Efficacy and toxicity of praziquantel in helminth-infected barbel (Barbus barbus L.).

This study evaluated efficacy and toxicity of the pyrazinoisoquinoline anthelmintic praziquantel (PZQ) in barbel infected with metacercariae of Diplostomum spathaceum and adult Pomphorhynchus laevis, and assessed antioxidant biomarkers and the lipid peroxidation response in juvenile barbel post-treatment. The estimated 96-hr LC50 of PZQ was 28.6 mg/L. For evaluation of efficacy, barbel naturally infected with D. spathaceum were exposed to a 10 and 20 mg/L PZQ 4-day bath treatment. Both concentrations were 100% effective against D. spathaceum and significantly (p < .01) affected the activity of catalase, superoxide dismutase, glutathione reductase and glutathione-S-transferase as well as levels of reduced glutathione in liver and muscle. The efficacy of orally administered PZQ was assessed in adult barbel naturally infected with P. laevis. Fish were administered 10, 30 and 50 mg/kg of body weight and examined via gut dissection after 6 days. The 50 mg/kg dose significantly decreased the intensity of infection. Praziquantel is a feasible bath treatment for barbel infected with D. spathaceum and has potential for oral treatment of broodfish infected with P. laevis.

Effects of long-term exposure to simazine in real concentrations on common carp (Cyprinus carpio L.).

The effects of a 90 day simazine exposure at concentrations of 0.06 (reported concentration in Czech rivers), 1, 2, and 4 µg L⁻¹ were assessed in one-year-old common carp (Cyprinus carpio L.). Its influence on biometric parameters, hematology, blood biochemistry, liver biomarkers, and histology was investigated. Biometric parameters of common carp exposed to simazine at 0.06 µg L⁻¹ showed no differences from untreated fish. Simazine concentrations of 1, 2, and 4 µg L⁻¹ caused significant (p<0.01) increase of hepatosomatic indices relative to controls. Hematological profiles showed significant (p<0.01) decrease in leukocyte count relative to controls at all concentrations. Biochemical profiles of common carp exposed to simazine at all concentrations showed significant (p<0.01) increase in activity of alkaline phosphatase. In addition, at concentrations of 1 and 2 µg L⁻¹, there was a significant increase in alanine aminotransferase (p<0.05), and, at 4 µg L⁻¹, a significant increase in total protein (p<0.05), albumins (p<0.05), and alanine aminotransferase (p<0.05) compared with controls. Renal histology revealed severe hyaline degeneration of the epithelial cells of caudal kidney tubules in fish at all exposure levels compared to controls. Chronic exposure of common carp to simazine caused significant shifts in hematological, biochemical, and biometric profiles, and histopathological changes. The results of this study indicate that chronic exposure of simazine has altered multiple physiological indices in fish hematology and biochemistry, which potentially may be a biomarker of simazine toxicity; however, before these parameters are used as special biomarkers for monitoring residual simazine in aquatic environment, more detailed experiments in laboratory need to be performed in the future.

Effects of sub-chronic exposure to terbutryn in common carp (Cyprinus carpio L.).

The sub-chronic effects of terbutryn at concentrations 0.02 (reported concentration in Czech rivers), 4, 20, and 40 microg L(-1) were assessed in one-year-old common carp (Cyprinus carpio L.) exposed for 28 days and compared to a non-treated control group. Its influence on biometric parameters, hematology, blood biochemistry, and histology was investigated. Exposure to terbutryn at 0.02 microg L(-1) showed no observable effect, whereas exposure to 4, 20, and 40 microg L(-1) showed significantly higher erythrocyte counts, ammonia levels, aspartate aminotransferase, lactate dehydrogenase, creatine kinase, and lactate, but significantly lower mean corpuscular volume, mean corpuscular hemoglobin, and creatine. Cell shape changes and lipid inclusions were found in hepatocytes, and there was destruction of caudal kidney tubules when compared to control fish.

Effects of bifenthrin on some haematological, biochemical and histopathological parameters of common carp (Cyprinus carpio L.).

