Antioxidant role of propolis extract against oxidative damage of testicular tissue induced by insecticide chlorpyrifos in rats

Pesticides induce oxidative stress leading to generate free radicals and alternate the antioxidant or oxygen free radical scavenging enzyme system. This study was conducted to investigate the oral toxicity of chlorpyrifos toward male rat and the oxidative stress of the sub-lethal dose (9 mg/kg; 1/25 LD₅₀) on the lipid peroxidation level (LPO), reduced glutathione content (GSH) and antioxidant enzymes; catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities of testicular tissue. Also, the protective effects of propolis extract (50 mg/kg b.w.) alone or in combination with chlorpyrifos were investigated. The oral administration of chlorpyrifos significantly caused elevation in LPO level by 1.79-fold as compared to control. The activities of antioxidant enzymes including CAT, SOD, GPx and GST were decreased significantly (23.66%, 27.75%, 29.13% and 11.52%) as well as the level of GSH decreased by 21.97% in testicular tissue as compared to control animals. Co-administration of propolis extract with chlorpyrifos or alone in male rats decreased LPO level, normalized CAT, SOD GPx and GST activities, while GSH content was increased in testicular tissue. We conclude that propolis extract significantly reduces chlorpyrifos-induced oxidative stress in rat testis and the protective effect of the pre-treatment with propolis extract as attenuating agent could be due to its antioxidant properties.     

Modulation of ethion-induced hepatotoxicity and oxidative stress by vitamin E supplementation in male Wistar rats

Organophosphorus insecticides (OPIs) may induce oxidative stress leading to generation of free radicals and alteration in antioxidant system of animals. Many studies reported that enzymatic and non-enzymatic antioxidant may play protective role against OPIs induced toxicity in human and rats. The aim of present study was to investigate the possible protective role of vitamin E on ethion-induced hepatotoxicity in rats using qualitative, quantitative and biochemical approaches. Adult male albino rats of Wistar strain were randomly divided into four groups; each group consists of six animals. Animals were treated for a period of 28 days. Group I (control group received corn oil); Group II [ethion treated (2.7 mg/kg bw/day)]; Group III (vitamin E treated (50 mg/kg of bw/day)]; Group IV (ethion + vitamin E treated). Animals were sacrificed after 7, 14, 21 and 28 days by decapitation and liver tissue was used for the measurement of proteins, lipid peroxidation (LPO), reduced glutathione (GSH) content and activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) glutathione reductase (GR) and glutathione-S-transferase (GST). Erythrocytes were analyzed for acetyl cholinesterase activity. The result of this study shows that in vivo administration of ethion caused a significant induction of oxidative damage in liver tissue as evidenced by increased level of LPO and decreased GSH content. Ethion toxicity also led to a significant increase in the activities of SOD, CAT, GPx and GST in liver tissue. In addition, decrease in GR activity was observed in ethion administered rats compared to control. Histopathological findings revealed that exposure to ethion caused damage in liver tissue. However, simultaneous supplementation with vitamin E restored these parameters partially. In conclusion, the results of the current study revealed that ethion-induced toxicity caused lipid peroxidation, alterations in the antioxidant enzymes and histopathological changes in liver. Supplementation of vitamin E exhibited protective effect by inhibiting ethion-induced toxicity in liver and erythrocytes.     

Subacute chlorpyrifos-induced oxidative stress in rat erythrocytes and the protective effects of catechin and quercetin

This study examined the effects of chlorpyrifos in the rat erythrocyte antioxidant system and evaluated the ameliorating effects of catechin and quercetin on the oxidative damage induced by chlorpyrifos. Sexually mature male Wistar rats were given chlorpyrifos (5.4 mg/kg, 1/25 of the oral LD₅₀), catechin (20 mg/kg), quercetin (20 mg/kg), catechin plus chlorpyrifos, and quercetin plus chlorpyrifos daily via gavage for four weeks. No statistical differences were found in the catechin-only and quercetin-only groups compared with the control group. By the end of the fourth week, chlorpyrifos alone increased the levels of malondialdehyde (MDA) and decreased superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities compared with the control group in rat erythrocytes. In the catechin-plus-chlorpyrifos and quercetin-plus-chlorpyrifos groups, there were statistically significantly decreased MDA levels and increased SOD, CAT, and GPx activities compared with the chlorpyrifos-only group. Thus, it appears that catechin and quercetin ameliorate chlorpyrifos-induced oxidative stress in rat erythrocytes in vivo.     

