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1.
Pak J Biol Sci ; 16(24): 1873-83, 2013 Dec 15.
Article in English | MEDLINE | ID: mdl-24517002

ABSTRACT

The emergence of various diseases specifically severe diseases such as bronchial asthma is associated with apoptosis of lymphocytes. One of the major biochemical features of apoptosis is chromosome DNA fragmentation implemented by apoptotic nucleases. The inactivation of these apoptotic nucleases produces undigested DNA and is linked to a number of autoimmune disorders. Instead of this we have studied the enzymatic activities of the cytoplasmic and nucleic proteins of lymphocytes from healthy donors and patients with bronchial asthma. The study of enzymatic activities of the nuclease of lymphocytes was assessed by flow cytometry, spectrofluorimetry and electrophoresis method in agarose gel. In the peripheral blood cells of healthy donors undergoing apoptosis, we found a DNAse activated by Ca2+ and Mg2+ ions. Lymphocytes of patients with bronchial asthma contain DNAses, the activity of which depends on the seriousness of the desease. In patients cells, the activity of the Mn2+-dependent DNAse increases, whereas the activity of the Ca2+, Mg(2+)-dependent DNase decreases. Taking into consideration the role of the Ca2+, Mg(2+)-dependent DNAse in apoptosis, we can propose that there is a link between the reduction of the rate of apoptosis of lymphocytes in patients with bronchial asthma and the dysfunction of the induction of "apoptotical" Ca2+, Mg(2+)-dependent nuclease. According to the results obtained, we can assume that why apoptosis of lymphocytes resist in patients with bronchial asthma is a reduction in concentration of endocellular calcium and an increase of manganese ions content, which results in the triggering of activation mechanism for Mn(2+)-dependent endonuclease activity. This leads to the change of DNA fragmentation nature in lymphocytes and as a consequence, to disorders in process of apoptotic bodies' formation, thus, hindering apoptosis of lymphocytes in patients with bronchial asthma.


Subject(s)
Apoptosis , Asthma/pathology , Deoxyribonucleases/metabolism , Lymphocytes/pathology , Asthma/diagnosis , Asthma/enzymology , Asthma/immunology , Calcium/metabolism , Case-Control Studies , DNA Fragmentation , Electrophoresis, Agar Gel , Enzyme Activation , Flow Cytometry , Humans , Lymphocytes/enzymology , Lymphocytes/immunology , Manganese/metabolism , Severity of Illness Index , Spectrometry, Fluorescence
2.
Mali Med ; 27(2): 19-24, 2012.
Article in French | MEDLINE | ID: mdl-30049075

ABSTRACT

OBJECTIVE: Observing the concentrations of free thyroxine (FT4) and thyrotropin (TSH), in infants born in Cotonou, Benin to establish the profile of neonatal thyroid disturbance. DESIGN AND SUBJECTS: The detection of thyroid immune status was done by measuring the antibodies to thyroglobulin (Tg Ab Anti) and Antibody and Anti Thyroperoxidase (Anti TPO Ab) ratio. Blood was collected from 177 neonates aged 0 to 7 days. RESULTS: We measured free thyroxine, thyrotropin , and antibodies to thyroglobulin, Anti Thyroperoxidase and detected a prevalence of dysfunction of the thyroid gland in neonates is from 28% for hypothyroidism, 2.25% of hyperthyroidism. Among hypothyroid, there was a frank hypothyroidism of 53%, hypothyroidism in 25% Primary, secondary hypothyroidism of 20% and hypothyroidism unspecified 2%. Also 73.33% of hypothyroid shows an antibody against thyroglobulin above the threshold of normality and 41.18% of euthyroid have a high Anti thyroglobulin Antibody This allows us to suggest lymphocytic thyroiditis. CONCLUSION: The results of our studies show the onset of thyroid disease after neonatal hypothyroidism very pronounced. This is probably due to a transfer of the Anti- thyroglobulin Antibody of maternal origin to the fetus during pregnancy.


