Malathion-induced Oxidative Stress Research Articles

Rutin protects against gamma-irradiation and malathion-induced oxidative stress and inflammation through regulation of mir-129-3p, mir-200C-3p, and mir-210 gene expressions in rats’ kidney

Kidney injury represents a global concern, leading to chronic kidney disease. The organophosphate insecticide malathion (MT) demonstrates environmental disturbance and impairment of different mammalian organs, including kidneys. Likewise, gamma-irradiation (IRR) provokes destructive effects in the kidneys. Rutin is a flavonoid glycoside that exhibits nephro-protective and radio-protective properties. This manuscript focused on investigating the protective response of rutin on MT- and IRR-triggered kidney injury in rats. Rats were randomly divided into eight groups of twelve: G1 (C), control; G2 (Rutin), rutin-treated rats; G3 (IRR), gamma-irradiated rats; G4 (MT), malathion-treated rats; G5 (IRR/MT), gamma-irradiated rats treated with malathion; G6 (IRR/Rutin), gamma-irradiated rats treated with rutin; G7 (MT/Rutin), rats treated with malathion and rutin; and G8 (IRR/MT/Rutin), gamma-irradiated rats treated with malathion and rutin, every day for 30 days. The results demonstrated that rutin treatment regulated the biochemical parameters, the oxidative stress, the antioxidant status, and the inflammatory responses due to the down-regulation of the renal NF-κB p65 protein expression. Moreover, it amended the activity of acetylcholinesterase (AchE), angiotensin ACE I, and ACE II-converting enzymes. Besides, it regulated the iNOS, eNOS, miR-129-3p, miR-200c, and miR-210 gene expressions and bradykinin receptor (B1R and B2R) protein expressions. Histopathological examinations of the kidney tissue confirmed these investigated results. It could be concluded that rutin demonstrated nephro/radioprotection and counteracted the toxicological effects triggered in the kidney tissues of IRR, MT, and IRR/MT intoxicated rats, via regulating miR-129-3p, miR-200c-3p, and miR-210-3p gene expressions, which consequently regulated B2R protein expressions, ACE II activity, and HIF-1α production, respectively.

Protective Effect of Melatonin Against Malathion Induced Alterations in Antioxidant Defense System and Morphology of Erythrocytes in Wistar Rats

Malathion intoxication has been shown to produce oxidative stress due to the generation of free radicals and alter the antioxidant defense system in erythrocytes. Previous studies have shown the ameliorative role melatonin against oxidative stress induced by generation of free radicals. Present study was designed to investigate the protective effect of melatonin against malathion induced oxidative stress. For this purpose, male Wistar rats were randomly divided into four groups: Control; Melatonin (10mg/Kg body weight) group; Malathion (250mg/Kg body weight) treated group; Malathion + Melatonin treated group. Animals were administered an acute dose of malathion orally. The result of this study shows that in vivo administration of malathion caused inhibition in AChE activity in erythrocytes. Malathion intoxication also significantly increased the oxidative damage as evidenced by increased level of LPO and GSH content. The Inhibition of GSH level and increased lipid peroxidation in erythrocytes was relieved in malathion + melatonin group. Enhanced activities of SOD, CAT, GR and GPx were observed in erythrocytes of malathion treated rats as compared to control group. Moreover, melatonin supplementation in malathion treated rats maintain normal level of antioxidant enzymes as compared to malathion treated rats which indicates that melatonin provide protection against malathion-induced oxidative stress in erythrocytes. No significant change in the membrane bound enzymes such as Na+/K+-ATPase, Mg2+-ATPase and Ca2+-ATPase was observed in malathion intoxicated rats. Findings of scanning electron micrographs of erythrocytes revealed that both the malathion treated and malathion+melatonin treated groups exhibited morphological changes in erythrocytes. However, concomitant melatonin supplementation normalized the morphological alterations in erythrocytes induced by malathion toxicity. In conclusion, melatonin supplementation may ameliorate malathion-induced oxidative imbalance by enhancing the glutathione level, reducing lipid peroxidation and normalizing antioxidant enzyme activities in erythrocytes.