The aim of this study was to assess the effect of bifenthrin on common carp (Cyprinus carpio L.). The 96-h LC50 value of Talstar EC 10 (active substance 100 g l(-1) bifenthrin) was found to be 57.5 microg l(-1). Examination of haematological and biochemical profiles and histological tissue examination was performed on common carp after 96 h of exposure to Talstar EC 10 (57.5 microg l(-1)). The experimental group showed significantly higher (P < 0.01) values of plasma glucose, ammonia, aspartate aminotransferase and creatine kinase as well as the relative and absolute monocyte count, compared with the control group. Histological examination revealed teleangioectasiae of secondary gill lamellae and degeneration of hepatocytes. The bifenthrin-based Talstar EC 10 pesticide preparation was classified as a substance strongly toxic for fish.

Effects of subchronic nitrite exposure on rainbow trout (Oncorhynchus mykiss).

Subchronic toxicity of nitrite in rainbow trout (Oncorhynchus mykiss; mean mass ± S.D., 18.9 ± 1.3g) was assessed in a 28-day trial. The influence of nitrite on fish mortality, growth rate, haematology, blood biochemistry, and gill histology was observed. Survival was not affected by exposures up to 1 mg l(-1) NO(2)(-) (at 10 mg l(-1) Cl(-)). On the basis of growth rate inhibition data, the values of NOEC (28 d LC(0)) and LOEC (28 d LC(10)) were estimated at 0.01 and 0.2 mg l(-1) NO(2)(-), respectively. At 0.01 mg l(-1) NO(2)(-) (the lowest concentration tested), there was segmental hyperplasia of the respiratory epithelium of secondary lamellae and elevated glucose and decreased potassium. Elevated nitrite concentrations were found in blood plasma of fish exposed to concentrations of 1.0 mg l(-1) NO(2)(-) and higher, and in muscle tissue at the highest concentration 3.0 mg l(-1) NO(2)(-). Plasma and muscle nitrite levels were lower than those in the ambient water in all experimental groups.

Effects of deltamethrin on rainbow trout (Oncorhynchus mykiss).

The aim of this study was to assess the effect of deltamethrin on rainbow trout (Oncorhynchus mykiss). Control and experimental group of fish were exposed to Decis EW 50 pesticide preparation (active substance 50g/l of deltamethrin). The acute semistatical toxicity test lasting 96h was performed on rainbow trout juveniles. The 96hLC(50) value of Decis EW 50 was 0.02mg/l. Examination of haematological and biochemical profile and histological tissue examination was performed on 1-2-year-old rainbow trout after 96h of exposure to Decis EW 50 in a concentration of 0.02mg/l. The experimental group showed significantly lower values (p<0.05) of plasma glucose, alanine aminotransferase, cholinesterase and significantly higher (p<0.05) values of erythrocyte count, haemoglobin content, haematocrit and plasma total protein, albumins, ammonia, aspartate aminotransferase, creatinekinase and calcium compared to the control group. The deltamethrin-based Decis EW 50 pesticide preparation was classified among substances strongly toxic for fish.

Involvement of L-arginine-nitric oxide system in the response of isolated trachea to reactive oxygen species.