BUT: La détermination des concentrations de thyroxine libre (T4 libre) et de thyrotropine (TSH), chez 177 nouveaux nés âgés de 0 à 7 jours à Cotonou au Bénin a permis d'établir le profil de perturbations thyroïdiennes néonatales. MATÉRIELS ET MÉTHODE: L'état thyroïdien immunitaire a été mis en évidence par le dosage des anticorps anti thyroglobuline (Ac Anti Tg) et Anticorps anti Thyroperoxydase (Ac Anti TPO). RÉSULTATS: La prévalence du dysfonctionnement de la glande thyroïde chez les nouveaux nés a été de 28% d'hypothyroïdie et 2,25 % d'hyperthyroïdie. Parmi les hypothyroïdiens, on note une hypothyroïdie franche de 53%, une hypothyroïdie primaire de 25%, une hypothyroïdie secondaire de 20% et une hypothyroïdie indéterminée de 2%. Aussi 73,33% des hypothyroïdiens présentent-ils un taux d'anticorps anti thyroglobulines supérieur au seuil de la normalité et 41,18% des euthyroïdiens, un taux élevé d'anticorps anti thyroglobulines. Ceci a permis de suggérer une thyroïdite lymphocytaire. CONCLUSION: Les résultats des travaux ont montré l'apparition des affections thyroïdiennes néonatales par une l'hypothyroïdie très prononcée. Celle-ci est probablement due à un transfert de l'anticorps anti thyroglobuline d'origine maternelle vers le fœtus pendant la gestation.

3.
ISRN Vet Sci ; 2012: 915729, 2012.
Article in English | MEDLINE | ID: mdl-23738133

ABSTRACT

An experiment was carried out to define the optimal rate of palm-press fibres in growing rabbits' diet. In total, 64 weaned rabbits (35 days old) of Beninese breed were divided in 16 groups of 4 rabbits (2 males and 2 females) each. During six weeks, rabbits were fed with 4 complete diets containing 0% (F0, control), 5% (F5), 10% (F10), and 15% (F15) of fibres from a palm oil industry. Results demonstrated that up to 15 of palm-press fibres can be included efficiently in growing rabbits' diet. The daily feed intake was not significantly affected by the diet (P > 0.05). At 13 weeks old, the average live weights of rabbits were 1788.5 g, 1805.0 g, 1718.5 g, and 1801.3 g in respectively, F0, F5, F10 and F15 groups. No mortality of rabbits was recorded. Compared to F0, the feed conversion ratio and feeding cost decreased in the group of rabbits fed F15 diet. The carcass yield was similar between diets.

4.
Article in French | AIM (Africa) | ID: biblio-1264120

ABSTRACT

Les perturbations thyroidiennes sont connues pour etre un probleme de sante dans presque tous les pays du monde. Au Benin; rien n'est fait afin de comprendre l'ampleur et l'evolution de ces perturbations. But : Nous avons initie ce travail dans le but d'etablir le profil des differents types de perturbations. La ville de Tanguieta au Nord du Benin a ete choisie comme ville d'etude. Methode : nous avons recueilli le sang veineux chez 320 individus dans la population selectionnee selon les criteres bien definis (sexe; age profession) 51;87dans la commune urbaine de Tanguieta (Brouniessou et Biakou) et 48;13dans la commune rurale de Taiacou (Nafayoti et Tahongou). Les analyses suivantes ont ete realisees : Dosage de T3; T4 libre; TSH ultra sensible par la technique d'ELISA. Resultats : Les perturbations thyroidiennes apparaissent chez les deux sexes (32dans la population masculine et 46;11dans la population feminine). D'une facon generale 41;4des sujets preleves avaient une perturbation thyroidienne ; avec un taux de perturbations le plus elevee dans le village de Tahougou et le moins elevee dans le village de Brouniessou. Les perturbations thyroidiennes touchent les cultivatrices et menageres (48) les cultivateurs (35;84) et les eleves (32;61). Les perturbations thyroidiennes sont abondantes dans la ville et regions environnantes de Tanguieta. Elles touchent principalement les femmes (hypothyoidies : 19;68. 13;43des hommes entre 45-60 ans sont ont une hyperthyroidie. Les autres perturbations thyroidiennes (taux isolement eleves de T3; T4 libre ou TSH) sont evaluees a 7;5. Conclusion : Les perturbations thyroidiennes sont presentes dans cette region de Benin. Une etude approfondie sur les autres indicateurs biologiques (facteurs goitrigenes) permettra d'elucider profondement la question


