Malathion In Rats Research Articles

Efficiency of Thyme and Oregano Essential Oils in Counteracting the Hazardous Effects of Malathion in Rats.

The widespread use of MLT may pose numerous hazards to animal breeding, health, and resilience due to the presence of MLT residues in animal feedstuffs, pastures, hay, and cereals. Many medicinal plants provide what is called a generalized anti-toxic remedy. The current study examined hazardous biochemical and histological reactions to MLT and the efficiency of ThEO and OEO essential oils as anti-toxic therapies to return to a natural state after MLT exposure. A total of 75 male albino rats were randomly assigned to two groups: (i) C - MLT, comprising 25 rats, served as the control group; and (ii) C + MLT, with 50 rats that were exposed to 5 mg/kg/BW. After exposure to MLT for 21 days, a return to normal status was determined by subdividing the C + MLT group into two equal groups: ThEO and OEO were used as treatments, with 100 mg/kg body weight of thyme and oregano essential oils, respectively, being administered for 21 days. The results showed a significant decrease in body weight gain (BWG) and final weight (FW) compared to C - MLT, while the therapeutic effects of ThEO and OEO enhanced FW and BWG. Our results indicated that MLT exposure resulted in deficient serum liver function, but that OEO and ThEO therapy brought about a significant improvement in liver enzyme function. Although there was no significant difference in serum aspartate transaminase (AST) or alkaline phosphatase (ALK-Ph) and a significant drop in alanine transaminase (ALT) and acetyl choline-esterase (AChE) levels, the C + MLT group showed hepatic fibrosis in the third stage. Furthermore, histological sections of the OEO and ThEO groups showed reduced hepatocellular damage, inflammation, and hepatic fibrosis. However, there was a significant increase in serum creatinine between the C + MLT and C - MLT groups following exposure to MLT. Histological sections of renal tissue from rats treated with OEO and ThEO showed reduced tubular damage, reduced interstitial inflammation, and preserved renal tissue architecture. In conclusion, OEO and ThEO are potential compounds for use as anti-toxic therapies to return to a natural state after MLT exposure. These compounds could serve as an experimental therapeutic approach against natural toxins, providing a solution to the problems of raising livestock that are exposed to nutritional toxicity.

Effect of ginger on hepatotoxicity and nephrotoxicity induced by malathion in rats

Effect of ginger on hepatotoxicity and nephrotoxicity induced by malathion in rats

Potential role of a newly AChE reactivator in the depressive-like behavior induced by malathion

AChE inhibition caused by exposure to organophosphate (OP) compounds is strongly related to behavioural disorders such as depression. Malathion is an OP that already has a relationship between its exposure and behavioural changes, although few data still have its effects in a longer exposure protocol. In addition, intoxication therapy is based on the use of atropine-oxime which still has its controversial efficacy depending on the type of compound. For this, (3Z)-5-Chloro-3-(hydroxyimino)indolin-2-one (Cℓ-HIN), a compound that has properties of isatin and oxime in its structure, have shown reactivating properties in the activity of AChE that have been added to antidepressant-like effects in rats exposed to malathion in acute protocol. In this sense, effects of Cℓ-HIN on the depressive-like behaviour and AChE activity were evaluated in a protocol of subchronic exposure to malathion in rats. Male wistar rats were co-treated with Cℓ-HIN [5 mg/kg, p.o.] and/or malathion [1 or 10 mg/kg, i.p] for 20 days. The exposure to both doses of malathion increased immobility time of rats on the forced swimming test (FST). Besides, malathion inhibited the AChE activity in the prefrontal cortex of rats, but any significant difference was observed in the hippocampus. Cℓ-HIN protected against increased immobility time in the FST of those rats exposed to a dose of 1 mg/kg of malathion. Similarly, Cℓ-HIN was able to reactivate AChE activity only in that group exposed to the lowest dose of malathion. Collectively, the results of this study suggest that Cℓ-HIN is an oxime capable of reactivating AChE inhibited and presents na antidepressant-like effect in cases of prolonged exposure to malathion.

