Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 18

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
Organophosphate insecticides affect health. The effects could be divided into four groups: an acute cholinergic toxicity, organophosphate-induced delayed neuropathy (OPIDN), intermediate syndrome, long-term neuropsychological and neurophysiological effect. Acute organophosphate intoxication may lead to changes in serum enzyme activities indicative of liver damage. Patients acutely intoxicated with organophosphates and hospitalised for that reason showe symptoms of liver damage; disturbed liver functions were observed in workers of plants producing those insecticides. In persons exposed to those compounds, as well as in the experimental animals, the liver damage does not involve the cholinergic mechanism. It is suppesed that reactive oxygen species are involved in that liver damage.
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.
Zbadano wpływ podania chlorfenwinfosu w jednorazowej dużej dawce na aktywność enzymów antyoksydacyjnych i stężenie diadehydu malonowego we krwi szczurów.
Zbadano wpływ podania chlorfenwinfosu na aktywność enzymów wątrobowych w surowicy krwi i homogenacie wątroby szczura, 48 h po podaniu tego związku w dawce jednorazowej.
The aim of this study was to investigate the effect of chlorfenvinphos administered at a single dose of 0.02 LD50 on the activity of serum of liver damage indicatory enzymes, such as β-glucoronidase (BGR), acid phosphatase (AcP) and alanine and aspartate aminotransferases (ALT and AST), as well as on the activities of superoxide dismutase (SOD) and catalase (CAT) in erythrocytes and liver. The animals were divided into two groups: the control group, which received oil, and the experimental groups, which received oil solution of chlorfenvinphos at a dose of 0.02 LD50. After 1, 24 and 48 hours of intoxication with chlorfenvinphos the blood samples were collected and livers were quickly removed. This study indicates that acute intoxication with chlorfenvinphos administered at a dose of 0.02 LD50 leads to liver function disturbances, which is a likely result of increased generation of reactive oxygen species.
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.
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.
Chlorfenvinphos is an organophosphate insecticide widely used alone or in combination in Poland. In the present study, the influence of chlorfenvinphos on the activity of mitochondrial antioxidative system as well as hydrogen peroxide concentration was examinated. The experiments were conducted on male Wistar rats of 180±20g body weight. The animals 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 in doses of 0.02 LD50, 0.1 LD50 or 0.5 LD50. After 1, 24, 48 hours the livers were quickly removed. Liver mitochondria were isolated as described elsewhere. Glutathione peroxidase, superoxide dismutase, isocitrate dehydrogenase activity as well as reduced glutathione and hydrogen peroxide concentrations were determined in liver mitochondria using BIOXYTECH Assay kits produced by OXIS International, Inc., Portland, USA. The results of this work indicate that chlorfenvinphos induces oxidative stress to rat liver mitochondria. In acute chlorfenvinphos intoxication, we demonstrated that the key role in the oxidative mitochondrial damage play MnSOD and GSH pool, as well as accumulation of hydrogen peroxide.
Chlorfenvinphos, 2-chloro-1-(2,4-dichlorofenyl)vinyl diethyl phosphate, is an organophos-phate insecticide widely used in Poland singly or in mixture. The present study was undertaken to determine chlorfenvinphos-induced lipid peroxidation and to show whether acute intoxication with chlorfenvinphos alters the antioxidant system in the erythrocytes and serum. The study was conducted on male Wistar rats divided into two groups. The animals of control group were given olive oil intragastrically by a stomach tube, the animals of experimental group received oil solution of chlorfenvinphos (CVP) at a dose of 0.02, 0.1 or 0.5LD50. The blood was collected via heart puncture at the 1st, 24th and 48th hour after treatment. We determined the erythrocytes concentration of glutathione, the activities of glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase as well as the serum concentration of ascorbic acid, á-to-copherol and malondialdehyde. We observed the stimulation of enzymatic and nonenzymatic antioxi-dant system and lipid peroxidation in the erythrocytes and serum of chlorfenvinphos intoxicated rats.
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.
The aim of this paper was to examine the activity of lysosomal enzymes after intoxication with chlorfenvinvos and dichlorvos - phosphoorganic insecticides. Investigations were carried out on male Wistar rats weighing 180-230 g. Rats were divided into two groups: control and treated. Rats of treated group were receiving oil solution of chlorfenvinvos at doses of 0.5 LD50 or 0.1 LD5(), determinations were performed after 1 and 24 hours after treatment or dichlorvos in the dose equal to 0.5 LD50 estimations were performed after 1 h only. Rats of control group were given equivalent volume of oil. Activities of beta-glucuronidase and acid phosphatase in the blood serum and lysosomal fraction of rat liver homogenate were determined. It was found that the level of ChE inhibition and increase of BGR activity in the serum were dependant on chemical structure of used compound, dose and time after treatment. It was observed that increase of hydrolases activities in serum was accompanied by the decrease in its activity in the lysosomal fraction of liver homogenate.
Badano wpływ chlorfenwinfosu na aktywność aminotransferaz (AspAT, AlAT) w surowicy krwi i frakcjach homogenatu wątroby szczurów otrzymujących insektycyd w dawce 0,5 LD50 bądź 0,1 LD50 Stwierdzono wzrost aktywności AlA T w surowicy krwi (1 i 24 h) oraz przejściowy wzrost aktywności Asp A T, a także zmiany aktywności badanych aminotransferaz we frakcjach homogenatu wątroby.
Celem pracy było zbadanie wpływu chlorfenwinfosu, w dawce jednorazowej, na stężenie mleczanów i glukozy w surowicy krwi oraz na obraz glikogenu w wątrobie.
Objective: To study the levels of malonyldialdehyde, marked as the concentration of substances reacting with thiobarbituric acid in liver, brain, serum and kidney in subacute intoxication with low doses of chlorfenvinphos, an organophosphate insecticide. Materials and Methods: The study used male Wistar rats, body weight 250 – 280g. The animals received intragastrically, by a gastric tube, once daily 0.1ml/100g of olive oil (the control group) or oil solution of chlorfenvinphos at a dose of 0.02LD50 (0.3 mg/kg b.w.) (the experimental groups). After 14 and 28 days of the experiment, blood samples were collected by cardiac puncture to obtain serum; liver, kidney and brain sections were taken from the animals in anaesthesia. The level of malonyldialdehyde (as TBA RS) was determined in homogenates of the organs and in serum. Additionally, serum cholinesterase activity was determined. Results: There was an increase in the tissues as well in the serum malonyldialdehyde level. Proportionally the highest increase in TBARS , as compared to the control, was observed in the liver on day 28 of chlorfenvinphos administration and in the kidney on day 14 of the exposure. Conclusion: In subacute chlorfenvinphos intoxication, lipid peroxidation is increased in the rat liver, serum, kidney and brain, which may cause various health effects in the population exposed to its action.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.