scholarly journals The Insecticidal Activity of Rhinella schneideri (Werner, 1894) Paratoid Secretion in Nauphoeta cinerea Cocroaches

Toxins ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 630
Author(s):  
Allan Leal ◽  
Etiely Karnopp ◽  
Yuri Correia Barreto ◽  
Raquel Soares Oliveira ◽  
Maria Eduarda Rosa ◽  
...  
Keyword(s):  
Isolated Heart ◽  
Acetylcholinesterase Activity ◽  
Nauphoeta Cinerea ◽  
Rhinella Schneideri ◽  
Heart Preparation ◽  
Dose Dependent Decrease ◽  
Ld50 Value ◽  
Nerve Muscle ◽  
Dose Dependent

Rhinella schneideri is a common toad found in South America, whose paratoid toxic secretion has never been explored as an insecticide. In order to evaluate its insecticidal potential, Nauphoeta cinerea cockroaches were used as an experimental model in biochemical, physiological and behavioral procedures. Lethality assays with Rhinella schneideri paratoid secretion (RSPS) determined the LD50 value after 24 h (58.07µg/g) and 48 h exposure (44.07 µg/g) (R2 = 0.882 and 0.954, respectively). Acetylcholinesterase activity (AChE) after RSPS at its highest dose promoted an enzyme inhibition of 40%, a similar effect observed with neostigmine administration (p < 0.001, n= 5). Insect locomotion recordings revealed that RSPS decreased the distance traveled by up to 37% with a concomitant 85% increase in immobile episodes (p < 0.001, n = 36). RSPS added to in vivo cockroach semi-isolated heart preparation promoted an irreversible and dose dependent decrease in heart rate, showing a complete failure after 30 min recording (p < 0.001, n ≥ 6). In addition, RSPS into nerve-muscle preparations induced a dose-dependent neuromuscular blockade, reaching a total blockage at 70 min at the highest dose applied (p < 0.001, n ≥ 6). The effect of RSPS on spontaneous sensorial action potentials was characterized by an increase in the number of spikes 61% (p < 0.01). Meanwhile, there was 42% decrease in the mean area of those potentials (p < 0.05, n ≥ 6). The results obtained here highlight the potential insecticidal relevance of RSPS and its potential biotechnological application.

scholarly journals In vitro alteration of receptors for vasoactive intestinal peptide changes the in vivo localization of mouse T cells.

1984 ◽  
Vol 160 (4) ◽  
pp. 1054-1069 ◽  
Author(s):  
C A Ottaway
Keyword(s):  
T Cells ◽  
Vasoactive Intestinal Peptide ◽  
Receptor Expression ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Mesenteric Lymph Nodes ◽  
Dose Dependent Decrease ◽  
Dose Dependent

The capacity of T lymphocytes exposed in vitro to the neuropeptide vasoactive intestinal peptide (VIP) to bind VIP in vitro and to migrate to different tissues in vivo has been studied. VIP treatment of T cells resulted in a time- and dose-dependent loss of the ability of T cells to specifically bind radioiodinated VIP. Altered binding was due to a decrease in the expression of cellular receptors for VIP on the treated cells rather than an alteration in the affinity of the cells for the neuropeptide. Alteration of VIP receptor expression was not associated with a change in the expression of Thy-1, Lyt-1, or Lyt-2 surface markers by the treated cells. VIP treatment of T cells in vitro resulted, however, in a dose-dependent decrease in the ability of the treated cells to localize in mesenteric lymph nodes (MLN) and Peyer's patches of recipient animals at early times after cell transfer, and this was due to a selective decrease in the rate of accumulation of the treated cells in these tissues. There was no alteration in the distribution of VIP-treated cells in the blood, spleen, liver, or other major organs of the recipient animals. It is concluded that the presence of VIP receptors on T cells facilitates the entry of T cells into MLN and Peyer's patches in vivo, and it is proposed that this effect is mediated by T cell-VIP interactions in the vicinity of the specialized endothelium of those tissues.

