Carteolol hydrochloride reduces visible light-induced retinal damage in vivo and BSO/glutamate-induced oxidative stress in vitro

The purpose of this study was to determine whether carteolol eye drops, a β-adrenoceptor antagonist used as an intraocular hypotensive agent, has protective effects against the light-induced oxidative stress in retina. Dark-adapted pigmented rats were pre-treated with topical carteolol ophthalmic solution or saline and then exposed to visible light. The effects on electroretinogram (ERG), morphology, oxidative stress, and expression of mRNAs in the retinas were determined. The l-buthionine-(S,R)-sulfoximine (BSO)/glutamate-induced oxidative stress in 661 W cells, a murine photoreceptor cell line, was evaluated by cell death assays, production of reactive oxygen species (ROS), and activation of caspase. In vivo studies showed that exposure to light caused a decrease in the amplitudes of ERGs and the outer nuclear layer (ONL) thickness and an increase of the 8-hydroxy-2′-deoxyguanosine (8-OHdG)-positive cells in the ONL. These changes were significantly reduced by pre-treatment with carteolol. Carteolol also significantly up-regulated the mRNA levels of thioredoxin 1 and glutathione peroxidase 1 compared to saline-treated group. Moreover, carteolol and timolol, another β-adrenoceptor antagonist, significantly inhibited BSO/glutamate-induced cell death and reduced caspase-3/7 activity and ROS production in vitro. Therefore, carteolol could protect retina from light-induced damage with multiple effects such as enhancing the antioxidative potential and decreasing the intracellular ROS production.     

Evaluation of DNA damage in Chinese toad (Bufo bufo gargarizans) after in vivo exposure to sublethal concentrations of four herbicides using the comet assay

Chinese toad, Bufo bufo gargarizans, is frequently found in rice fields, muddy ponds, wetlands and other aquatic ecosystems in China. Because of its habitat, it has many chances of being exposed to pesticides, such as acetochlor, butachlor, chlorimuron-ethyl, and paraquat, which are extensively used in rice or cereal fields. Amphibians may serve as model organisms for determining the genotoxic effects of pollutants contaminating these areas. In the present study DNA damage was evaluated in the Chinese toad using the comet assay, as a potential tool for the assessment of ecogenotoxicity. The first step was to determine the acute toxicity of the above-mentioned herbicides. In acute tests, tadpoles were exposed to a series of relatively high concentrations of acetochlor, butachlor, chlorimuron-ethyl, and paraquat for 96 h. The LC₅₀ (96 h) of acetochlor, butachlor, chlorimuron-ethyl and paraquat were measured as 0.76, 1.32, 20.1 and 164 mg·l⁻¹, respectively. Also, negative effects on the behavior of tadpoles were observed with acetochlor, butachlor, and paraquat. Secondly, the comet assay was used for detecting DNA damage in Chinese toad tadpoles exposed to sublethal concentrations of four herbicides. Significant (P < 0.05) concentration-dependent increase in DNA damage (as indicated by tail length, tail moment, olive tail moment) were observed from erythrocytes of tadpoles exposed to sublethal concentrations of acetochlor, butachlor, paraquat, and methyl methanesulfonate, except chlorimuron-ethyl. To our knowledge, this is the first report describing the use of Bufo bufo gargarizans for genotoxicity assessment of herbicides.     

Catechol metabolites of zeranol and 17β-estradiol: a comparative in vitro study on the induction of oxidative DNA damage and methylation by catechol-O-methyltransferase

The current study examines whether the occupation of firefighting contributes to exposure to polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and dioxin-like polychlorinated biphenyls (PCBs). We compared serum dioxin concentrations and congener profiles of current firefighters (n=13) with those of men who have ceased employment as firefighters (n=17) and with men employed in occupations other than firefighter (n=10). We found that compared to former or non-firefighters, current firefighters have higher levels of dioxins primarily due to the contribution of PCBs and to a lesser extent PCDFs. PCDFs were significantly higher in former firefighters compared to non-firefighters (p<0.05). Comparisons with studies performed by other investigators suggest that local environmental conditions contribute to some of the elevation of PCBs. The congeners 1,2,3,4,6,7,8-heptachlorodibenzodioxin and PCB-114 were significantly higher in current firefighters when compared to former or non-firefighters. Moreover, levels of these congeners were inversely correlated with years since employed as firefighter (Spearman r=-0.610, p=0.009 and Spearman r=-0.53, p=0.03, respectively). The classes of dioxins show an overall decline with years since employed as firefighters, this decline is most evident with PCDDs (Spearman r=-0.46, p=0.06). Together, the combination of evidence supports firefighting as a source of exposure to dioxins.     