The aim of this study was to investigate the effect of reactive oxygen species (ROS), generated by electrolysis of Krebs-Henseleit solution (GE-KHS), on isolated guinea pig trachea and to assess the possible involvement of nitric oxide (NO) in the observed effects. The isolated trachea was superfused in GE-KHS, generating H2O2 and hypochlorous acid (HOCl), both of which slowly increased in the organ bath and reached final stable concentrations of 42 and 63 microM, respectively, at the rate of 20 ml/min(-1), and 261 and 245 microM, respectively, at the rate of 5 ml/min(-1). ROS GE-KHS-induced relaxation of tracheal rings was preceded by a small transient contraction in 40% and 65% of experiments when tracheal rings were superfused at the rate of 20 ml/min(-1) and 5 ml/min(-1), respectively. Removal of tracheal epithelium abolished the relaxation of the trachea induced by ROS GE-KHS and unmasked or potentiated trachealis contraction. The ROS GE-KHS-induced changes in trachealis tension were accompanied by an increase in thiobarbituric acid reactive substances (TBARS) and a decrease in nonprotein (NP) thiols in the trachea. These changes were inhibited by treatment with the antioxidant N-acetylcysteine (100 microM). Pretreatment of tracheal rings with the inhibitor of NO synthase (NOS) N(omega)-nitro-L-arginine (L-NOARG; 100 microM) for 20 min prior to exposure to ROS GE-KHS decreased the ROS GE-KHS-induced relaxation. When L-NOARG (100 microM) was present in the superfusing solution, not only 20 min before but also during superfusion with ROS GE-KHS, the evoked trachealis relaxation was reduced in the first 15 min but was enhanced in the 30th min. This late enhancement of relaxation was accompanied by a 12-fold increase in nitric oxide metabolites (NO(x)). ROS GE-KHS-induced elevation of TBARS levels in the trachea was decreased to 63% by pretreatment with L-NOARG (100 microM). Elevation of TBARS levels induced by incubation of brain liposomes with a hydroxyl radical generating system was decreased to 90% by L-NOARG (10, 100 microM), while the antioxidant stobadine (100 microM) nearly completely inhibited the evoked lipid peroxidation. In comparison with Trolox, L-NOARG exerted a slight scavenging effect on the 1,1-diphenyl-2-picrylhydrazyl radical. The presence of L-arginine and D-arginine in the superfusion fluid for 15-20 min before and during exposure of the trachea to ROS GE-KHS inhibited trachealis relaxation. Results indicate that epithelium derived NO may participate in the response of guinea pig trachea to ROS GE-KHS. The presence of L-NOARG in the bathing fluid during superfusion with ROS GE-KHS gave rise to NO(x), with relaxing activity. L- and D-arginine induced an inhibition of the relaxatory response to ROS GE-KHS and partially prevented a ROS-induced decrease in NP thiols. The involvement of the small antioxidant effects of L-NOARG and L- and D-arginine in the above mentioned actions of L-NOARG and L-arginine requires additional investigation.

Reactive oxygen species induced smooth muscle responses in the intestine, vessels and airways and the effect of antioxidants.

Numerous experimental data confirm the importance of reactive oxygen species (ROS) in physiological activities of smooth muscles and in the pathogenesis of various diseases with altered function of smooth muscles. The present study shows that smooth muscles of the intestine, airways and vessels, as well as their epithelium, endothelium and innervations, might be important targets of the ROS action. We demonstrated differences among the actions of various ROS (endogenous, exogenous, produced enzymatically, non-enzymatically) as well as among their actions in different smooth muscle tissues. Our results indicate that ROS are involved in changes in muscle tone, membrane conductance, calcium homeostasis, calcium-dependent processes, as well as in eicosanoid and nitric oxide metabolism. The effects of antioxidative enzymes (superoxide dismutase, catalase), of several drugs of natural origin (e.g. Kampo Medicines) and synthetic agents (e.g. stobadine, nitrosopine, ACE inhibitors) suggest that smooth muscle tissues are useful models to study ROS action and drug intervention in ROS induced injuries.

Effect of propentofylline on [3H]-leucine incorporation into protein of postischemic rat brain.

The effect of propentofylline on regional [3H]-leucine incorporation into brain proteins was investigated during early reperfusion following permanent occlusion of vertebral arteries and reversible occlusion of the common carotid arteries of awake rats. In rats subjected to 5 min ischemia/50 min reperfusion the total brain radioactivity and TCA-precipitable radioactivity were reduced in the cerebellum, medulla oblongata, hypothalamus, cortex, striatum and hippocampus and the fractional protein radioactivity was decreased in the cortex, striatum and hippocampus. Propentofylline pretreatment at a dose of 25 mg/kg p.o. daily for 14 days completely reversed the reduction in total radioactivity and partially reversed the reduction in TCA-precipitable radioactivity in all brain regions studied and decreased the reduction in fractional protein radioactivity in the hippocampus. The results suggest that the protective effect of propentofylline on transient ischemia-induced brain damage may be related to improvement of [3H]-leucine incorporation into brain proteins.

Protective action of vinpocetine against experimentally induced gastric damage in rats.

The efficacy of vinpocetine (CAS 42971-09-5) to prevent gastric mucosal damage induced by several noxious agents and its antisecretory effect were studied in rats. Vinpocetine administered orally or intraperitoneally inhibited the development of gastric lesions induced by 96% ethanol in a dose-dependent way. The highest protective activity was observed when vinpocetine was given intraperitoneally 30 min before ethanol, and its effect was still significant when administered 120 min before ethanol exposure. Oral administration of vincamine also displayed gastroprotective action in this model. Pretreatment with indometacin counteracted the protective action of vinpocetine against ethanol-induced damage, suggesting the involvement of a prostaglandin-mediated mechanism. The protective effect of vinpocetine was compared with that of prostaglandin E2, sucralfate, and tripotassium dicitrate bismuthate. The antiulcer activity of vinpocetine was demonstrated also in gastric injury induced by phenylbulazone and in chronic gastric ulcer induced by acetic acid. Histamine-stimulated gastric acid secretion in pylorus-ligated rats was partially inhibited by vinpocetine administered intraduodenally. The activity of vinpocetine established in these experiments is indicative of its potential clinical value as a gastroprotective agent.