Antidepressant-like effect of (3Z)-5-Chloro-3-(hydroxyimino)indolin-2-one in rats exposed to malathion: Involvement of BDNF-Trkβ pathway and AChE

BackgroundOrganophosphorus pesticides exert their toxic effects mainly by the inhibition of acetylcholinesterase (AChE), which is related to emotional disorders, such as depression. Atropine-oximes therapy is commonly used; however, the efficacy of oximes in the reactivation of AChE has been inconsistent. The objective of this study was to investigate the possible neuroprotective effect of (3Z)-5-Chloro-3-(hydroxyimino)indolin-2-one (Cℓ-HIN), a compound that combines the isatin and oxime functional groups, in rats exposed to malathion. The effect of Cℓ-HIN on the AChE activity and the BDNF-Trkβ pathway in the prefrontal cortex of malathion-exposed rats were tested. MethodsWistar male rats were co-treated with Cℓ-HIN [50 mg/kg (p.o.) (3 mL/kg)] and/or malathion [250 mg/kg (i.p.) (5 mL/kg)] and performed behavioral tests twelve hours after these exposures. ResultsThe Cℓ-HIN reversed the increased immobility time in the forced swimming test and the decreased grooming time in the splash test induced by malathion, but any significant difference was observed in locomotion analysis. These results demonstrate the antidepressant-like effect of Cℓ-HIN. The cortical AChE activity was reactivated by Cℓ-HIN in rats exposed to malathion. Malathion induced an increase in Trkβ and a decrease in BDNF levels in the prefrontal cortex of rats, which were avoided by Cℓ-HIN. ConclusionThese findings support the hypothesis that Cℓ-HIN is an AChE reactivator with antidepressant-like properties, which is related to the improvement of BDNF-Trkβ signaling after acute exposure to malathion in rats. Thus, the results allow suggesting the potential use of Cℓ-HIN as an oxime-based therapy against the neurotoxic effects of malathion.

Resveratrol attenuates malathion-induced liver damage by reducing oxidative stress.

BACKGROUND:Malathion is an organophosphate insecticide which disrupts the antioxidant system of the body. Resveratrol is a phytoestrogen and antioxidant of the red grape.AIM AND OBJECTIVE:This study was designed to evaluate the effects of resveratrol against toxic effects of malathion to the liver of rats.MATERIALS AND METHODS:In this study, 48 male rats were randomly assigned to 8 groups: control normal (saline) and malathion control-treated groups (50 mg/kg), resveratrol groups (2, 8, and 20 mg/kg), and malathion + resveratrol-treated groups (2, 8, and 20 mg/kg). Treatments were administered intraperitoneally daily for 14 days. Griess technique was assessed for determined serum nitrite oxide level. Aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase concentrations were determined for liver functional disturbances. In addition, thiobarbituric acid reactive species, antioxidant capacity, the diameter of hepatocytes, and the central hepatic vein (CHV) were investigated.RESULTS:Malathion administration significantly improved liver malondialdehyde (MDA) and nitrite oxide level, the mean diameter of CHV and hepatocyte, and liver enzymes and decreased tissue ferric-reducing ability of plasma (FRAP) level compared to the normal control group (P < 0.01). The resveratrol and resveratrol + malathion treatments at all doses significantly reduced the mean diameter of hepatocyte and CHV, liver enzymes, kidney MDA, and nitrite oxide levels and increased tissue FRAP level compared to the malathion control group (P < 0.01).CONCLUSION:It seems that resveratrol administration improved liver injury induced by malathion in rats.

Resveratrol attenuates malathion-induced renal damage by declining oxidative stress in rats

Background: Malathion is the most organophosphates which are capable to produce free radicals and induce disturbance in body antioxidant. Resveratrol is an herbal polyphenol and it has been beneficial antioxidant effects during short‑term administration. This study was designed to evaluate the effects of resveratrol against damage induced by malathion to the kidneys of rats. Materials and Methods: Forty‑eight Wistar rats divided randomly into eight groups (n = 6): sham (saline) and malathion control treated groups (27 mg/kg); resveratrol groups (2, 8, and 20 mg/kg); and resveratrol + malathion‑treated groups (2, 8, and 20 mg/kg). Treatments were administered intraperitoneally and gavage daily for 45 days. Parameters related to the function and the histology of the kidneys were evaluated and statistically analyzed from kidney and blood serum samples in respect of the groups. Results: Malathion administration increased significantly Bowman’s space, qualitative histopathology indices, kidney malondialdehyde (MDA) level, blood urea nitrogen (BUN), creatinine, and nitrite oxide levels and decreased significantly total antioxidant capacity (TAC) level and diameter and number of renal corpuscles compared to the Sham group (P < 0.001). The resveratrol and resveratrol + malathion treatments in a dose‑dependent manner reduced significantly Bowman’s space, qualitative histopathology indices, kidney MDA level, BUN, creatinine, and nitrite oxide levels and increased significantly TAC level and diameter and number of renal corpuscles compared to the malathion control group (P < 0.001). Conclusion: It seems that resveratrol administration in a dose‑dependent manner improved kidney injury induced by malathion in rats.

