Biomedical subjects

C Barja-Fidalgo

Publications and source records attributed to C Barja-Fidalgo.

25 records · Page 2Linked to original sources

PubMed1993

Rat paw edema and leukocyte immigration induced by plant lectins.

Lectins from Dioclea grandiflora (DG) and Canavalia brasiliensis (CB) were compared with Concanavalin A (ConA) for their ability to induce paw edema and peritoneal cell immigration in rats. ConA caused a slight edema with a peak at 1 h after injection, while DG or CB induced a pronounced and long-lasting edema that reached a maximum at about 6 h. Different antiinflammatory drugs partially inhibited the edema. alpha-D-glucose (GLU) partially blocked the edema caused by ConA and markedly inhibited that due to CB, but had no effect on the edema induced by DG. alpha-Methyl mannoside (alpha-MM) blocked the edema caused by DG and ConA, but did not affect that caused by CB. At doses much lower than those used to induce paw edema, the lectins promoted an intense accumulation of neutrophil and mononuclear cells in the rat peritoneal cavity. CB and DG were more potent than ConA, which also presented a different profile of cell immigration. GLU significantly inhibited leukocyte accumulation caused by all lectins. alpha-MM impaired ConA- and DG-induced cell immigration, but only partially inhibited CB. Thus, despite their physicochemical similarities with ConA, DG and CB have more powerful pro-inflammatory effects. This difference seems to be related to their sugar-binding properties. However, while ConA- and DG-induced effects were inhibited more by alpha-MM than by GLU, CB-induced effects were inhibited more by glucose.

Animals↗

PubMed1992

Role of resident macrophages in canatoxin-induced in vivo neutrophil migration.

Canatoxin (Cntx), a toxic protein purified from Canavalia ensiformis seeds, was shown to have lipoxygenase-mediated effects either in vivo or in vitro. Data here show that Cntx induced a dose-dependent migration of neutrophils and mononuclear cells when injected into rat peritoneal cavities. Furthermore, Cntx was able to induce neutrophil migration into pleural cavities and into air pouches. These effects were inhibited by dexamethasone but not by inhibitors of arachidonic acid metabolism (indomethacin, NDGA, and BW-755c) or by a PAF antagonist (BN 52021). In the peritoneal cavity Cntx caused an increase in vascular permeability inhibited by dexamethasone and BW-755c. Neutrophil migration induced by this toxin was dependent on the number of resident macrophages, since the migratory effect was enhanced by increasing the peritoneal macrophage population with thioglycollate pretreatment and was diminished when this population was reduced by peritoneal wash. It was also observed that Cntx induced release of a chemotactic factor from macrophage monolayers in vitro. Dexamethasone blocked this release but did not affect in vivo neutrophil recruitment induced by that factor. These data suggest that Cntx-induced neutrophil migration may be mediated by the same macrophage-derived neutrophil chemotactic factor released by other stimuli such as LPS, IL-1, and INF-gamma.

Animals↗

PubMed1992

Pharmacological characterization of rat paw edema induced by canatoxin, the toxic protein from Canavalia ensiformis (jack bean) seeds.

Intraplantar injection of canatoxin (CNTX) induced a dose-dependent rat hind-paw edema which was distinguished by two phases. In the first phase, observed between 0 and 2 hr after CNTX injection, there was an increase in paw volume, with no apparent involvement of inflammatory phagocytic cells. The second phase, beginning at about the 3rd hr, was characterized by an intense cellular infiltration at the site of administration which was coincident with a further increase in paw swelling. The edema was maximum at 6 hr after injection and disappeared within 48 hr at doses of 50-100 micrograms, while at doses of 200-300 micrograms edema was present in excess of 48 hr. The pharmacological studies suggested that CNTX-induced edema is a multi-mediated phenomenon. Histamine, serotonin, PAF and prostaglandins are likely involved in the first phase. Lipoxygenase metabolites, probably leukotrienes, seem to play a major role in the second phase, and may account for the development of cellular infiltration in the inflammatory site.

Animals↗

PubMed1992

Canatoxin induces activation on mice peritoneal macrophages.

Canatoxin (CNTX), the toxic protein from Canavalia ensiformis seeds, injected into the peritoneal cavities of mice (10 micrograms/cavity) induced a significant neutrophil migration (10.5 +/- 0.5 x 10(6) cells/cavity) after 4 h. A later migratory effect (48 h) on mononuclear cells, predominantly macrophages, was also observed (controls: 7 +/- 0.9; CNTX: 17 +/- 2.0 x 10(6) cells/cavity). These CNTX-elicited macrophages, when compared to resident cells (R) or cells elicited by thioglycollate (TG), had an increased content of the lysosomal enzyme N-acetyl-beta-D-glucosaminidase (R: 4.5 +/- 0.5; TG: 7.2 +/- 1.0; CNTX: 20.2 +/- 3.0 mU/10(6) cells) and a greater (> or = 100%) phagocytic activity. The data suggest that CNTX-stimulated macrophages presented some characteristics of activated cells.

Acetylglucosaminidase↗

PubMed1991

Lipoxygenase-mediated secretory effect of canatoxin the toxic protein from Canavalia ensiformis seeds.

Canatoxin was shown to induce serotonin release from rabbit platelets and rat brain synaptosomes, as well as to release insulin from isolated pancreatic islets. All these effects were dose-dependent and were inhibited by lipoxygenase inhibitors, such as nordihydroguaiaretic acid and esculetin, but not by indomethacin, a cyclooxygenase inhibitor. The data suggest that canatoxin-induced secretory effect results from the activation of the lipoxygenase pathway which would elicit exocytosis. Thus, canatoxin might be a useful tool for the study of biological events that involve lipoxygenase mediation.

Animals↗

PubMed1991

Canatoxin, a plant protein, induces insulin release from isolated pancreatic islets.

Canatoxin (CNTX), the toxic protein purified from Canavalia ensiformis, has been shown to induce secretion from different cellular systems through a mechanism involving a lipoxygenase-mediated pathway. Here it is shown that CNTX causes insulin release from isolated rat pancreatic islets. This effect is time and dose dependent, occurs in the absence as well in the presence of glucose, and is markedly reduced at lower temperatures (15 C). At 1-2 microM, the insulinotropic effect of CNTX is equivalent to that of 20 mM glucose, and the two responses are not additive. The stimulatory effect of CNTX is not caused by a toxic or lytic effect of the toxin on the islets, since islets once exposed to CNTX are able to respond a new insulinotropic stimulus. The phospholipase inhibitor mepacrine impairs insulin release induced by either CNTX or glucose. Indomethacin, an inhibitor of the cyclooxygenation of arachidonic acid, fails to affect insulin release, but two lipoxygenase inhibitors block it, and epinephrine reduces it. These data suggest that CNTX may act on islets through the same pathway as that used by glucose, with both effects being mediated by lipoxygenases.

Animals↗

PubMed1988

The secretory effect of canatoxin on rat brain synaptosomes involves a lipoxygenase-mediated pathway.

Canatoxin (CNTX), a neurotoxic protein, is known to activate platelet secretion and aggregation in vitro through a lipoxygenase-dependent pathway. This study shows that CNTX also induces time and dose-dependent serotonin secretion from rat brain synaptosomes. The secretory effect induced by 6 microM CNTX was similar to that elicited by 150 mM KCl. Nordihydroguaiaretic acid (500 microM) completely abolished CNTX-induced serotonin release while 150 microM indomethacin had no effect. These data suggest the involvement of the lipoxygenase pathway in neurotransmitter release elicited by CNTX as occurs in the platelet.

Animals↗