Effect of oxidative stress on (3H)N-methylscopolamine binding and production of thiobarbituric acid reactive substances in rat cerebral cortex membranes.

We investigated the effect of lipid peroxidation, in vitro induced by H2O2 or FeSO4 and ascorbic acid, on binding properties of muscarinic receptors in rat cerebral cortex membranes. Simultaneously the concentrations of thiobarbituric acid reactive substances (TBARS) were measured to assess the extent of lipid peroxidation. In conditions of increased TBARS levels the density of (3H)N-methylscopolamine [(3H)NMS] binding sites in rat cerebral cortex membranes was not affected. Decreased numbers of (3H)NMS binding sites observed in the presence of high concentrations of H2O2 (100 and 1000 mmol.l-1) accompanied by a decrease of TBARS levels might be related to a nonspecific effect of H2O2 on cellular proteins.

[The effect of BL 343 Ac, a beta-adrenolytic, on the cervical ganglion]. / Pôsobenie betaadrenolytika BL 343 Ac na ganglion cervicale.

The activity of the newly synthetized substance BL 343 Ac (propyl-3-acetyl-4[/2-hydroxy-3-isopropyl amino/propoxy] carbanylate of hydrochloride), a beta 1-adrenolytic with sympathomimetic activity was investigated by means of the electrophysiological method of sucrose gap. Its effect on the membrane potential of a population of neurons of the superior cervical ganglion (GCS) of the cat was analyzed with the aim to contribute to the knowledge on the selectivity of action of this substance. In the GCS of the cat, which contains predominantly beta 2-adrenoceptors, BL 343 Ac given in concentrations from 0.01 to 50 mumol.l-1 and after single application into the superfusion stream close to the ganglion in doses from 0.01 to 1,000 nmol did not induce an unequivocal change in the membrane potential or a response comparable to that elicited by isoprenaline. No blocking effect of the substance BL 343 Ac (0.01-50 mumol.l-1) was observed on isoprenaline induced depolarization of the cat GCS. The obtained results indicate that BL 343 Ac fails to exert either beta 2-adrenomimetic or beta 2-adrenolytic effect on the GCS of the cat. (Fig. 2, Ref. 11.)

Effect of the steroidal alkaloid buxaminol-E on blood pressure, acetylcholinesterase activity and (3H)quinuclidinyl benzilate binding in cerebral cortex.

Pharmacological properties of the steroidal alkaloid buxaminol-E isolated from Buxus sempervirens varietas bullata were studied in relation to the cholinergic nervous system. In anaesthetised cats buxaminol-E (1.25 mumol/kg) initially induced a small short-lasting increase in blood pressure followed by marked hypotension. Atropine (1.47 mumol/kg) inhibited the hypotensive effect almost completely and methylatropine (1.47 mumol/kg) partially. Buxaminol-E and the muscarinic agonists McN-A-343 and bethanechol inhibited the binding of the muscarinic antagonist (3H)quinuclidinyl benzilate in cat and rabbit cerebral cortex membranes in decreasing order of potency. In about 10-fold higher concentrations they also inhibited acetylcholinesterase activity in cat cerebral cortex in the same order of potency. The results suggest that the hypotensive effect of buxaminol-E could be due to both central and peripheral activation of muscarinic receptors, and to a lesser degree to inhibition of acetylcholinesterase activity.

[The central effects of a steroid alkaloid, Buxaminol-E, in conscious cats]. / Centrálne úcinky stereoidného alkaloidu Buxaminolu-E u bdelých maciek.