Protective effects of Nigella sativa oil on propoxur-induced toxicity and oxidative stress in rat brain regions

Propoxur (PPr) is a widely used broad spectrum carbamate insecticide mainly used to control household pests. Because of the widespread use of pesticides for domestic and industrial applications, evaluation of their neurotoxic effects is of major concern to public health. The aim of the present study was to evaluate the possible protective effects of Nigella sativa oil (NSO), an antioxidant agent, against PPr-induced toxicity and oxidative stress in different brain regions of rats including cerebellum, cortex and hippocampus. In the present study, 32 male Sprague-Dawley rats were used and divided into four equal groups. Group 1 was allocated as the control group. Groups 2-4 were orally administered 1 ml/kg/bw/day NSO, 8.51 mg/kg/bw/day PPr or NSO plus PPr, respectively, for 30 days. Lipid peroxidation (LPO), protein carbonyl content (PCC) and acetylcholine esterase activity (AChE) were determined. Enzymatic antioxidant activities [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST)] and non-enzymatic antioxidants [reduced glutathione (GSH)] were determined. PPr treatment significantly increased the levels of LPO, PCC and oxidized glutathione (GSSG) in brain regions. On the contrary, levels of GSH and the activities of SOD, CAT, GSH-Px, GST and AChE were significantly decreased. NSO treatment to PPr intoxicated rats restored such biochemical parameters to within control levels except GST activity, emphasizing its antioxidant role. We conclude that NSO significantly reduces PPr-induced toxicity and oxidative stress in rat brain regions via a free radicals scavenging mechanism.     

Amelioratory effect of vitamin E on organophosphorus insecticide diazinon-induced oxidative stress in mice liver

Considering that the involvement of reactive oxygen species (ROS) has been implicated in the toxicity of organophosphate insecticides (OPIs), the aim of this study was to investigate the ameliorative properties of vitamin E (vitE) against the subchronic effect of diazinon (DZN) on oxidative damage markers such as lipid peroxidation (LPO) and the antioxidant defense system (ADS) in the liver of male MFI albino mice. The groups were intraperitoneally (i.p) administered with either vehicle or vitE (100 mg/kg body weight) or ¼ LD₅₀ of DZN (16.25 mg/kg b.w.) or ½ LD₅₀ of DZN; 32.5 mg/kg b.w) or ¼ LD₅₀-DZN + vitE or ½ LD₅₀ + vitE every consecutive day for 14 days. Hepatic damage markers analysis revealed that alanine transferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) were significantly decreased in both DZN doses. Also, the significantly increased levels of biomarkers of oxidative stress as LPO and protein carbonyl (PC) and the decreased antioxidant defenses like reduced glutathione (GSH), and free radical scavenger enzymes viz., catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione reductase (GSH-Rx) were noted in DZN-treated groups as compared to control group. Distinctly lower levels of GSH and increased levels of LPO, along with alterations in endogenous antioxidant enzymes were evident in hepatic toxicity of DZN which is dose-dependent. Hepatic specific marker enzymes were restored to normalcy in mice supplemented with vitE following treatment with DZN which otherwise was decreased in the DZN-treated mice. The results show that co-treatment of vitE with DZN prevents or diminishes the oxidative stress of DZN-treated mice and may act as a putative protective agent against DZN-induced liver tissue injury.     

Lipid peroxidation and oxidative stress in rat erythrocytes induced by chlorpyrifos and the protective effect of zinc

Male and female rats were orally administered chlorpyrifos at a dose of 6.75 mg kg⁻¹ body weight for 28 consecutive days. An additional chlorpyrifos group received zinc (227 mg l⁻¹) in drinking water throughout the experimental duration. Two groups more served as controls; one received water only and the other received zinc in drinking water. Administration of chlorpyrifos resulted in a significant increase in lipid peroxidation (LPO) level and significant decrease in the activities of superoxide dismutase (SOD), glutathione-s-transferase (GST), catalase (CAT) and acetylcholinesterase (AChE) in erythrocytes of male and female rats. In contrast, zinc-chlorpyrifos treatment showed insignificant differences (p ? 0.05-0.01), compared to control results, regarding LPO, SOD, GST and CAT. In case of AChE, supplementation of zinc showed little alteration in the activity of this enzyme in the rats treated with chlorpyrifos. It can deduce that chlorpyrifos induced oxidative stress and lipid peroxidation in erythrocytes of male and female rats. The overall results reveal the pronounced ameliorating effect of zinc in chlorpyrifos-intoxicated rats and variation in the response of male and female animals regarding alteration in the level of some biochemical parameters and LPO.     