Subject(s)
Benin , Goiter , Iodine/deficiency , Thyroid Hormones
5.
Am J Physiol Gastrointest Liver Physiol ; 290(1): G66-73, 2006 Jan.
Article in English | MEDLINE | ID: mdl-16081764

ABSTRACT

Coordination of intercellular Ca2+ signals is important for certain hepatic functions including biliary flow and glucose output. Prostaglandins, such as PGF2alpha and PGE2, may modify these hepatocyte functions by inducing Ca2+ increase, but very little is known about the organization of the Ca2+ signals induced by these agonists. We studied Ca2+ signals induced by PGF2alpha and PGE2 in fura-2 AM-loaded hepatocyte doublets. Even though both prostaglandins induced Ca2+ oscillations, neither PGF2alpha nor PGE2 induced coordinated Ca2+ oscillations in hepatocyte doublets. Gap junction permeability (GJP), assessed by fluorescence recovery after photobleaching, showed that this absence of coordination was not related to a defect in GJP. Inositol (1,4,5)trisphosphate [Ins(1,4,5)P3] assays and the increase in Ins(1,4,5)P3 receptor sensitivity to Ins(1,4,5)P3 observed in response to thimerosal suggested that the absence of coordination was a consequence of the very small quantity of Ins(1,4,5)P3 formed by these prostaglandins. Furthermore, when PGE2 and PGF2alpha were added just before norepinephrine, they favored the coordination of Ca2+ signals induced by norepinephrine. However, GJP between hepatocyte doublets was strongly inhibited by prolonged (>or=2 h) treatment with PGF2alpha, thereby preventing the coordination of Ca2+ oscillations induced by norepinephrine in these cells. Thus, depending on the time window, prostaglandins, specially PGF2alpha, may enhance or diminish the propagation of Ca2+ signals. They may therefore contribute to the fine tuning of Ca2+ wave-dependent functions, such as nerve stimulation, hormonal regulation of liver metabolism, or bile secretion, in both normal and pathogenic conditions.


Subject(s)
Calcium Signaling/drug effects , Calcium/metabolism , Dinoprost/pharmacology , Dinoprostone/pharmacology , Hepatocytes/drug effects , Hepatocytes/metabolism , Animals , Cell Membrane/metabolism , Dinoprost/metabolism , Dinoprostone/metabolism , Female , Gap Junctions/metabolism , Hepatocytes/cytology , Inositol 1,4,5-Trisphosphate/metabolism , Membrane Potentials/drug effects , Membrane Potentials/physiology , Norepinephrine/pharmacology , Rats , Receptors, Prostaglandin/metabolism
6.
Article in French | AIM (Africa) | ID: biblio-1264262

ABSTRACT

Nous avons etudie l'effet de la chloroquine sur la production du peroxyde d'hydrogene par la thyroide de porc et les modifications morphologiques induites. Trois groupes experimentaux ont ete constitues : porcs temoin (sans traitement); porcs traites a la chloroquine et porcs traites a la chloroquine associee a l'iodure de sodium. Nous avons demontre que l'administration de la chloroquine a induit dans la thyroide de porc; un elargissement des lumieres folliculaires; un aplatissement de l'epithelium glandulaire et une augmentation brutale de la production d'H202 suivie d'une stabilisation. D'apres nos resultats; la chloroquine n'aurait donc pas d'effet direct sur l'enzyme la NAD(P)H oxydase. Cette etude suscite de nouvelles questions et devra etre poursuivie sur d'autres molecules utilisees dans le traitement du paludisme. Mots cles : chloroquine; goitre experimental; goitre colloide; production d'H2O2


Subject(s)
Animal Experimentation , Chloroquine , Goiter , Hydrogen Peroxide , Thyroid Gland
7.
Arch Physiol Biochem ; 104(7): 826-32, 1996 Dec.
Article in French | MEDLINE | ID: mdl-9221105