Evaluation of the Protective Effects of Hydroalcoholic Extract of Satureja avromanica Against Malathion-induced Oxidative Stress in the Liver: An Experimental Study

Background: Studies have shown that organophosphorus pesticides such as malathion induces oxidative stress injury and tissue damage.
 Objectives: This research aimed to determine the effects of the hydroalcoholic extracts of Satureja Avromanica (SA) on the liver function of malathion-poisoned animals.
 Methods: Twenty-eight rats were divided into four groups of the control, SA (20 mg/kg), malathion+SA, and malathion. Animals received malathion 150 mg/kg and SA 20 mg/kg for one week through intraperitoneal injection. Then, their liver and blood samples were extracted, and alanine aminotransferase, aspartate aminotransferase concentrations in serum as well as biomarkers of oxidative stress such as Lipid Peroxidation (LPO), Total Antioxidant Capacity (TAC) and Total Thiol Groups (TTG) in the liver tissue were measured.
 Results: The results showed that the SA administration reduced the level of liver LPO compared with that in the malathion group. Also, receiving SA increased liver TAC and TTG levels in rats, which this difference was significant compared with the malathion group. Besides, the SA group showed a significant decrease in liver enzyme levels, compared with the malathion-treated group.
 Conclusion: According to the results, SA exerted protective effects against malathion poisoning, through reduction of oxidative stress. Therefore, SA may be an antioxidant to counteract the harmful effects of malathion poising in liver tissue.

Protective effects of thymoquinone and diallyl sulphide against malathion-induced toxicity in rats.

Malathion is a potent organophosphate insecticide that inhibits acetylcholinesterase (AChE) enzyme. Our experimental objective was to investigate the beneficial effects of diallyl sulphide (DAS) and thymoquinone (TQ) against malathion-induced oxidative stress in rat cerebral, hepatic, and renal tissues. For 30days, rats received corn oil alone (negative control) or malathion by intragastric gavage (200mg/kg daily), either alone (positive control) or combined with oral DAS (200mg/kg daily) or TQ (10mg/kg daily) (treatment groups). Later, blood samples were collected via direct cardiac puncture and tissue samples were obtained for biochemical analysis. Malathion administration was associated with significant increases (p < 0.05) in the serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, γ-glutamyl transferase, cholesterol, urea, creatinine, and 8-OHdG (DNA damage biomarker), as well as significant (p < 0.05) decreases in theserum levels of total proteins, albumin, triglycerides, and AChE. Moreover, it significantly increased thetissue concentrations of malondialdehyde and nitric oxide and reduced tissue glutathione concentration and activities of antioxidant enzymes (glutathione peroxidase, superoxide dismutase, and catalase). Treatment of malathion-intoxicated rats with DAS or TQ significantly minimized these biochemical and oxidative effects with more frequent reversal to normal ranges of serum biomarkers, tissue oxidative markers, and antioxidant enzymes in the TQ group. In conclusion, treatment with DAS or TQ ameliorated the biochemical and oxidative effects of malathion, probably through reducing the generation of reactive oxygen and nitrogen radicals, as well as enhancing the antioxidant defense mechanisms.

The protective effects of the antioxidant N-acetylcysteine (NAC) against oxidative stress-associated apoptosis evoked by the organophosphorus insecticide malathion in normal human astrocytes