Preventive effects of cannabis on neurotoxic and hepatotoxic activities of malathion in rat

Objective: To investigate the effect of Cannabis sativa extract on the development of neuro- and hepato-toxicity caused by malathion injection in rats. Methods: The extract of Cannabis sativa was obtained from the plant resin by chloroform treatment. Δ-Tetrahydrocannabinol content of the extract (20%) was quantified using gas chromatography–mass spectrometry. The doses of cannabis extract were expressed as Δ -tetrahydrocannabinol content of 10 or 20 mg/kg. Malathion (150 mg/kg) was intraperitoneally administered followed after 30 min by the cannabis extract (10 or 20 mg/kg, subcutaneously). Rats were euthanized 4 h later. Malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide and paraoxonase-1 (PON-1) activity were determined in brain and liver. Brain 5-lipoxygenase and butyrylcholinesterase (BChE) activity were measured as well. Histopathological examination of brain and liver tissue was also performed. Results: Compared to controls, malathion resulted in increased oxidative stress in brain and liver. MDA and nitric oxide concentrations were significantly increased (P

The Effect of Satureja avromanica Maroofi Extract on Oxidative Stress Induced by Malathion in Rats

The Effect of Satureja avromanica Maroofi Extract on Oxidative Stress Induced by Malathion in Rats

ATP depletion and oxidative damage of hepatic cells following acute exposure to malathion in rat: beneficial role of porphyrin–fullerene nanoparticles carrying magnetic magnesium

ATP depletion and oxidative damage of hepatic cells following acute exposure to malathion in rat: beneficial role of porphyrin–fullerene nanoparticles carrying magnetic magnesium

Protective effects of caffeic acid against hypothalamic neuropeptides alterations induced by malathion in rat.

Exposure to pesticides is suspected to cause human health problems. Our study aimed to evaluate preventive effects of caffeic acid (3,4-dihydroxycinnamic acid) in the hypothalamus against malathion-induced neuropeptides gene expression alterations. Malathion at 100 mg/kg was administered intragastrically to rats alone or in combination with caffeic acid at 100 mg/kg during 4 weeks. A molecular expression of hypothalamic neuropeptides and plasmatic cholinesterase activity was investigated. Furthermore, we used in silico analysis, known as computational docking, to highlight the nature of acetylcholinesterase-malathion/caffeic acid interactions. Our findings showed differences in the responses and indicate that caffeic acid reversed malathion-induced decrease in corticotropin-releasing hormone mRNA but not brain-derived neurotrophic factor which presented an increased tendency. We suggest that caffeic acid can interact with acetylcholinesterase as the primary target of organophosphorus compounds. Results predict that caffeic acid can block partly the acetylcholinesterase gorge entrance via π-π stacking interaction with Tyr 124 and Trp 286 residues of the peripheral site leading to its stricture. Under this condition, we suggested that acetylcholine trafficking toward the catalytic site is ameliorated compared to malaoxon according to their sizes.