3,3′,5′-Triiodothyronine inhibits ontogenetic development of iodothyronine-5′-deiodinase in the liver of the neonatal mouse

1988 ◽  
Vol 119 (2) ◽  
pp. 181-188 ◽  
Author(s):  
Doo Chol Han ◽  
Kanji Sato ◽  
Yuko Fujii ◽  
Minoru Ozawa ◽  
Hidehito Imamura ◽  
...  
Keyword(s):  
Single Injection ◽  
Inhibitory Effect ◽  
Antagonistic Effect ◽  
Time Dependent ◽  
Dependent Manner ◽  
Neonatal Mice ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Abstract. To elucidate the effect of rT3 on iodothyronine-5′-deiodinating activity (I-5′-DA) in the liver of neonatal mice, rT3 was injected sc on the 5–8th day after birth and I-5′-DA in the liver was determined. A single injection of rT3 (0.01–1 μg/g) inhibited the ontogenetically developing I-5′-DA in a dose- and time-dependent manner. The inhibitory effect was reversible and specific for I-5′-DA. Lineweaver-Burk analysis revealed that the time- and dose-dependent decrease in the enzyme activity was due to a decrease in Vmax with no alteration in Km values (5 × 10−8 mol/l). The maximal inhibitory effect was observed at a dose of 1 μg rT3/g, whereas the inhibitory effect was diminished at greater doses (4–10 μg/g), probably owing to a contamination with T4 of the rT3 preparation administered. Furthermore, consistent with our previous in vitro findings, rT3 inhibited the I-5′-DA induced by T3 in the liver of neonatal mice. These findings suggest that rT3 inhibited I-5′-DA in the liver of neonatal mice by decreasing the amount of enzyme available to the substrate and that rT3 also elicited an antagonistic effect against T3 in the induction of I-5′-DA in vivo.

Oral aluminum administration to rats with normal renal function. 1. Impairment of erythropoiesis

1998 ◽  
Vol 17 (6) ◽  
pp. 312-317 ◽  
Author(s):  
Graciela Garbossa ◽  
Gladys Gálvez ◽  
María E Castro ◽  
Alcira Nesse
Keyword(s):  
Osmotic Fragility ◽  
Hemoglobin Concentration ◽  
Local Effect ◽  
Erythroid Progenitor ◽  
Al Content ◽  
Erythroid Progenitor Cells ◽  
Cell Life ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Aluminum (Al) toxicity has been mainly investigated in uremic patients although healthy subjects and patients without renal insufficiency are not exempt from its potential deleterious effects. This experimental study aims to elucidate the action of different doses of Al citrate on in vivo erythropoiesis and find out whether the metal exerts a local toxic effect upon the bone marrow late erythroid progenitor cells. The groups in the first experimental series were: C1 (n=5) controls and TAl-1 (n=5) rats receiving 1 mmol Al citrate/g body weight/day by gavage. Colony-forming units-erythroid (CFU-E) development was inhibited in the TAl-1 group, but the median osmotic fragility (MOF) and hematocrit (Ht) values were similar to those of the C1 group. The groups in the second series were C2 (n=5) controls and TAl-2 (n=5) rats receiving Al citrate in drinking water (100 mmol/l). The TAl-2 group showed decreased Ht, hemoglobin concentration, MOF and red blood-cell life-span values (P50.05), and a marked inhibition of the CFU-E development (P50.01). Serum and bone Al concentrations were increased in both Al-treated groups (P50.01). There was a dose-dependent increase in bone Al levels (P50.01) and a dose-dependent decrease of CFU-E development (P50.05). The CFU-E development was inversely correlated with the bone Al content (r=70.79; P50.05). The results demonstrate that even very low doses of Al citrate impair erythropoiesis in vivo and higher doses exert a deleterious action on both CFU-E and mature erythrocytes. This might show a local effect of Al on CFU-E caused by the bone sensitivity to the metal accumulation.

AM reverses pressor response to ET-1 independently of NO in rat coronary circulation

2001 ◽  
Vol 281 (3) ◽  
pp. H1178-H1183 ◽  
Author(s):  
Pietari Kinnunen ◽  
Jarkko Piuhola ◽  
Heikki Ruskoaho ◽  
István Szokodi
Keyword(s):  
Perfusion Pressure ◽  
Pressor Response ◽  
Vasoconstrictor Response ◽  
Heart Preparation ◽  
Simultaneous Activation ◽  
Nos Inhibitor ◽  
Dose Dependent Decrease ◽  
Dose Dependent ◽  
Constrictor Response ◽  
Coronary Vasoconstrictor

Endothelin-1 (ET-1) elicits a vasoconstrictor response via ETA receptors, whereas simultaneous activation of ETB receptors triggers the release of nitric oxide (NO), which may limit the constrictor effect of ET-1. Recently, stimulation of ETB receptors has been shown to increase the secretion of adrenomedullin (AM), a newly identified vasorelaxing peptide. The present study was designed to see whether AM can oppose the vasoconstrictor response to ET-1. In the isolated perfused paced rat heart preparation, infusion of ET-1 at concentrations of 1 nmol/l for 30 min induced a significant coronary vasoconstriction, whereas it had no effect on perfusion pressure at a dose of 0.08 nmol/l. N ω-nitro-l-arginine methyl ester (l-NAME; 300 μmol/l), a potent inhibitor of NO synthase (NOS), did not change the perfusion pressure when added alone to the perfusion fluid but it unmasked the constrictor effect of ET-1 at both concentrations. In the presence of l-NAME, AM (0.03 to 1 nmol/l) markedly reversed the pressor response to ET-1 at both concentrations. Administration of AM (0.03 and 1 nmol/l) alone resulted in a dose-dependent decrease in perfusion pressure, which was not modified in the presence of l-NAME. In conclusion, the coronary vasoconstrictor response to ET-1 is markedly augmented in the presence of a NOS inhibitor. This constrictor response is substantially reversed by AM. Our results indicate that AM may serve as a paracrine modulator of ET-1-induced vasoconstriction independently of the NO pathway.