Malathion is one of the most widely used organophosphorus insecticides in agriculture. However, malathion may be involved in the etiology of human brain dysfunction. Induction of ROS has been proposed as a mechanism of malathion-induced poisoning cases, but there are few data regarding the effects of malathion on oxidative stress-associated neurotoxicity in human glial cells. The aim was to explore the mechanism underlying effects of malathion on neurotoxicity in Gibco® Human Astrocytes (GHA cells) and evaluate the protective effects of the antioxidant (N-acetylcysteine, NAC). Cell viability was measured by the cell proliferation reagent (WST-1). Antioxidant enzymes (glutathione peroxidase and catalase) were measured by an ELISA reader. Cell cycle distribution and ROS productions were detected by flow cytometry. Cell cycle-related protein levels (cyclin E1, CDK2, cyclin A2, CDK1/CDC2, or cyclin B1) and apoptotic protein levels (Bcl-2, Bax, and cleaved caspase-9/caspase-3) were analyzed by Western blotting. In GHA cells, treatment with malathion (10–25 μM) for 24 h concentration-dependently induced cytotoxicity and cell cycle arrest. In terms of oxidative stresses, malathion elevated intracellular ROS levels, but reduced glutathion and antioxidant enzyme levels. Treatment with NAC (5 μM) reversed malathion-induced oxidative stress responses, and prevented malathion-evoked apoptosis by regulating apoptotic protein expressions. Together, in GHA cells, NAC mediated inhibition of malathion-activated mitochondrial apoptotic pathways that involved cell cycle arrest and ROS responses. These data provide further insights into the molecular mechanisms behind malathion poisoning, and might suggest that NAC with its protective effects may be a potential compound for prevention of malathion-induced brain injury.

The subchronic exposure to malathion, an organophosphate pesticide, causes lipid peroxidation, oxidative stress, and tissue damage in rats: the protective role of resveratrol.

The present study was planned to evaluate the protective role of resveratrol (Res) against subchronic malathion exposure in rats over four weeks. In total, 48 Wistar rats were used and divided equally into six groups. The groups were designed as the control group (received only a rodent diet and tap water), the corn oil group (0.5 ml corn oil by the oral route), and the malathion group (100 mg kg-1 day-1 by the oral route). Other three groups received malathion (100 mg kg-1 day-1) plus Res (5, 10, and 20 mg kg-1 day-1, respectively) by the oral route. Malathion increased malondialdehyde and 8-OHdG levels, whereas it decreased glutathione levels. Also, acetylcholinesterase, superoxide dismutase, and catalase activities were found to be low in the blood, liver, kidney, heart, and brain tissues. Biochemical parameters were not notably changed in all groups. In contrast, Res treatment inverted malathion-induced oxidative stress, lipid peroxidation, and activity of enzymes. Additionally, malathion-induced histopathological changes in the liver, kidney, heart, and brain were ameliorated by Res treatment. These results demonstrate that malathion increases oxidative stress and decreases the antioxidant status while Res has a protective function against malathion toxicity in rats.

Antioxidant effect of curcumin against exposure to malathion in Cyprinus carpio.

The aim of this study was to determine protective effects of curcumin on oxidant/antioxidant parameters in Cyprinus carpio exposed to malathion. The fish were exposed to two sublethal concentrations of malathion (0.5 and 1 mg/L), and curcumin (100 mg per kg of fish weight) was simultaneously administered for 14 days. Malondialdehyde level and superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase activities were monitored in liver, kidney and gills, which were collected at the end of the experiment. The results revealed a significant increase in the malondialdehyde levels of the groups that were exposed to malathion. Also, malathion exposure caused a significant increase in superoxide dismutase, catalase, and glutathione-S-transferase activities and a significant decrease in glutathione peroxidase activity. Treatment with curcumin attenuated the malathion-induced oxidative stress by significantly decreasing the levels of malondialdehyde in the tissues. In addition, curcumin reversed the superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase activities. In conclusion, this study demonstrated that malathion caused oxidative stress and negative alterations on the antioxidant enzyme activities of the fish. However, this toxic effect was neutralised by the administration of curcumin.