Propoxur-induced oxidative DNA damage in human peripheral blood mononuclear cells: protective effects of curcumin and α-tocopherol

The present study enumerates the attenuating effects of curcumin and α-tocopherol against propoxur induced oxidative DNA damage in human peripheral blood mononuclear cells (PBMC). Cultured cells were isolated from peripheral blood of healthy volunteers, and were exposed to varying concentrations of propoxur (0–21?μg/ml) for 6, 12, and 24?h, and in combination with curcumin (9.2?μg/ml) or α-tocopherol (4.3?μg/ml) or both. Cytotoxic effect of propoxur was examined by MTT assay. The role of oxidative stress beneath the cytotoxicity of propoxur was evaluated by the measurement of reduced glutathione (GSH), malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OH-dG) levels in cell lysate. A concentration-dependent cell death, depletion of GSH, an increase in the level of both MDA and 8-OH-dG were observed. Co-treatment with curcumin or α-tocopherol significantly attenuates depleted GSH, decrease in MDA and 8-OH-dG levels in propoxur exposed cells (p?相似文献   

Dynamic oxidative stress and DNA damage induced by oestrogen deficiency and protective effects of puerarin and 17β-oestradiol in ovariectomized rats

Oxidative stress plays an essential role in the pathogenesis of cardiovascular diseases and osteoporosis resulting from oestrogen deficiency in the postmenopausal period. In this report, we observed a dynamic change of oxidative stress and DNA damage after ovariectomy in female rats. We then compared phytoestrogen puerarin and 17β‐oestradiol (E₂) in their effects on oestrogen deficiency‐induced oxidative stress and DNA damage. Serum total antioxidant capacity (TAC), malondialdehyde (MDA) and lymphocytes DNA damage (comet%) were measured. There was a gradual increase in oxidative stress in the ovariectomized (OVX) rats over time after ovariectomy, as compared to rats receiving sham operation. OVX rats that were on puerarin and E₂ showed increased TAC and decreased MDA in the serum, as well as decreased lymphocytes comet%. Puerarin appeared to have a more powerful protective effect on DNA oxidative damage than E₂. The study indicates that postmenopausal women may benefit from phytoestrogen puerarin.     

DNA damage in lead-exposed hepatocytes: coexistence of apoptosis and necrosis?

The aim of the present study was to investigate the coexistence of oxidative DNA damage and apoptosis- and necrosis-related DNA damage, and to correlate with ultrastructural changes in hepatocyte nuclei in the lead-nitrate-exposed liver. Adult male Wistar rats were exposed to 0, 0.5, and 1% lead nitrate for 60 days, and the livers were sampled the next day. Ultrastructurally, hepatocyte nuclei showed no apoptosis-related morphological changes, but showed necrotic changes. Competitive enzyme-linked immunosorbent assay showed no change in 8-oxo-dG activity (P?>?0.05), but immunohistochemistry showed its localization in hepatocytes, Kupffer cells, endothelium, and bile ductule epithelium. TUNEL-labeled DNA breaks presenting 3'-OH ends increased in hepatocytes in all functional zones of the portal acini and bile ductule epithelium (zones I>III>II). In situ oligo ligation revealed the existence of DNA breaks bearing duplex 3' overhangs and 5' P-blunt ends in hepatocytes of all functional zones and bile ductule epithelium. In conclusion, both apoptosis- and necrosis-related DNA damage coexist without significant oxidative DNA damage. Hepatocytes display changes related to necrosis, but not those related to apoptosis.     

Girl or boy? Prenatal lead,cadmium and mercury exposure and the secondary sex ratio in the ALSPAC study

The aim of this study was to evaluate the effect of prenatal exposure to lead, cadmium and mercury levels on the secondary sex ratio. Whole blood samples were collected from pregnant women enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC) study at a median gestational age of 11 weeks and were analyzed for lead, cadmium and mercury. Regression analysis was used to identify associations between maternal lead, cadmium and mercury levels and the secondary sex ratio with adjustment for confounders. There was no evidence for associations between maternal lead, cadmium or mercury levels and the secondary sex ratio in this sample. It appears unlikely that alterations in the secondary sex ratio are influenced by exposure to heavy metals, but further work should be done in large cohorts in other countries to confirm these findings.     

