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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.
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EN
The aim of this paper was to study the activity of liver superoxide dismutase and catalase and the concentration of liver malondialdehyde in rats intoxicated with chlorfenvinphos, an organophosphate widely used as an insecticide. The study was carried out on male Wistar rats weighing 180-230 g. The rats were divided into two groups: examined - receiving oil solution of chlorfenvinphos in doses of 0.5 LD50, and 0.1 LD50, and control group - receiving oil. The activity of superoxide dismutase (SOD), catalase (CAT) and concentration of malondialdehyde (MDA) were determined after 1, 24 and 48 hours of intoxication. We observed an increase in the liver activity of SOD in further period of intoxication with chlorfenvinphos in both doses and a decrease of liver SOD activity in the rats intoxicated with the higher dose. The CAT activity in liver of the treated rats increased at the 1st hour of experiment with a dose of 0.5 LD50 and at the Ist hour and the 24th hour after intoxication with a dose 0.1 LD50. Hepatic concentration of MDA showed a decrease at the 24th hour of intoxication with chlorfenvinphos and an increase at the 48th hour of intoxication with the higher dose and returned to control value for the rats intoxicated with the lower dose. SOD and CAT play a major role in the maintaince of the physiological level of reactive form of oxygen. When reactive oxygen species generation exceeds capability of redox degrading systems, MDA levels increase. The results obtained suggest that reactive oxygen species in liver injury might be caused by chlorfenvinphos.
EN
The aim of this paper was to examine the effects of chorfenvinphos on serum concentrations of transition metals, hydrogen peroxide and malondialdehyde (a lipid peroxidation index), and on the activity of superoxide dismutase in erythrocytes. Male Wistar rats were treated with vehicle or 0.02, 0.1 and 0.5 x LD50 of chlorfenvinphos and samples were collected at 1, 24 and 48 hr after treatment. The experiments were approved by the Local Ethics Committee. We demonstrated a decreased concentration of copper serum, which is accompanied by the increased activity of superoxide dismutase. The changes observed in the concentrations of copper can be explained by its displacement from serum to erythrocytes. We also observed increased levels of zinc serum (after intoxication with CVP at doses of 0.02 and 0.1 x LD50) and iron, as well as enhancement in hydrogen peroxide serum and malondialdehyde concentration. The changes in serum Zn concentration probably resulting from cellular membrane damage and the increase in serum iron concentration, is probably caused by its release from haemoglobin. The changes of serum Fe levels seems to have no effect on lipid peroxidation. We concluded that in acute intoxication with chlorfenvinphos — organophosphorus insecticide, the non-cholinesterase mechanismes are involved.
EN
The aim of this study was to determine the effect of acute intoxication with chlorfenvinphos on the liver reduced glutathione (GSH) level and the activities of two enzymes involved in glutathione metabolism, as well as the activity of catalase (CAT), glucose-6-phosphate dehydrogenase (G6PDH) and the level of liver hydrogen peroxide. The concentration of malondialdehyde (MDA) was determined as lipid peroxidation index. Rats were divided into two groups: the control group, which received oil intragastrically by stomach tube, and the experimental groups, which received oil solution of chlorfenvinphos (CVP) in doses of 0.02 LD50, 0.1 LD50 or 0.5 LD50. After 1, 24, 48 hours of intoxication with chlorfenvinphos, the livers were quickly removed and placed in iced 0.9% NaCl containing 0.16 mg/ml heparin. The liver glutathione peroxidase (GPx) and reductase (GR) activities as well as GSH and hydrogen peroxide levels were determined using Bioxytech Assay kits. CAT activity was determined by Aebi method, G6PDH activity was measured using Sigma Assay kit. MDA level was determined by Buege and Aust method. The changes of examined parameters of antioxidative system as well as lipid peroxidation index were found. The correlation between MDA concentration and the elements of enzymatic and non-enzymatic antioxidative system was determined. A statistically significant correlation was found only between MDA level and G6PDH activity. In conclusion, it is suggested that G6PDH play a key role in the defence against oxidative stress induced by intoxication with chlorfenvinphos.
EN
This study was intendent to examine if N-acetylcysteine (NAC) changes liver GSH levels and influences ChE serum activity in rats intoxicated with chlorfenvinphos. The studies were conducted on male Wistar rats of 200±20 g body weight. One group of rats was pretreated with 0.1% water solution of NAC. NAC was administered in drinking water 24h before intoxication. The control groups received oil intragastrically by stomach tube in the amount of 0.1ml/100g (I), immediately or after NAC pretreatment. The experimental groups received oil solution of chlorfenvinphos in a dose of 0.02 LD50 or 0.1 LD50 immediately or after pretreatment with NAC. One and 24 hours after intoxication with chlorfenvinphos (or after NAC pretreatment) the blood samples were collected and livers were quickly removed and placed in iced 0.9% NaCl containing 0.16 mg/ml heparin. ChE serum activity and GSH level were measured. The results of this study demonstrated the changes in serum ChE activity and liver glutathione levels in the rats after administration of chlorfenvinphos at single doses. The results reported here indicate that NAC influences a decreased level of GSH in the liver of chlorfenvinphos-intoxicated rats and does not prevent ChE inhibition.
PL
Celem pracy było zbadanie wpływu chlorfenwinfosu, w dawce jednorazowej, na stężenie mleczanów i glukozy w surowicy krwi oraz na obraz glikogenu w wątrobie.
EN
The aim of this work was to estimate the effect of chlorphenvinphos on the concentration of lactate and glucose in blood serum and glycogen in the liver. The test animals received oil alone or oil solution of chlorphenvinphos at 0.5 or 0.1 LD50. The test material was collected at hour 1, 24 and 48 since the exposure. The following were assayed: serum glucpse by the Biochem Test, serum lactate by the Sigma test, and liver glycogen by the histological method. It was found that exposure to a single dose of chlorphenvinphos resulted in reduced number of glycogen granules, vacoulated degeneration of hepatocytes and colliguative necrosis. The changes were more evident in the animals exposed to the higher dose of the pesticide. The acute poisoning with chlorphenvinphos resulted also in hyperglycaemia and lactate acidosis.
PL
Przedstawiono wyniki badań wpływu dwóch insektycydów (bromfenwinfos i chlorfenwinfos) oraz herbicydu glifosat, a także ich metabolitów oraz zawartych w preparatach pestycydowych potencjalnych zanieczyszczeń, na erytrocyty i jednojądrzaste komórki krwi człowieka (głównie limfocyty).
EN
Chem. and physiol. properties of bromfenvinphos, chlorfenvinphos and glyphosate were reviewed with 22 refs. Their metabolites and potential impurities were also taken into consideration.
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