ABSTRACT

Calcium loading of a rat parotid microsomal fraction is greatly increased by an ATP-regenerating system (phosphocreatine and creatine phosphokinase). This effect is neither a consequence of a rise in the ATP concentration nor of an increased formation of inorganic phosphate originating from hydrolysis of ATP or phosphocreatine. Addition of ADP to the incubation medium provokes an inhibition of Ca2+ influx and a stimulation of Ca2+ efflux by the microsomal fraction. These results suggest that the stimulation of Ca2+ uptake by the ATP-regenerating system is due, at least in part, to an increase of Ca2+ influx and a slowing down of Ca2+ efflux as consequence of a decrease of ADP availability. It is proposed that the effect of ADP on Ca2+ movements could account for the action of certain agonists on intracellular Ca2+ concentration. Moreover, the InsP3 responsive Ca2+ pool was also shown to be enlarged by the ATP-regenerating system without modification of InsP3 sensitivity.


Subject(s)
Adenosine Diphosphate/pharmacology , Adenosine Triphosphate/metabolism , Calcium/metabolism , Microsomes/metabolism , Parotid Gland/metabolism , Adenosine Triphosphatases/metabolism , Animals , Biological Transport , Calcium Radioisotopes/metabolism , Creatine Kinase/metabolism , Inositol 1,4,5-Trisphosphate/metabolism , Ionomycin/pharmacology , Ionophores/pharmacology , Male , Parotid Gland/ultrastructure , Phosphocreatine/metabolism , Rats , Rats, Sprague-Dawley
8.
C R Seances Soc Biol Fil ; 189(2): 281-8, 1995.
Article in French | MEDLINE | ID: mdl-8590226

ABSTRACT

The variations in the intracellular free calcium concentration, [Ca2+]i, have been studied in isolated acini of rat parotid gland with a fluorescent probe, fura-2. In unstimulated acini, [Ca2+]i amounted to a basal value of 180 nM. Isoproterenol used at a concentration of 200 microM, in the presence of a beta-adrenergic blocker, caused a net increase of [Ca2+]i to a mean of 90 nM above basal values. This increase was suppressed by phentolamine, an alpha-adrenergic blocker. A weak increase of [Ca2+]i of 47 nM was also obtained when acini were incubated with 1 microM isoproterenol. This effect was suppressed with 0.1 microM propranolol which, at this concentration, specifically antagonizes the beta-adrenergic receptors. We conclude that isoproterenol at 1 microM, increases the [Ca2+]i by stimulating beta-adrenergic receptors. This effect is not reproduced by forskoline. Our results suggest that this isoproterenol effect on [Ca2+]i is independent of the formation of cyclic AMP. Moreover, when the isoproterenol concentration is high (200 microM), the increase of [Ca2+]i could be through an activation of alpha-adrenergic receptors.


Subject(s)
Calcium/analysis , Isoproterenol/pharmacology , Parotid Gland/chemistry , Animals , Carbachol/pharmacology , Drug Administration Schedule , Isoproterenol/administration & dosage , Male , Parotid Gland/drug effects , Propranolol/pharmacology , Rats , Rats, Sprague-Dawley
9.
J Cell Physiol ; 157(3): 493-501, 1993 Dec.
Article in English | MEDLINE | ID: mdl-8253860