Concurrent generation of nitric oxide and superoxide damages surfactant protein A

1994 ◽  
Vol 267 (3) ◽  
pp. L242-L249 ◽  
Author(s):  
I. Y. Haddad ◽  
J. P. Crow ◽  
P. Hu ◽  
Y. Ye ◽  
J. Beckman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Xanthine Oxidase ◽  
Protein A ◽  
Surfactant Protein ◽  
Simultaneous Generation ◽  
Tyrosine Residues ◽  
Dose Dependent Decrease ◽  
Dose Dependent

The conditions under which nitric oxide (.NO) may modulate or promote lung injury have not been identified. We hypothesized that .NO-induced injury results from peroxynitrite, formed by the reaction of .NO with superoxide. The simultaneous generation of .NO and superoxide by 3-morpholinosydnonimine (SIN-1, 0.1-2 mM) resulted in oxidation of dihydrorhodamine, a marker of peroxynitrite production, and a dose-dependent decrease in the ability of SP-A to enhance lipid aggregation. Western blot analysis of SIN-1 exposed SP-A samples, overlaid with a polyclonal antibody against nitrotyrosine, were consistent with nitration of SP-A tyrosine residues. Superoxide dismutase (100 U/ml), L-cysteine (5 mM), xanthine oxidase (10 mU/ml) and xanthine (500 microM), or urate (100 microM) prevented the SIN-1-induced dihydrorhodamine oxidation and injury to SP-A. .NO alone, generated by S-nitroso-N-acetylpenicillamine plus 100 microM L-cysteine, or superoxide and hydrogen peroxide, generated by pterin and xanthine oxidase in the absence of iron, did not damage SP-A or oxidize dihydrorhodamine. We concluded that peroxynitrite, but not .NO or superoxide and hydrogen peroxide, in concentrations likely to be encountered in vivo, caused nitrotyrosine formation and decreased the ability of SP-A to aggregate lipids.

Myocardial work load is a major determinant of norepinephrine-induced left ventricular dysfunction

1994 ◽  
Vol 266 (2) ◽  
pp. H531-H539 ◽  
Author(s):  
F. J. Bosso ◽  
F. D. Allman ◽  
C. F. Pilati
Keyword(s):  
Energy Demand ◽  
Work Load ◽  
Left Ventricular ◽  
Lv Function ◽  
Lv Dysfunction ◽  
High Concentrations ◽  
Dose Dependent Decrease ◽  
Dose Dependent

This study was conducted to determine whether increased myocardial energy demand plays a role in norepinephrine (NE)-induced left ventricular (LV) dysfunction. A range of arterial pressure-heart rate (P-R) products (myocardial energy demand) was produced in both conscious and pentobarbital sodium-anesthetized rabbits with the same dose of NE (10 micrograms priming bolus plus 2.5 micrograms.kg-1 x min-1 for 2.5 h). After NE treatment, LV function was evaluated in vitro and found to be markedly diminished in the rabbits that had an elevated P-R product. In contrast, LV function was not significantly affected when the P-R product was maintained near control levels during NE treatment. In separate experiments, rabbit hearts were isolated and exposed to NE (10,000 or 50,000 pg/ml) for 2.5 h under low P-R product conditions. These hearts exhibited a dose-dependent decrease in LV function that was modest compared with that observed in rabbits that had elevated P-R products during in vivo NE treatment. Our results suggest that high concentrations of NE may cause modest degrees of LV dysfunction independently of increases in myocardial energy demand, but the LV dysfunction is exacerbated when myocardial energy demand is elevated.

scholarly journals The effect of tributyltin on human eosinophylic leukemia EoL-1 cells

2008 ◽  
Vol 13 (1) ◽  
Author(s):  
Jolanta Sroka ◽  
Przemysław Włosiak ◽  
Anna Wilk ◽  
Justyna Antonik ◽  
Jarosław Czyż ◽  
...  
Keyword(s):  
Human Blood ◽  
Human Fibroblasts ◽  
Basic Function ◽  
Organotin Compounds ◽  
Cellular Model ◽  
Dose Dependent Decrease ◽  
Dose Dependent