Association of inflammatory response and oxidative injury in the pathogenesis of liver steatosis and insulin resistance following subchronic exposure to malathion in rats

Insulin resistance and risk of type 2 diabetes are the most important complications following exposure to organophosphorous (OPs) pesticides. Regarding the importance of liver on metabolic pathways regulation, in particular blood glucose homeostasis, we focused on liver inflammation and oxidative damages in a subchronic model of toxicity by malathion. Adult male Wistar rats of body weight 200–250g were used for the study. Malathion (200mg/kg b.w./day) was administered to rats by oral intubation for 28 days. Glycemic and insulin resistance indices, markers of liver injury, markers of inflammation and oxidative stress were assessed. Malathion-treated rats showed increased glycemia, insulinemia and glycated hemoglobin level, HOMA-IR and HOMA-β indices, plasma activities of hepatocellular enzymes, lipid peroxidation index, CD3+/CD4+ and CD3+/CD4+ and pro-inflammatory cytokines when decreased antioxidant status in liver was noted. Most of our study indicates that malathion promotes insulin resistance, inflammation and Hepatosteatosis in subchronic model of exposure. On the basis of biochemical and molecular findings, it is concluded that insulin resistance induced by malathion occurs through oxidative stress and related pro-inflammatory markers in a way to result in a reduced function of insulin in liver cells.

Potential hepatoprotective effects of vitamin E and selenium on hepatotoxicity induced by malathion in rats

The aim of this present study was to analyze the hepatotoxic effect of malathion in adult male rats and evaluate the possible hepatoprotective effect of vitamin E and/or selenium. Oral administration of malathion for 45 days significantly induced marked hepatic injury as revealed by increased activity of the plasma enzymes (alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and gamma-glutamyl transferaseGGT). Oral administration of vitamin E and selenium in combination with malathion exhibited a significant protective effect by lowering the elevated plasma levels of the previous enzymes. Light microscopic investigation revealed that malathion exposure was associated with necrosis of hepatocytes, marked changes of liver tissues in the form of dilated veins, hemorrhagic spots and some degenerative signs of hepatocytes. Co-administration of vitamin E and selenium with malathion to rats showed mild histopathological changes. Thus, it appears that vitamin E and/or selenium ameliorate malathion hepatotoxicity but are not completely protective. Key words: Malathion, rats enzymes, selenium, vitamin E.

Lipid peroxidative damage on hypothalamo-pituitary-adrenal axis following subchronic exposure to malathion in rats

Lipid peroxidative damage on hypothalamo-pituitary-adrenal axis following subchronic exposure to malathion in rats

DNA Damage after Acute and Chronic Treatment with Malathion in Rats

Malathion is an insecticide widely used in agriculture and in public health programs that when used indiscriminately in large amounts can cause environmental pollution and risk to human health. However, it is possible that during the metabolism of malathion, reactive oxygen species can be generated, and malathion may produce oxidative stress in intoxicated rats that can be responsible for alterations in DNA molecules related in some studies. As a result, the present study aimed to investigate the DNA damage of cerebral tissue and peripheral blood in rats after acute and chronic malathion exposure. We used single cell gel electrophoresis (Comet assay) to measure early damage in hippocampus and peripheral blood and the Micronucleus test in total erythrocytes samples. Malathion was administered intraperitoneally once a day for one day (acute) or for 28 days (chronic) protocols (in both protocols, malathion was administered at 25, 50, 100, and 150 mg/kg). Our results showed that malathion (100 and 150 mg/kg) increased the DNA damage index in the peripheral blood and in the hippocampus after both chronic and acute treatment. Malathion increased the frequency of micronuclei only in chronic treatment at 150 mg/kg dose, and induced a cytotoxic dose-dependent decrease in the frequency of polychromatic erythrocytes in the peripheral blood of rats. In conclusion, since malathion increased both the peripheral blood and hippocampus DNA damage index using the Comet assay and increased the frequency of micronuclei in the total peripheral blood, it can be regarded as a potential mutagen/carcinogenic agent.

Biochemical evaluation of hepatic damage in subchronic exposure to malathion in rats: Effect on superoxide dismutase and catalase activities using native PAGE

The aim of this study was the evaluation of the hepatic damages following a subchronic exposure to malathion, an organophosphorus (OP) insecticide. Malathion was administered intragastrically in 1 ml corn oil containing 100 mg/kg Body Weight daily for 32 days. Malondialdehyde (MDA) concentration superoxide dismutase (SOD) and catalase (CAT) activities were analysed using a non-denaturing electrophoresis. The serum activities of Pseudocholinesterase (PchE), aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) were determined. Malathion exposure leads to a significant decrease in AchE activity, an increase in hepatic MDA, and in serum ASAT and ALAT activities. A positive correlation between serum transaminases levels and hepatic MDA was demonstrated. These results indicate that malathion exposure induced lipid peroxidation LPO, a process of degradation of membrane lipids, involving the deterioration of the cellular integrity. We have recorded a slight increase in antioxidant enzymes activities. This leads us to suggest an insufficient elimination of free radicals, causing cytotoxic effects. To cite this article: R. Rezg et al., C. R. Biologies 331 (2008).