Hepatoprotective effect of Zataria Multiflora Boiss against malathion-induced oxidative stress in male rats

This study was aimed to evaluate the protective effects of methanolic extract of Zataria Multiflora Boiss (Z. multiflora) against oxidative stress induced by malathion (MT) in male Wistar rats in comparison to N-acetylcysteine (NAC). Rats were randomly divided into 6 groups (n: 8) and treated daily for 28 days. They received MT (150 mg/kg), Z. multiflora methanolic extract (50, 100, and 200 mg/kg), and NAC (200 mg/kg) alone or in combination. This study included a histopathological examination of liver tissue in parallel with measurement of serum aminotransferases. Activities of antioxidant enzymes, total glutathione (GSH), and lipid peroxidation end products in plasma and tissue were also measured. Subacute exposure of rats to MT resulted in a significant morphological change in tissue, an increase in plasma aminotransferases, and oxidative damage. Both NAC and Z. multiflora at the dose of 200 mg/kg significantly reduced MT-induced oxidative stress by inhibiting lipid peroxidation, increasing the content of glutathion, and restoring the activities of superoxide dismutase and catalase. Biochemical and histological observations also showed a dose dependent hepatoprotective effect of Z. multiflora extract against subacute exposure to MT.

Oleuropein alleviates malathion-induced oxidative stress and DNA damage in rats

The effects of acute exposure to 250 mg/kg malathion and the protective effects of 20 mg/kg oleuropein, both administered intraperitoneally, were evaluated in Wistar male rats. Malathion administration increased malondialdehyde, nitric oxide, 8-hydroxy-2′-deoxyguanosine, total oxidant status, and DNA damage, yet decreased total antioxidant activity, superoxide dismutase, and catalase activities in blood, liver, and kidney. Administration of oleuropein reversed malathion-induced oxidative stress, lipid peroxidation, DNA damage, and antioxidant enzyme activity.

Hepatoprotective and Renoprotective Effects of Lavender (Lavandula stoechas L.) Essential Oils Against Malathion-Induced Oxidative Stress in Young Male Mice.

We aimed in the present study to investigate the hepato- and nephroprotective effects of Lavandula stoechas essential oils (LSEO) against malathion-induced oxidative stress in young male mice as well as the possible mechanism implicated in such protection. Animals were divided into eight groups of 12 each: Control, malathion (200 mg/kg b.w.); Various doses of LSEO (10, 30, and 50 mg/kg b.w.), malathion+various doses of LSEO. Malathion and LSEO were daily per orally (p.o.) administered by intragastric gavage during 30 days. We initially found that malathion treatment induced body weight gain decrease as well as a clear nephro- and hepatotoxicity as assessed by significant relative liver and kidney weight increase and related hemodynamic parameters deregulation. Malathion exposure of mice also induced a considerable perturbation of metabolic parameters. On the other hand, we showed that malathion administration was accompanied by an oxidative stress status assessed by an increase of malondialdehyde (MDA) and hydrogen peroxide (H2O2) levels as well as a depletion of sulfhydril group content (-SH) and antioxidant enzyme activities such as catalase (CAT) and glutathione peroxidase (GPx), total superoxide dismutase (SOD), Cu/Zn-SOD, Mn-SOD, and Fe-SOD in the kidney and liver. More importantly, LSEO treatment abolished all malathion-induced body gain loss, liver and kidney relative weight increase, hemodynamic and metabolic disorders, as well as hepatic and renal oxidative stress. In conclusion, our data suggest that LSEO exerted potential hepato- and nephroprotective effects against malathion-induced oxidative stress in mice. The beneficial effect of LSEO might be related, in part, to its antioxidant properties.