Effect of lead exposure on some biological indices related to porphyrin metabolism and the activity of erythrocyte pyrimidine 5′-nucleotidase in the mice

The urinary excretion of -aminolevulinic acid (ALA) and coproporphyrin (CP) isomers (I and III) was investigated in mice exposed to lead in drinking water (200 and 500 ppm) for 14 or 30 days. Furthermore, the inhibition of pyrimidine 5-nucleotidase (P5N) and -aminolevulinic acid dehydratase (ALAD) was studied in the same mice. In the lead-exposed mice, urinary excretion of ALA was significantly elevated (12-times control), while that of CP remained unchanged. This discrepancy on the urinary excretion may be of interest. The P5N activity in both erythrocytes and bone marrow cells was significantly inhibited by exposure to lead. However, the degree of inhibition was greater in the erythrocytes (45% inhibition) than in the bone marrow cells (25% inhibition). The inhibition of ALAD was much higher in erythrocytes (90% inhibition) than in liver (20–40% inhibition). The increase in erythrocyte protoporphyrin and the decrease in both hemoglobin and hematocrit were not observed in mice exposed to lead under the above conditions.     

Prophylactic effect of α-linolenic acid and α-eleostearic acid against MeHg induced oxidative stress,DNA damage and structural changes in RBC membrane

The present study was undertaken to evaluate under in vivo condition the effects of α-linolenic acid and α-eleostearic acid against methyl mercury (MeHg) induced oxidative stress. Male albino rats were divided into six groups. Group 1 was under normal control and Group 2 was treated with methyl mercury chloride (MeHgCl; 5 mg/kg BW/day). Groups 3, 4, 5 and 6 were orally treated with different doses of the two fatty acids (0.5% and 1.0% of total lipid given for each kind of linolenic acid isomer) along with MeHgCl (5 mg/kg BW). Comet assay of blood lymphocytes showed that administration of α-linolenic acid reduced DNA damage significantly (P < 0.05). Results also showed that activity of antioxidant enzymes of plasma and brain tissue and total antioxidant capacity in plasma decreased significantly due to oxidative stress generated by MeHgCl. Administration in higher dose of both kind of linolenic acid restored all the activities of the antioxidant enzymes and also reduced lipid peroxidation and increased total antioxidant capacity in plasma. Both kinds of linolenic acid successfully maintained the RBC membrane integrity which was totally disrupted and became flat due to MeHgCl stress. α-Linolenic acid was more efficient antioxidant than α-eleostearic acid against oxidative DNA damage.     

The effects of lead exposure on placental NF-κB expression and the consequences for gestation

The present study was designed to investigate the toxicity of lead exposure on the placenta at different dosages and the relationship with placental expression of NF-κB. A total of 67 unrelated Han Chinese pregnant women and 108 Wistar rats were included in this study. The rats were randomly divided into four groups for consumption of water with or without 0.025% lead acetate during various gestational periods; blood samples and placenta were harvested for analysis. Blood lead content was determined by atomic absorption spectrophotometry. Placental NF-κB expression was evaluated by immunohistochemistry. Placental cytoarchitecture was examined by histopathology and electronic microscopy. Fetal body weight, body length and placental weight was significantly lower (p < 0.05) in the lead-exposed rats compared to controls. Maternal blood lead levels in the rats negatively correlated with placental weight (r = 0.652, p < 0.01). Rat placenta showed focal necrosis in the decidua with trophoblast degeneration and fibrin deposition. Mitochondria were swollen and decreased in number, rough endoplasmic reticula were distended and ribosomal number on membranes decreased. In the human placenta, we did not find abnormal cytoarchitecture. On the other hand, placental expression of NF-κB in lead-exposed rats was significantly higher than that in controls and the expression of NF-κB in human placenta was positively correlated with maternal blood lead levels (r = 0.663, p < 0.01). These findings suggest that lead exposure at various gestational periods produce varied effects, with NF-κB activation following lead exposure. Injury to cytoplasmic organelles may interfere with the nutrition and oxygen exchange between mother and fetus, which may be contribute to abnormal pregnancy outcomes.     

