Full-text resources of CEJSH and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl

Results found: 3

first rewind previous Page / 1 next fast forward last

Search results

help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
EN
Objectives: The aim of the study was the assessment of local tolerance to nickel implants during 9 months observation in guinea pigs sensitized to nickel before implantation and non-sensitized ones. Materials and Methods: Three groups of guinea pigs were included in the study: 10 sensitized to nickel by the guinea pig maximization test; 10 previously nonsensitized and 10 in control group. In 20 animals (except control group) the nickel implants were inserted in the muscle of the back. After 9 months of observation, the animals were patch-tested with 5% nickel sulfate. Also percentage of eosinophils in peripheral blood was examined. Next, the tissue surrounding the implant and skin from the area of patch tests were collected for the histological examination. Results: In 70% of previously sensitized animals, the patch test confirmed the sensitivity to nickel. In 60% of previously non-sensitized animals, a positive reaction to nickel occurred. The results of patch tests in control group were negative. Percentage of eosinophils in peripheral blood was fourfold higher in animals sensitized to nickel than in control group. In histological examination, in the tissue surrounding the implant a dissimilarity concerning the intensity of cellular infiltration was observed between animals previously allergic and non-allergic to nickel. In the 2 of 10 previously sensitized guinea pigs quite severe inflammatory reactions in the inside of connective tissue capsule were noted which may indicate a local allergic reaction. The histological images of skin collected from the positive patch test site corresponded with the typical allergic contact dermatitis. Conclusions: Nickel implants may cause primary sensitization to nickel. The nature of the histological changes in the tissues around the implants in guinea pigs sensitized to nickel may correspond to an allergic reaction. The examination of percentage of eosinophils in blood of guinea pigs may be useful in assessing the allergenic activity of metal alloys containing nickel.
EN
Objectives: Diisocyanates (DIC) are highly reactive, low-molecular-weight chemicals which are the leading cause of occupational asthma (OA). The aim of the study was to analyze certain aspects of the pathogenesis of allergic infl ammation in the airways induced by toluene diisocyanate (TDI) in an experimental model in mice. Materials and Methods: The experiment was carried out on 50 female BALB/cJ/Han/IMP mice, which were exposed by inhalation (intranasal and in the inhalation chamber) to toluene diisocyanate (2,4-TDI). After the experiment, the bronchoalveolar lavage fluid (BALF) was collected from the animals, and the composition of the induced infl ammatory cells, and the concentrations of certain cytokines (IL-4, IL-5, TNF-α) were evaluated. Results: The total number of cells in BALF of the examined group of mice was signifi cantly higher compared to the control mice. There was also a signifi cant increase in neutrophils and eosinophils in the study group compared to the controls. The number of lymphocytes and macrophages did not differ signifi cantly between the two groups. A statistically signifi cant increase in the level of TNF-α was shown to occur in the group exposed to toluene diisocyanate in comparison to the control group. The concentration of IL-4 increased in the study group, compared to the control one, but the differences did not reach the level of signifi cance, p > 0.05. Such difference was not observed for IL-5. Conclusions: We developed a murine model of TDI-induced asthma which caused the infl ux of infl ammatory cells like eosinophils and neutrophils in the bronchoalveolar lavage fl uid (BALF) in the TDI-treated mice. The increase of the concentration of some proinfl ammatory cytokines (TNF-α, IL-4) in BALF from the exposed mice was also observed.
EN
Background: Organophosphates are cholinesterase (ChE) inhibitors with worldwide use as insecticides. Stress response, evidenced by a dramatic and relatively long-lasting (several hours) rise in the plasma glucocorticoid concentration is an integral element of the organophosphate (OP) poisoning symptomatology. In rodents, corticosterone (CORT) is the main glucocorticoid. There are several reports suggesting a relationship between the stressor-induced rise in CORT concentraion (the CORT response) and the activity of the cerebral and peripheral ChE. Thus, it seems reasonable to presume that, in OP intoxication, the rise in plasma CORT concentration may somehow affect the magnitude of the OP-induced ChE inhibition. Metyrapone (MET) [2-methyl-1,2-di(pyridin-3-yl)propan-1-one] blocks CORT synthesis by inhibiting steoid 11β-hydroxylase, thereby preventing the CORT response. Chlorfenvinphos (CVP) [2-chloro-1-(2,4-dichlorophenyl) ethenyl diethyl phosphate] is an organophosphate insecticide still in use in some countries. Material and Methods: The purose of the present work was to compare the CVP-induced effects - the rise of the plasma CORT concentration and the reduction in ChE activity - in MET-treated and MET-untreated rats. Chlorfenvinphos was administered once at 0.0, 0.5, 1.0 and 3.0 mg/kg i.p. Metyrapone, at 100 mg/kg i.p., was administered five times, at 24-h intervals. The first MET dose was given two hours before CVP. Conclusion: The following was observed in the MET-treated rats: i) no rise in plasma CORT concentration after the CVP administration, ii) a reduced inhibition and a faster restitution of blood and brain ChE activities. The results suggest that MET treatment may confer significant protection against at least some effects of OP poisoning. The likely mechanism of the protective MET action has been discussed.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.