Oxidative stress, steroid hormone concentrations and acetylcholinesterase activity in Oreochromis niloticus exposed to chlorpyrifos

We investigated the endocrine disrupting effects of chlorpyrifos-ethyl which is suspected to be originated from oxidative stress. Initially, the 96 h LC₅₀ values of chlorpyrifos in juvenile and adult of Oreochromis niloticus were determined to be 98.67 μg/L and 154.01 μg/L, respectively. Sub-lethal concentrations of chlorpyrifos-ethyl (5 ppb, 10 ppb, 15 ppb) were administrated to adult fish for 15 and 30 days. Fish were then left to depurate for 15 days in pesticide-free water. Gonadal somatic indices, serum sex steroids as indicators of reproductive function and cortisol level as indicator of stress condition were measured to observe the endocrine disruption effects of chlorpyrifos-ethyl. Gonadal glutathione S-transferase and antioxidant enzyme activities and lipid peroxidation as indicators of oxidative stress were also measured. Acetylcholinesterase activity was measured as a marker of chlorpyrifos toxicity. Results showed that serum estradiol, testosteron and cortisol levels in fish exposed to chlorpyrifos were lower than those of the control fish while gonad somatic indices did not change during the experiments. After 30 days, chlorpyrifos exposure decreased GST activity, and increased SOD enzyme activity by up to 215-446% compared with the control, suggesting there was a oxidative stress. No statistically significant differences between GPx and CAT specific activities, protein contents and lipid peroxidation were determined between control and treatment groups in all exposure concentrations and periods. Acetylcholinesterase activity decreased (45.83-77.28%) in gonad tissues. After recovery serum estradiol and testosteron levels were similar to those of the control levels. An increase in the GST and SOD enzyme activities were determined. Cortisol level and AChE activity in all exposure groups decreased after the depuration period, and fish were unable to overcome the stress of chlorpyrifos. Thus, this study revealed that after chlorpyrifos treatments there exists a protective function of antioxidant enzymes against lipid peroxidation in gonad tissue of O. niloticus. There also exist lower testosteron and estradiol levels in exposed fish than those of the control fish without any alterations in oxidative stress, which is attributed to the capability of chlorpyrifos to impair steroid hormone levels.     

Biochemical effects of acute phoxim administration on antioxidant system and acetylcholinesterase in Oxya chinensis (Thunberg) (Orthoptera: Acrididae)

The study was undertaken to evaluate the effects of different concentrations of phoxim on acetylcholinesterase (AChE) and esterase (EST) activities, and antioxidant system after topical application to Oxya chinensis. The results showed that phoxim inhibited AChE activity, and did not cause significant changes in the EST activity and the levels of malondialdehyde (MDA) and reduced glutathione (GSH). After phoxim administration, superoxide (SOD) and catalase (CAT) activities showed a biphasic response with an initial increase followed by a decline in their activities. Glutathione reductase (GR) and glutathione peroxidase (GPx) activities were inhibited in comparison with the control. Glutathione S-transferase (GST) activity showed irregular changes. Its activity increased significantly at the concentrations of 0.06 and 0.12 μg/μL and decreased at the concentrations of 0.09 and 0.24 μg/μL compared with the control. Changes in SOD, CAT, GST, GPx, and GR activities indicated that phoxim caused oxidative damage in O. chinensis. However, no significant changes in MDA content suggested that these enzymes played important roles in scavenging the oxidative free radicals induced by phoxim in O. chinensis. The formation of oxygen free radicals might be a factor in the toxicity of phoxim.     

Chronic chlorpyrifos-induced oxidative changes in the testes and pituitary gland of Wistar rats: Ameliorative effects of vitamin C

Chlorpyrifos (CPF), a chlorinated organophosphate insecticide that is widely used in agriculture and public health, has been implicated in male reproductive toxicity. Apart from acetylcholinesterase inhibition, CPF has been shown to induce changes characteristic of oxidative stress. Therefore, the aim of the present study was to evaluate the effects of vitamin C on oxidative changes in the testes and pituitary gland of rats chronically exposed to CPF. Twenty adult male Wistar rats were divided into four groups of five animals each: Group I (S/oil) received soya oil (2 ml/kg); Group II (VC) was administered with vitamin C (100 mg/kg); Group III (CPF) was given CPF (10.6 mg/kg; ∼1/8th LD₅₀); Group IV (VC + CPF) was pretreated with vitamin C (100 mg/kg) and then given CPF (10.6 mg/kg), 30 min later. The regimens were administered orally by gavage once daily for 15 weeks. Thereafter, the rats were sacrificed and the testes and pituitary glands were evaluated for the concentration of malonaldehyde (MDA) and activities of superoxide dismutase (SOD) and catalase (CAT). The result shows that CPF increased MDA concentration and reduced activities of SOD and CAT, which were ameliorated by pretreatment with vitamin C.     