Buxaminol-E injected i.v. to conscious cats evoked hypothermia, tachypnoe, anorexia, salivation, defecation, decrease of spontaneous activity and sensitivity to painful stimulus and agitation during its administration. The above mentioned effects of B--E, with the exception of the antinociceptive action which was not examined and of the initial excitation, were observed also after intracerebroventricular (i.c.v.) administration of B--E, and they were depressed by atropine administered i.c.v. Our findings suggest a central cholinergic action of B--E in conscious cats. Paroxysmal tonic-clonic convulsions and circling observed only after i.c.v. administration of B--E and piloerection, ataxia and urination were not inhibited by atropine administered i.c.v.

[A dexterity test in school-age children]. / Test obratnosti u detí skolního veku.

In a group of 50 children of school age a dexterity test was performed. The group comprised children who, when born, were mature, immature or hypotrophic. The authors describe the method of the test, its physiological background and value. From the results of the test ensues that there is no difference between boys and girls, no difference in practice and gnosis, no difference between the right and left hand, the result of the test does not depend on age. Maturity, prematurity or hypotrophy caused significant differences in the results of the test. As according to statistical criteria the group is sufficiently numerous, the submitted results of the test can be used as standards in school children who were born mature, premature or hypotrophic. The submitted battery of tests is a suitable method for testing of dexterity. In the conclusion the authors give output data for paediatric and teaching practice.

[Relations between postnatal weight loss and feeding of newborn infants with breast milk]. / Beziehungen zwischen der postnatalen Gewichtsabnahme und der Ernährung der Neugeborenen mit Muttermilch.

Data presented in this study prove that in term neonates as well as in premature newborns the normal postnatal fall of the body weight is of a smaller extend when breast milk, especially breast milk from their own mothers, is used for nutrition.

Trachealis responses induced by vincamine and vinpocetine; inhibition by indomethacin and Ca2+ dependence.

Vincamine in low concentrations induced a sustained contraction of the isolated guinea pig trachealis with long latency and slow onset and, in high concentrations, it induced relaxation which was potentiated in the precontracted trachealis. Vinpocetine had actions similar to those of vincamine on trachealis, however its relaxant effect was more pronounced. The vincamine-induced trachealis contraction was not changed by substance P desensitization, was reduced by tetrodotoxin, nifedipine and low Ca2+ high Mg2+ solution and increased in nominally Ca2+-free solution. The vincamine-induced relaxation of precontracted trachealis was increased by guanethidine and was not affected by propranolol, high Mg2+-low Ca2+ solution and tetrodotoxin. Vincamine- and vinpocetine-induced trachealis contraction as well as vinpocetine-induced relaxation at basal tension were abolished by indomethacin. Vincamine in a low concentration shifted to the left the concentration-effect curve for CaCl2 in the K+-depolarized trachealis, and shifted it to the right at a high concentration. Our results indicate that the contractile and relaxant actions of vincamine and vinpocetine on the guinea pig trachealis may be due to the generation of prostaglandins and to changes in the membrane Ca2+ fluxes and/or the intracellular Ca2+ distribution.

The actions of histamine in cat and rabbit superior cervical ganglia.

Depolarization of the cat superior cervical ganglion (SCG) evoked by histamine was antagonized by mepyramine. Histamine-induced depolarization, indicated by changes in the negative and positive afterpotentials of ganglionic action potentials, was decreased by pretreatment with aminophylline. In the cat SCG, histamine evoked stimulus bound decremental oscillatory potentials (SBDOP). In the rabbit SCG, only depolarization and no SBDOP were observed after the administration of histamine. Histamine-induced SBDOP were increased by isoprenaline and decreased by Leu-enkephalin pretreatment. Our results indicate that histamine evokes depolarization and an increase in excitability of the cat SCG which seems to be mediated by H1-receptors.

Antihistaminic activity of stobadine in the peripheral and central nervous system.

Stobadine in low doses induced hyperpolarization, and in high doses depolarization and inhibition of transmission in the cat superior cervical ganglion. The ganglionic depolarizing action of histamine was inhibited by stobadine in low doses. Stobadine partially depressed ganglionic responses to isoprenaline, serotonin, M1 muscarinic agonist McN-A-343 and clonidine only in high doses. Stobadine administered into the third cerebral ventricle of anaesthetized cats evoked dose-dependent hypotension without changes in heart rate. Intracerebroventricular (i.c.v.) administration of histamine evoked hypertension followed by hypotension. Both effects were inhibited by i.c.v. pretreatment with stobadine. These results indicate that in nervous tissue stobadine antagonises histamine responses presumably due to H1-receptor stimulation.