Boron attenuates malathion-induced oxidative stress and acetylcholinesterase inhibition in rats

Organophosphorus compounds cause oxidative stress and lead to alterations in antioxidant status in organisms. In this study, the effects of subchronic exposure to malathion and the protective effects of boron (B) were evaluated in 48 Wistar rats, which were divided equally into six groups. For 28 d, the control group received a normal diet and tap water, the corn oil group received a normal diet and 0.5 mL of corn oil by gastric gavage and the malathion group received a normal diet and malathion (100 mg/kg/d) by gastric gavage. During the same period, each of the three other groups received a different dosage of B (5, 10 and 20 mg/kg/d, respectively) and malathion (100 mg/kg/d) by gastric gavage. Malathion administration during the period increased malondialdehyde, nitric oxide and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, as well as markers of liver function, yet decreased acetylcholinesterase, reduced glutathione, superoxide dismutase, and catalase activities in blood, liver, kidney and brain tissues. Administration of B in a dose-dependent manner also reversed malathion-induced oxidative stress, lipid peroxidation (LPO) and antioxidant enzyme activity. Moreover, B exhibited protective action against malathion-induced histopathological changes in liver, kidney and brain tissues. These results demonstrate that, if used in a dose-dependent manner, B decreases malathion-induced oxidative stress, enhances the antioxidant defense mechanism and regenerates tissues in rats.

Oxidative stress in freshwater fish, Labeo rohita as a biomarker of malathion exposure

This study examined the effect of lethal (4.5 μg/l) and sublethal (0.45 μg/l) malathion levels on oxidative stress responses of the freshwater edible fish, Labeo rohita. Fish were exposed to lethal (1-4 days) and sublethal (1, 5, 10, and 15 days) periods. In the present study, catalase and protease activity, hydrogen peroxide, malondialdehyde, protein carbonyls, and free amino acids levels increased in the gill, liver, and kidney tissues of fish exposed to lethal and sublethal concentrations of malathion except protein content. Time- and concentration-dependent induction/reduction of the above parameters by lethal and sublethal concentrations of malathion was observed in the tissues (the gill, liver, and kidney) of L. rohita. Thus, the results clearly infer oxidative damage and decline in antioxidant defense due to malathion-induced oxidative stress.

Lactobacillus casei protects malathion induced oxidative stress and macromolecular changes in Caenorhabditis elegans

Malathion induced oxidative stress (OS) leads to the inevitable accumulation of free radicals and eventual alteration of antioxidant enzymes in various biological systems. Lactic acid bacteria (LAB), renowned for its probiotic potentials has been clinically accepted and recommended for consumption as a dietary supplement for its anti-oxidant efficacy. But the idea of treating malathion-induced OS by LAB has been in the dark. Thus, the present study is intended to investigate the protective antioxidant potential of Lactobacillus casei against malathion-induced biochemical alterations by employing the nematode Caenorhabditis elegans as model system. C. elegans exposed to malathion and L. Casei were examined for toxicity by assessing various stress markers including, reactive oxygen species (ROS), hydrogen peroxide (H2O2), protein carbonyl content (PCC) and lipid peroxidation (LPO). In addition, the levels of antioxidative enzymes such as catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and reduced glutathione (GSH) also were assessed. According to the results, C. elegans exposed to malathion showed a significant increase in the accumulation of stress markers and a decrease in the levels of antioxidative enzymes, when compared to their respective controls. Interestingly, C. elegans pretreated with L. casei significantly increased the levels of SOD and GSH and, while exposing the pretreated C. elegans with malathion, the levels of antioxidative and stress marker enzymes were rescued and reduced respectively, thereby showing that the L. casei pretreatment protects the in vivo system from malathion-induced OS. Furthermore, the FT-IR spectroscopy results suggested the protective efficacy of L. casei as an antioxidant in preventing the malathion induced damage to macromolecules such as DNA, lipids and protein. Thus, the present study reports for the first time that L. casei could be a promising biotherapeutic agent against malathion induced OS.

Protective effect of NAC against malathion-induced oxidative stress in freshly isolated rat hepatocytes.