Influence of Green Tea on Haematological and Lung Histological Disorders Induced by Malathion in Rats

Influence of Green Tea on Haematological and Lung Histological Disorders Induced by Malathion in Rats

Behavioral effects and ChE measures after acute and repeated administration of malathion in rats

Organophosphorus compounds such as malathion are environmental contaminants that may evoke neurobehavioral responses including anxiety and depression. In this study, after a functional observational battery, rats were tested in an open field and temperature test to better define doses used in subsequent experiments. Then, we investigated the effects of acute and repeated treatment with malathion on elevated plus-maze and forced-swim test, which are validated animal models to observe for anxiety- and depressive-related behaviors, respectively. We found that both acute and repeated malathion administration induced anxiogenic and depressive-like responses at doses that affected neither locomotion nor systemic temperature. Biochemical assays demonstrated inhibition of cholinesterase activity by these effective doses.

Influence of dietary ginger ( Zingiber officinales Rosc) on oxidative stress induced by malathion in rats

Pesticide chemicals may induce oxidative stress leading to generation of free radicals and alterations in antioxidants or oxygen free radical (OFR) scavenging enzymes. Hence, the effect of subchronic malathion ( O,O-dimethyl- S-1,2, bis ethoxy carbonyl ethyl phosphorodithioate) exposure was evaluated on lipid peroxidation, glutathione and related enzymes and OFR scavenging enzymes in albino rats. Administration of malathion (20 ppm) for 4 weeks increased the malondialdehyde (MDA) levels in serum, activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in erythrocytes and glutathione reductase (GR) and glutathione S-transferase (GST) in serum. However, it decreased the glutathione (GSH) level in whole blood. Concomitant dietary feeding of Zingiber officinales Rosc (ginger 1%, w/w) significantly attenuated malathion induced lipid peroxidation and oxidative stress in these rats. These results indicate the possible involvement of free radicals in organophosphate-induced toxicity and highlight the protective action of ginger, an indigenous medicinal plant product.

Determination of the distribution of malathion in rats following various routes of administration by whole-body electronic autoradiography.

The distribution of [14C]-malathion, an organophosphorus pesticide, in rats after intravenous, oral and dermal administration was carried out using electronic autoradiography of whole body sections of treated animals. The study indicated that a major difference in the disposition of [14C]-malathion occurred following various routes of administration to rats. Following intravenous administration, the liver and kidney accumulated extremely high levels of the chemical. After oral administration, [14C]-malathion absorption from the stomach was slow and its excretion followed mostly the fecal route. Dermal application of [14C]-malathion may represent a high risk for exposure to the organophosphorus pesticide where the entire skin, not only the site of application, may act as reservoir for the compound.

Bioavailability and toxicological potential of lentil-bound residues of malathion in rats.

Lentil grains treated with malathion and stored under laboratory conditions for 12 months formed bound residues. Bioavailability and the effects of lentil-bound residues of malathion in rats were studied. The amount of bound residues in lentils treated with 14C-malathion at 10 ppm and 50 ppm gradually increased to 9.52% and 13.01% of the initially applied doses after 12 months. When rats were fed these 14C-bound residues, radioactivity excreted in urine accounted for 34.49% of the administered dose. In feces, 26.15% of given dose was methanol-extractable while 18.67% was determined as nonextractable. Various tissues including liver, kidney, fat and lungs contained 8.93% while radioactivity in expired air (14CO2) was low (1.51%). The results indicate that lentil-bound malathion residues are highly bioavailable to rats. Analysis of the lentil material containing bound residues indicated that the main compound was malathion. Lentil-bound malathion residues were administered to albino rats at 0.95 and 6.51 ppm in the feed for 3 months. Body weights were determined during and at the end of the experiment. Terminal organ weights were also determined and a number of blood chemistry parameters were examined. A significant reduction in serum cholinesterase activity and an increase in blood urea nitrogen and in white cell count suggest a toxocological potential of the bound residues.