ABSTRACT

The study was conducted on human leukemia (K 562) cells to characterize the mechanisms implicated in the regulation of the polyamine spermidine (Spd) transport process. The antagonists of calmodulin, trifluoperazine (TFP), W-7 (N-[6-aminohexyl]-5-chloro-1-naphthelenesulfonamide), or mellitin inhibited significantly polyamine Spd uptake in these cells. The translocation of calmodulin towards plasma membrane and a concomitant decrease in its contents in cytosol were directly correlated with the time course increases similar to that of Spd uptake, indicating that calmodulin is recruited towards plasma membrane during the Spd transport process. Diminution of free intracellular calcium, (Ca2+)i, by preincubating the cells in BAPTA (bis[2-amino-5-methylphenoxyl]-ethane-N,N,N',N',-tetraacetate) buffer inhibited Spd transport significantly. Addition of lanthanum (LAN), a molecule known to inhibit Ca2+ efflux via Ca(2+)-ATPase, curtailed Spd uptake by these cells. LAN inhibited Vmax, but not the Km, of Spd uptake, indicating that the former does not directly interact with the polyamine transporter; rather it regulates the transport process, probably via its action on Ca(2+)-ATPase. Calmodulin-stimulated uptake of 45Ca2+ by inside-out vesicles of K 562 cells, a measure of Ca(2+)-ATPase activity. Furthermore, addition of LAN inhibited both basal and calmodulin-stimulated activity of Ca(2+)-ATPase. Thapsigargin (THAP), a molecule known to elevate (Ca2+)i due to its action on the endoplasmic reticulum, increased Spd transport whereas addition of LAN inhibited THAP-stimulated Spd transport activity. THAP increased free (Ca2+)i in these cells, and a pre-addition of LAN to these cells curtailed the THAP-stimulated increases of (Ca2+)i concentrations. Addition of Spd brought about elevations in (Ca2+)i contents. Caffeine also increased (Ca2+)i in these cells; however, it failed to stimulate significantly the Spd uptake process, indicating that (Ca2+)i which is involved in the regulation of polyamine transport pathways does not belong to the calcium-induced calcium-release (CICR) pool. Replacement of Ca2+ from the incubation medium (i.e., 0% Ca2+) resulted in higher uptake activity as compared to that in 100% Ca2+ medium, demonstrating that in 100% Ca2+ medium the calcium efflux process is quickly compensated by calcium refilling/influx from the extracellular medium, while in 0% Ca2+ medium there is perpetual efflux of (Ca2+)i which contributes to higher Spd uptake process. The results of this study suggest that an increase in free (Ca2+)i and its release from the cells via Ca(2+)-ATPase, and concomitant activation of calmodulin, which controls Ca(2+)-pump activity, are involved in the regulation of the Spd uptake process in human leukemia cells.


Subject(s)
Calcium-Transporting ATPases/metabolism , Calcium/metabolism , Calmodulin/metabolism , Spermidine/metabolism , Biological Transport , Calmodulin/antagonists & inhibitors , Egtazic Acid/analogs & derivatives , Egtazic Acid/pharmacology , Humans , Lanthanum/pharmacology , Melitten/pharmacology , Sulfonamides/pharmacology , Terpenes/pharmacology , Thapsigargin , Trifluoperazine/pharmacology , Tumor Cells, Cultured
10.
Biochem Biophys Res Commun ; 175(3): 894-900, 1991 Mar 29.
Article in English | MEDLINE | ID: mdl-1850995

ABSTRACT

In this study, we report our data on the binding of D-myoinositol(1,4,5)P3 and of 6-deoxy D-myoinositol(1,4,5)P3 to a rat parotid microsomal fraction and their effect on Ca2+ release. The binding affinity and the potency of 6-deoxy Ins(1,4,5)P3 to induce Ca2+ release are about 100 times lower than those of Ins(1,4,5)P3. However, maximal concentrations of both inositol trisphosphates induce similar calcium efflux and present comparable displacement of radioligand binding. Experiments were performed to exclude that the microsomal preparations used display rapid metabolism of Ins(1,4,5)P3 or 6-deoxy Ins(1,4,5)P3 during binding and Ca2+ release. We also report that, in permeabilized rat parotid acini preparations, 6-deoxy Ins(1,4,5)P3 is about 100 times less potent than Ins(1,4,5)P3 in inducing Ca2+ release. These data indicate that removal of the hydroxyl group in position 6 of the Ins(1,4,5)P3 molecule severely reduces its binding affinity which seems, in a large part at least, responsible for the reported loss of potency in mobilizing Ca2+. Nevertheless, 6-deoxy Ins(1,4,5)P3 seems to be a full agonist for the release of Ca2+.


Subject(s)
Calcium Channels , Calcium/metabolism , Inositol 1,4,5-Trisphosphate/analogs & derivatives , Inositol 1,4,5-Trisphosphate/metabolism , Microsomes/metabolism , Parotid Gland/metabolism , Receptors, Cell Surface/metabolism , Receptors, Cytoplasmic and Nuclear , Animals , Binding, Competitive , Dose-Response Relationship, Drug , Inositol 1,4,5-Trisphosphate/pharmacology , Inositol 1,4,5-Trisphosphate Receptors , Kinetics , Microsomes/drug effects , Phosphoric Monoester Hydrolases/metabolism , Rats
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