Asian dust and titanium dioxide particles–induced inflammation and oxidative DNA damage in C57BL/6 mice

Inhaled particulate matter (PM) might influence many adverse health effects in human body, including increased exacerbations of pulmonary and cardiovascular diseases. In this study, we examined the associations between PM and pulmonary adverse effects. Two types of particles, Asian dust (AD) and titanium dioxide (TiO₂), were administered intratracheally to C57BL/6 mice. The mice were exposed to saline and saline suspensions of 20?mg/?kg of AD, TiO₂ particles twice a week for 12 weeks. Following exposure with these particles, the lungs were analyzed histopathologically by hematoxylin and eosin (H&E) and Masson’s trichrome (MT) staining. Oxidative injuries were determined by immunohistochemistry (IHC) for 8-oxoguanine in the lungs and Comet assays in peripheral blood mononuclear cells (PBMCs) of C57BL/6 mice. Mice exposed to AD and TiO₂ showed significant inflammatory changes and oxidative damages in the lungs as compared with the control group. DNA damage in PBMCs was also increased significantly in AD and TiO₂-exposed mice. However, lung fibrosis was minimal and there was no significant difference between PM exposed and control mice. Exposure to AD and TiO₂ particles–induced similar inflammatory damages in the lungs and elicited oxidative DNA damage in the PBMCs.     

Cat’s whiskers flavonoid attenuated oxidative DNA damage and acute inflammation: its importance in lymphocytes of patients with rheumatoid arthritis

Cleome gynandra L. (Capparidaceae) is one of the vegetables commonly known as ‘Hurhur’ and ‘Karaila’ in India, ‘Pe Hua Tsai’ in China and “Cat’s whiskers” in English. Present study was aimed to characterize previously isolated Cat’s whiskers flavonoid as 5-hydroxy-3, 7, 4′ -trimethoxyflavone (5HTMF) and to evaluate its effect on carrageenan-induced acute inflammation in rats and hydrogen peroxide induced DNA damage in mouse macrophages. The ex vivo effect of 5HTMF upon generation of free radicals in the mononuclear lymphocytes of patients with rheumatoid arthritis (RA) was also evaluated. 5HTMF not only reduce the swelling of hind paw in rats from 1 to 3 h of carrageenan injection but also decreased serum nitric oxide (NO) production. Toxic hydrogen peroxide induced oxidative DNA damage that was significantly decreased by 5HTMF. Though oxidative stress is a potential biomarker for determining disease activity in patients with RA, surprisingly 5HTMF inhibited the superoxide, hydroxyl and NO radicals in the isolated peripheral blood mononuclear lymphocytes of patients with RA. From the above study, it may be concluded 5HTMF attenuated acute inflammation by inhibiting NO and by protecting the oxidative DNA damage due to hydrogen peroxide scavenging property. It was also equally effective in scavenging the free radicals in lymphocytes of patients with RA. Collectively, our results indicate that 5HTMF as well as leafy vegetable of Cat’s whiskers may be a promising nontoxic food alternative in attenuating the oxidative stress, meriting further studies on other human inflammatory cells.     

IKKα kinase silencing increases doxorubicin-induced apoptosis through regulation of oxidative DNA damage response in colon cancer cells

The inhibitor of kappa B kinase alpha (IKKα) is demonstrated to be involved in the various aspects of cancer biology, from its initiation, to progression, metastasis, and drug resistance. The aim of this study was to investigate the role of IKKα in doxorubicin (DOX)-mediated induction in apoptosis in SW-480 colon cancer cells. Cells were transfected with siRNA against IKKα and treated with DOX. MTT assay was applied to measure SW-480 cell proliferation. The mRNA levels of γ-H2AX within cells were assessed by qRT-PCR. 8-Hydroxy-2′-deoxyguanosine was measured by ELISA. The formation of intracellular reactive oxygen species (ROS) was detected by fluorometry. The antioxidant activities of some enzymes were also determined. For evaluation of apoptosis, ELISA assay was applied. IKKα silencing dramatically increased the doxorubicin cytotoxic effects. In addition, IKKα silencing substantially overexpressed γ-H2AX in SW-480 cells. Furthermore, upon IKKα silencing, the levels of ROS were elevated and the antioxidant defense system was significantly weakened. In addition, IKKα silencing led to the enhancement of apoptotic cells in doxorubicin-treated SW-480 cells. Co-treatment of IKKα and doxorubicin led to the enhanced cellular cytotoxicity via robosting ROS formation, inducing oxidative DNA damage, and decreasing cellular antioxidant defense, and finally potent apoptosis induction in cancer cell lines.     