AbstractOrganotin compounds are chemicals that are widely used in industry and agriculture as plastic stabilizers, catalysts and biocides. Many of them, including tributyltin (TBT), have been detected in human food and, as a consequence, detectable levels have been found in human blood. As organotin compounds were shown to possess immunotoxic activity, we focused our attention on the effect of TBT on the basic determinants of the function of eosinophils, i.e. cell adhesiveness and motility. We used human eosinophylic leukemia EoL-1 cells, a common in vitro cellular model of human eosinophils. Here, we demonstrate that TBT causes a dose-dependent decrease in the viability of EoL-1 cells. When administered at sub-lethal concentrations, TBT significantly decreases the adhesion of EoL-1 cells to human fibroblasts (HSFs) and inhibits their migration on fibroblast surfaces. Since the basic function of eosinophils is to invade inflamed tissues, our results indicate that TBT, and possibly other organotin compounds, may affect major cellular properties involved in the determination of in vivo eosinophil function.

scholarly journals Effect of a CNS-Sensitive Anticholinesterase Methane Sulfonyl Fluoride on Hippocampal Acetylcholine Release in Freely Moving Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Tamotsu Imanishi ◽  
Muhammad Mubarak Hossain ◽  
Tadahiko Suzuki ◽  
Ping Xu ◽  
Itaru Sato ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Acetylcholinesterase Activity ◽  
Suitable Candidate ◽  
Freely Moving Rats ◽  
Freely Moving ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Sulfonyl Fluoride

Anticholinesterases (antiChEs) are used to treat Alzheimer’s disease. The comparative effects of two antiChEs, methanesulfonyl fluoride (MSF) and donepezil, on the extracellular levels of ACh in the hippocampus were investigated byin vivomicrodialysis in freely moving rats. MSF at 1 and 2 mg/kg produced a dose-dependent increase in ACh efflux from 10 min to at least 3 hrs after injection. At 2 mg/kg, the increase was still present at 24 hr. Donepezil at 1 mg/kg showed a similar but smaller effect, and, paradoxically, 2 mg/kg showed no consistent effect. MSF at 1 and 2 mg/kg decreased acetylcholinesterase activity in the hippocampus to 54.8 and 20.1% of control, respectively. These results suggest that MSF is a suitable candidate for the treatment of Alzheimer’s disease.

scholarly journals NADH changes during hypoxia, ischemia, and increased work differ between isolated heart preparations

2014 ◽  
Vol 306 (4) ◽  
pp. H529-H537 ◽  
Author(s):  
Anastasia M. Wengrowski ◽  
Sarah Kuzmiak-Glancy ◽  
Rafael Jaimes ◽  
Matthew W. Kay
Keyword(s):  
Energy Supply ◽  
Oxygen Supply ◽  
Heart Function ◽  
Isolated Heart ◽  
Supply And Demand ◽  
Half Maximum ◽  
Low Oxygen ◽  
Heart Preparation ◽  
Perfused Hearts

Langendorff-perfused hearts and working hearts are established isolated heart preparation techniques that are advantageous for studying cardiac physiology and function, especially when fluorescence imaging is a key component. However, oxygen and energy requirements vary widely between isolated heart preparations. When energy supply and demand are not in harmony, such as when oxygen is not adequately available, the imbalance is reflected in NADH fluctuations. As such, NADH imaging can provide insight into the metabolic state of tissue. Hearts from New Zealand white rabbits were prepared as mechanically silenced Langendorff-perfused hearts, Langendorff-perfused hearts, or biventricular working hearts and subjected to sudden changes in workload, instantaneous global ischemia, and gradual hypoxia while heart rate, aortic pressure, and epicardial NADH fluorescence were monitored. Fast pacing resulted in a dip in NADH upon initiation and a spike in NADH when pacing was terminated in biventricular working hearts only, with the magnitude of the changes greatest at the fastest pacing rate. Working hearts were also most susceptible to changes in oxygen supply; NADH was at half-maximum value when perfusate oxygen was at 67.8 ± 13.7%. Langendorff-perfused and mechanically arrested hearts were the least affected by low oxygen supply, with half-maximum NADH occurring at 42.5 ± 5.0% and 23.7 ± 4.6% perfusate oxygen, respectively. Although the biventricular working heart preparation can provide a useful representation of mechanical in vivo heart function, it is not without limitations. Understanding the limitations of isolated heart preparations is crucial when studying cardiac function in the context of energy supply and demand.

Sign in / Sign up

Export Citation Format

Share Document