peritoneal antigen-presenting cells (APC) in the induction of tolerance to EAE. Peritoneal cells (PC) pulsed in vivo with MBP were obtained from rats that had been intraperitoneally injected 2 h previously with soluble MBP (MBP-PC) and then inoculated in recipient rats before the induction of EAE. Our findings show that the i.p. treatment of the animals with MBP-PC before the immunization was able to diminish the incidence and severity of the disease, reduce the histological alterations, abrogate the proliferative response against MBP and change the pattern of the humoral response to MBP. Moreover, when spleen mononuclear cells (MNC) from tolerant animals were cultured together with spleen MNC from sick animals, a dose-dependent inhibition of the proliferative response was observed, arguing for the presence of a regulatory cell population in the tolerant animals. It is also demonstrated that the MBP-PC are activated and their capability of inducing suppression of EAE is highly associated with the enhanced expression of MHC class II IA molecule. Our results show that peritoneal cells pulsed in vivo with MBP are able to induce tolerance and suggest that the up-regulation of MHC class II on MBP-PC is a necessary event for tolerance induction in our model.

Animals↗
PubMed2001

Studies on a model of long term alcohol drinking.

This study investigated the effects of a dihydropyridine calcium channel antagonist in a free drinking model previously reported to show increased and 'uncontrolled' drinking. The results showed, rather than the previously reported increase in consumption, a gradual decrease in alcohol intake over 9-18 months. When the alcohol was withdrawn from one group of rats after 55 weeks free choice, the animals showed no behavioural signs of physical withdrawal, but they did demonstrate the expected elevated ethanol intake on reintroduction to ethanol after 2 weeks abstinence. A second group of rats were given 62 weeks free choice access to ethanol in groups of four, then transferred to single housing and baseline drinking levels established. Intraperitoneal injections of nimodipine 5 mg/kg, 20 mg/kg or Tween vehicle were then given once daily. Nimodipine had no effect on ethanol intake of animals with continuous access to ethanol, or of those animals withdrawn from ethanol and then reintroduced after 2 weeks of abstinence. However the unexpectedly low alcohol intake may have prevented any effects of nimodipine being seen.

Alcohol Drinking↗
PubMed2003

Evaluation of the toxicological effects of perfluorooctane sulfonic acid in the common carp (Cyprinus carpio).

In the present study we evaluated the toxicological effects of a scarcely documented environmental pollutant, perfluorooctane sulfonic acid (PFOS), on selected biochemical endpoints in the common carp, Cyprinus carpio. Juvenile organisms were exposed to PFOS through a single intraperitoneal injection (liver concentrations ranging from 16 to 864 ng/g after 5 days of exposure) and after 1 and 5 days effects were assessed in liver and serum of the exposed organisms. The investigation of the hepatotoxicity of PFOS included the determination of the peroxisome proliferating potential (peroxisomal palmitoyl CoA oxidase and catalase activity) and the compounds influence on the average DNA basepair length (ABPL) by agarose gel electrophoresis. Total antioxidant activity (TAA), cholesterol and triglyceride levels were monitored in the serum. After 1 day of exposure the ABPL was significantly increased in the 270 and 864 ng/g treatment groups. After 5 days of exposure significant increases relative to the control were observed for the 16, 270 and 864 ng/g treatment groups. Enzyme leakage from the liver was investigated by measurement of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities in the serum. At 561, 670 and 864 ng/g PFOS a significant increase in serum ALT activity became apparent after 5 days of exposure with values ranging from 159 to 407% relative to the control. For serum AST activity a significant increase for the 864 ng/g treatment group was observed with a value of 112% relative to the control. Determination of the polymorphonuclear leukocyte migration into liver tissue as assessed through myeloperoxidase (MPO) activity in liver, was used as an indicator for inflammation. It appeared that inflammation was not involved in the observed membranous enzyme leakage for the 561, 670 and 864 ng/g PFOS treatment groups. The results of this study suggest that PFOS induces inflammation-independent enzyme leakage through liver cell membranes that might be related to cell necrosis. Furthermore, results show that PFOS does not significantly affects serum antioxidant levels nor does it clearly induce peroxisome proliferation in carp. This study also points out that PFOS might interfere with homeostasis of the DNA metabolism. The results of these biochemical analyses were used to perform an initial hazard assessment study indicating that PFOS levels observed in tissues of wildlife populations could induce a clear rise in serum transaminase levels indicative for disruption of hepatocyte membrane integrity.

Alkanesulfonic Acids↗