GABA-mediated activated microglia induce neuroinflammation in the hippocampus of mice following cold exposure through the NLRP3 inflammasome and NF-κB signaling pathways

Chronic cold stress has long-term dramatic effects on the animal immune and neuroendocrine systems. As one of the important regions of the brain, the hippocampus is the main region involved in response to stressors. Nevertheless, the impact to the hippocampus following cold exposure and the underlying mechanism involved are not clear. To evaluate the response of the hippocampus during chronic cold stress, male C57BL/6 mice were exposed to 4 °C, 3 h per day for 1 week, after which neuroinflammation and the molecular and signaling pathways in the hippocampus response to cold stress were investigated. To confirm the potential mechanism, BV2 cells were treated with γ-aminobutyric acid (GABA) and BAY 11-7082 and MCC950, then the activation of microglia and key proteins involved in the regulation of inflammation were measured. We demonstrated that chronic cold stress induced the activation of microglia, the emergence of neuroinflammation, and the impairment of neurons in the hippocampus, which might be the result of GABA-mediated activation of nod-like receptor protein 3 (NLRP3) inflammasome and the nuclear factor kappa B (NF-κB) signaling pathway.     

Relationship between lead concentration in blood and the activities of erythrocyte pyrimidine 5′-nucleotidase and delta-aminolevulinate dehydratase in the mice exposed to lead

The relationship between the activities of both pyrimidine 5-nucleotidase (Py5N) and delta-aminolevulinate dehydratase (ALA-D) in erythrocytes and the concentration of lead in blood was investigated in the mice which were given ad libitum a drinking water containing lead of 10 to 500 ppm, for 30 days.From these results, it was demonstrated that the erythrocyte PySN activity is inhibited by lead and its activity level is negatively correlated with the concentration of lead in blood (r=–0.78). In addition, it was suggested that the erythrocyte Py5N activity is a better indicator in the exposure to relatively high lead concentration while the ALA-D is a more sensitive indicator for evaluating the lead exposure of low and moderate levels.     

Depression of glucose levels and partial restoration of pancreatic β-cell damage by melatonin in streptozotocin-induced diabetic rats

Diabetes mellitus is a common but serious metabolic disorder associated with many functional and structural complications. Glucose metabolism is disturbed due to an absolute or relative insulin deficiency. The experiment was carried out to determine the effect of melatonin on blood glucose and insulin concentrations, and histopathology of pancreatic β-cells in streptozotocin (STZ)-induced diabetic rats. The rats were randomly allocated into one of the four experimental groups: group A (control), group B (diabetic untreated), group C (diabetic treated with melatonin for 6 weeks) and group D (diabetic treated with melatonin for 8 weeks); each group contained ten animals. Diabetes was induced in B, C and D groups by a single intraperitoneal (i.p.) injection of STZ (50 mg/kg, freshly dissolved in 5 mmol/l citrate buffer, pH 4.5). The rats in melatonin-treated groups were subjected to the daily i.p injection of 10 mg kg⁻¹ of melatonin for 6 or 8 weeks starting the day after STZ injection. Control and diabetic untreated rats were injected with the same volume of isotonic NaCl as the melatonin treated groups. Almost all insulin-positive β-cells were degranulated, degenerated or necrotic in the STZ-treated rats leading to decrease in insulin secretion and an increase in blood glucose concentration. Melatonin treatment caused a sharp decrease in the elevated serum glucose, a slight increase in the lowered serum insulin concentrations and small partial regeneration/proliferation of β-cells of islets. It is concluded that the hypoglycemic action of melatonin could be partly due to small amelioration in the β-cells of pancreatic islets causing a slight increase in insulin secretion, it is mostly due to the extrapancreatic actions of the melatonin.     