Induction of oxidative stress by Organophosphate compounds (OPs) has been previously reported. In the present work, the mechanism of protective effects of N-acetylcysteine as a glutathion (GSH) prodrug against malathion-induced cell toxicity was investigated. In this work, freshly isolated rat hepatocytes were used to determine the effect of NAC on malathion-induced cytotoxicity, formation of reactive oxygen species (ROS) and mitochondrial dysfunction. Rat hepatocytes were isolated using collagenase perfusion and then cell viability, mitchondrial membrane potential (MMP) and ROS formation were determined using trypan blue exclusion, Rhodamine 123 fluorescence and fluorogenic probe, 2', 7' -dichlorofluorescin diacetate (DCFH-DA), respectively. Despite the protective effect of NAC on malathion-induced cell toxicity and MMP dysfunction, its efficacy against ROS formation was not adequate to completely protect the cells. Cytotoxic effects of malathion regardless of its cholinergic feature, is started with gradual free radical production but, the main factor that causes cell death, is mitochondrial dysfunction, so that reduction of ROS formation alone is not sufficient for cell survival, and the maintenance of mitochondrial integrity through different mechanisms is the most ameliorative factor specially at high levels of cell damage, as NAC seemed to protect cells with various fashions apart from ROS scavenging in concentrations higher than malathion's LC50.

Malathion‐induced oxidative stress, cytotoxicity, and genotoxicity in human liver carcinoma (HepG2) cells

Malathion is an organophosphate pesticide that is known for its high toxicity to insects and low to moderate potency to humans and other mammals. Its toxicity has been associated with the inhibition of acetylcholinesterase activity, leading to the interference with the transmission of nerve impulse, accumulation of acetylcholine at synaptic junctions, and subsequent induction of adverse health effects including headache, dizziness, nausea, vomiting, bradycardia, and miosis. Oxidative stress (OS) has been reported as a possible mechanism of malathion toxicity in humans. Hence, the aim of this study was to examine the role of OS in malathion-induced cytotoxicity and genotoxicity. To achieve this goal, MTT, lipid peroxidation, and single cell gel electrophoresis (Comet) assays were performed, respectively, to evaluate the levels of cell viability, malondialdehyde (MDA) production, and DNA damage in human liver carcinoma (HepG(2)) cells. Study results indicated that malathion is mitogenic at lower levels of exposure, and cytotoxic at higher levels of exposure. Upon 48 h of exposure, the average percentages of cell viability were 100% +/- 11%, 117% +/- 15%, 86% +/- 15%, 35% +/- 9%, and 27% +/- 7% for 0, 6, 12, 18, and 24 mM, respectively. In the lipid peroxidation assay, the concentrations of MDA produced were 12.55 +/- 0.16, 20.65 +/- 0.27, 31.1 +/- 0.40, 34.75 +/- 0.45, and 15.1 +/- 0.20 muM in 0, 6, 12, 18, and 24 mM malathion, respectively. The Comet assay showed a significant increase in DNA damage at the 24 mM malathion exposure. Taken together, our results indicate that malathion exposure at higher concentrations induces cytotoxic and genotoxic effects in HepG(2) cells, and its toxicity may be mediated through OS as evidenced by a significant production of MDA, an end product of lipid peroxidation.

Protection against malathion-induced oxidative stress in rat brain mitochondria by phosphodiesterase (PDE) type 4 selective inhibitor

Protection against malathion-induced oxidative stress in rat brain mitochondria by phosphodiesterase (PDE) type 4 selective inhibitor

Malathion-Induced Oxidative Stress in a Parasitoid Wasp: Effect on Adult Emergence, Longevity, Fecundity, and Oxidative and Antioxidative Response of Pimpla turionellae (Hymenoptera: Ichneumonidae)