Determination of lead in samples of zooplankton,water, and sediments in a Mexican reservoir: Evidence for lead biomagnification in lower/intermediate trophic levels?

We have determined lead concentration of water, sediment, and zooplankton samples of El Niágara, a reservoir in Aguascalientes, Mexico. Our results include the first report of bioconcentration factor (BCF) obtained in an actual ecosystem (as opposed to the experimental setups in the laboratory) for a rotifer species; Asplanchna brigthwellii (BCF ca. 49 300). The BCF of this predatory zooplanktonic species (A. brigthwellii) are up to four times greater than those of two grazing zooplanktonic species (Daphnia similis and Moina micrura). In this contaminated reservoir that lacks fishes, Asplanchna, and Culex sp. together with ducks and other bigger invertebrates might represent the top predators. Our data suggest that biomagnification of lead through at least one trophic level can occur in freshwater systems. Biomagnification in A. brigthwellii might be explained in part by predation of this voracious predator on young of the herbivorous cladoceran, M. micrura. Our findings stand opposite to the current theoretical framework where lead biomagnification occurs only in lower trophic levels.     

β-adrenergic receptor density and adenylate cyclase activity in lead-exposed rat brain after cessation of lead exposure

To understanding the reversible or irreversible harm to the -adrenergic system in the brain of lead-exposed rats, this study sets up an animal model to estimate the change in the sympathetic nervous system of brain after lead exposure was withdrawn. We address the following topics in this study: (a) the relationship between withdrawal time of lead exposure and brain -adrenergic receptor, blood lead level, and brain lead level in lead-exposed rats after lead exposure was stopped; and (b) the relationship between lead level and -adrenergic receptor and cyclic AMP (c-AMP) in brain. Wistar rats were chronically fed with 2% lead acetate and water for 2 months. Radioligand binding was assayed by a method that fulfilled strict criteria of -adrenergic receptor using the ligand [¹²⁵I]iodocyanopindolol. The levels of lead were determined by electrothermal atomic absorption spectrometry. The c-AMP level was determined by radioimmunoassay. The results showed a close relationship between decreasing lead levels and increasing numbers of brain -adrenergic receptors and brain adenylate cyclase activity after lead exposure was withdrawn. The effect of lead exposure on the -adrenergic system of the brain is a partly reversible condition.     

Alterations in Ca²⁺ homeostasis and oxidative damage induced by ethion in erythrocytes of Wistar rats: ameliorative effect of vitamin E

Organophosphate (OP) insecticides have been reported to induce oxidative stress due to lipid peroxidation and alteration in defense mechanisms. It is known that calcium content in erythrocytes plays a very important in normal physiology of cells. Erythrocytes are a very convenient model to understand the susceptibility of membrane to oxidative damage induced by various xenobiotic compounds. The aim of present study was to investigate the effects of ethion induced oxidative damage, alterations in membrane bound enzymes and Ca(2+) homeostasis and a possible protective role of vitamin E. Adult male albino rats of Wistar strain were orally administered ethion and vitamin E daily for 28 days. Animals were randomly divided into four groups: control; ethion treated (2.7 mg/kgbw/day); vitamin E treated (50mg/kg of bw/day); ethion+vitamin E treated. The animals were sacrificed after 7, 14, 21 and 28 days. Erythrocyte membranes were prepared and analyzed for protein, lipid peroxidation (LPO) and membrane bound ATPases. Furthermore, Ca(2+) homeostasis as function of time and concentration was evaluated in erythrocytes. The results from the present study show that in vivo administration of ethion resulted in oxidative damage to erythrocyte membranes as evident by increased lipid peroxidation. The increased LPO following ethion intoxication was accompanied by significant decrease in the activities of Na(+)/K(+)-ATPase, Mg(2+)-ATPase and Ca(2+)-ATPase and disturbed Ca(2+)homeostasis in erythrocytes. Furthermore, vitamin E treatment had a beneficial effect by decreasing lipid peroxidation; partially restoring activities of membrane bound ATPases and Ca(2+) homeostasis. The present study suggests that ethion exerts its toxic effect by increasing LPO, altering the activity of membrane bound enzymes and disturbing Ca(2+) homeostasis. Vitamin E treatment ameliorated the toxic effects of ethion suggesting its role as a potential antioxidant.