Effects of an organophosphorus insecticide, malathion, on survivorship and lipid peroxidation of the greater wax moth, Galleria mellonella (L.), pupae were investigated by rearing the newly hatched larvae on an artificial diet containing 0.01, 0.1, 1, 10, and 100 ppm of the insecticide. As bioindicators of long-term physiological stress responses, the adult emergence rate, longevity, and fecundity associated with lipid peroxidation level and antioxidant enzyme activity in the endoparasitoid Pimpla turionellae (L.) (Hymenoptera: Ichneumonidae) were determined by rearing the parasitoid on a factitious host, G. mellonella pupae treated with malathion. At 100 ppm, malathion significantly decreased pupation rate of G. mellonella larvae and the rate of adult emergence of the parasitoid from these pupae. This concentration resulted in a significant increase in the lipid peroxidation product malondialdehyde (MDA) in both the host and the parasitoid. Malathion at 1 and 10 ppm significantly increased pupation rate and lipid peroxidation level of G. mellonella pupae. The adult emergence rate of P. turionellae was significantly decreased from 63.7 to 20% by these concentrations, whereas MDA content was increased by two- and three-fold, respectively, compared with the control (45.3 +/- 3.2 nmol/ g protein). The longevity of adults was significantly extended from 52.5 +/- 5.7 to 75.7 +/- 6.3 d when the parasitoids emerged from host pupae exposed with 0.1 ppm malathion. At low concentrations (0.01 and 0.1 ppm), malathion significantly increased the number of eggs laid per female per day. However, the lowest concentration (0.01 ppm) had no significant effect on hatchability, whereas 0.1 ppm of the insecticide resulted in significant decrease in egg hatch compared with the control. A significant increase in total superoxide dismutase (SOD) activity for low concentrations of malathion (0.01-1 ppm) was found compared with the control. There was a significant positive correlation of SOD activities with adult longevity and fecundity. This study suggested that malathion-induced oxidative stress was causative factor in the deterioration of biological fitness and that increased SOD activities may have resulted in decreased oxidative damage, which retarded the rate of deteriorative physiological changes in P. turionellae in response to sublethal doses of malathion.

Malathion-Induced Oxidative Stress in a Parasitoid Wasp: Effect on Adult Emergence, Longevity, Fecundity, and Oxidative and Antioxidative Response of &lt;I&gt;Pimpla turionellae&lt;/I&gt; (Hymenoptera: Ichneumonidae)

Malathion-Induced Oxidative Stress in a Parasitoid Wasp: Effect on Adult Emergence, Longevity, Fecundity, and Oxidative and Antioxidative Response of &lt;I&gt;Pimpla turionellae&lt;/I&gt; (Hymenoptera: Ichneumonidae)

Malathion-induced Oxidative Stress in Rat Brain Regions

Malathion is a pesticide with high potential for human exposure. However, it is possible that during the malathion metabolism, there is generation of reactive oxygen species (ROS) and malathion may produce oxidative stress in intoxicated rats. The present study was therefore undertaken to determine malathion-induced lipid peroxidation (LPO), protein carbonylation and to determine whether malathion intoxication alters the antioxidant system in brain rats. Malathion was administered intraperitoneally in the acute and chronic protocols in the doses of 25, 50, 100 and 150 mg malathion/kg. The results showed that LPO in brain increased in both protocols. The increased oxidative stress resulted in an increased in the activity of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT), observed in cortex, striatum in the acute malathion protocol and hippocampus in the chronic malathion protocol. Our results demonstrated that malathion induced oxidative stress and modulated SOD and CAT activity in selective brain regions.

Lipid peroxidative damage on malathion exposure in rats

Lipid peroxidation is one of the major outcomes of free radical-mediated injury to tissue in vivo, including the central nervous system (CNS). The aim of this study was to examine whether malathion, a commonly used organophosphorus (OP), might induce oxidative stress in cerebrospinal fluid, blood serum and brain structures in male Wistar rats. Malathion was administered intraperitoneally in the doses of 25, 50, 100 and 150 mg/kg for 28 days. Oxidative damage was determined by measuring the thiobarbituric acid reactive species (TBARS) content, as an index of lipid peroxidation. TBARS concentration in the cerebrospinal fluid (CSF) and brain structures were increased, but a decrease in TBARS concentration in serum was observed. The results of the present study suggest the usefulness of TBARS measurement as a good biomarker in the estimation of malathion-induced oxidative stress affecting CSF and brain structures.