Ameliorative effect of lycopene on antioxidant status in Cyprinus carpio during pyrethroid deltamethrin exposure

The aim of the present study was to investigate the ameliorative properties of lycopene against the toxic effects of deltamethrin (DM) by examining oxidative damage markers such as lipid peroxidation and the antioxidant defense system components in carp (Cyprinus carpio). The fish were divided into seven groups of 15 fish each and received the following treatments: Group 1, no treatment; Group 2, orally administered corn oil; Group 3, oral lycopene (10 mg/kg body weight); Group 4, exposure to 0.018 μg/L DM; Group 5, exposure to 0.018 μg/L DM plus oral administration of 10 mg/kg lycopene; Group 6, exposure to 0.036 μg/L DM; and Group 7, exposure to 0.036 μg/L DM plus oral administration of 10 mg/kg lycopene. Treatment was continued for 14 days, and at the end of this period, blood and tissue (liver, kidney, and gill) samples were collected. Levels of malondialdehyde (MDA) and reduced glutathione (GSH) as well as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were determined in blood and tissues for measurement of oxidant-antioxidant status. A significant elevation in the level of MDA, as an index of lipid peroxidation, and reductions in antioxidant enzyme activities (SOD, CAT, and GSH-Px) and low molecular weight antioxidant (GSH) levels were observed in DM-exposed fish. Treatment with lycopene attenuated the DM-induced oxidative stress by significantly decreasing the levels of MDA. In addition, lycopene significantly increased the SOD, CAT, and GSH-Px activities and the level of GSH. The present results suggest that administration of lycopene might alleviate DM-induced oxidative stress.     

Influence of subacute and subchronic treatment of abcisic acid and gibberellic acid on serum marker enzymes and erythrocyte and tissue antioxidant defense systems and lipid peroxidation in rats

This study describes the subacute and subchronic effects of two plant growth regulators (PGRs) [abcisic acid (ABA) and gibberellic acid (GA₃)] on serum marker enzymes [aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatine phosphokinase (CPK) and lactate dehydrogenase (LDH), γ-glutamil transpeptidase (GGT)], antioxidant defense systems [reduced glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT)] and lipid peroxidation level (Malondialdehyde = MDA) in various tissues of rats. Rats (Sprague-Dawley albino) were exposed to 75 ppm (parts per million) of ABA and GA₃. Seventy-five parts per million of PGRs as drinking water was administered orally ad libitum for 25 and 50 days continuously. The PGRs treatments caused different effect on the serum marker enzymes, antioxidant defense systems and the content of MDA in comparison to those of control rats. Results show that ABA caused a significant decrease in serum LDH and CPK activity with both periods. Also, GA₃ significantly decreased serum AST, CPK, and LDH activity with subacute and decreased serum ALT, CPK, LDH, and GGT treated with subchronic periods. The lipid peroxidation end product MDA significantly increased in the erythrocyte, liver, brain, and muscle of rats treated with both the period of GA₃ without significantly change in the erythrocyte and muscle of rats treated with the subacute period of ABA. The GSH levels were significantly depleted in the erythrocyte and brain of rats treated with both the period of GA₃ without any change in the erythrocyte, liver, brain, and muscle of rats treated with both the period of ABA. Also GSH levels in the muscle significantly depleted with the subchronic period of GA₃. Antioxidant enzyme activities such as SOD significantly decreased in the erythrocyte, liver and brain tissues but increased in the muscle tissue of rats treated with both the periods of GA₃. Meanwhile, SOD significantly decreased in liver and brain, and increased in muscle of rats treated with both the period of ABA. While CAT significantly decreased in the all tissues of rats treated with both the period of GA₃, decreased in the liver and muscle of rats treated with both the periods of ABA too. On the other hand, the ancillary enzyme GPx and GR activity in the erythrocytes, liver, brain and muscle were either significantly depleted or not changed with two periods of PGRs. The drug metabolizing enzyme GST activity significantly decreased in the brain of rats treated with subacute period of PGRs but increased in the erythrocytes of rats treated with subacute period of GA₃. As a conclusion, ABA and GA₃ had significantly increased the activity of hepatic damage enzymes. Also the rats resisted to oxidative stress via antioxidant mechanism. However, the antioxidant mechanism could not prevent the increases in lipid peroxidation in rat’s tissues. These data, along with changes, suggest that PGRs produced substantial systemic organ toxicity in the erythrocyte, liver, brain, and muscle during the period of a 25-day subacute and 50-day subchronic exposure.     

Exposure to streptomycin alters oxidative and antioxidative response in larval midgut tissues of Galleria mellonella

Although antibiotics have different molecular modes of actions, increasing evidence for their secondary effects suggests that they disturb cellular homeostasis by generating free radical intermediates that trigger lipid peroxidation, which leads to oxidative stress. Streptomycin is an antibiotic insecticide used to control pest insects and microbial diseases of agricultural crops. We investigated the biochemical basis for pro-oxidative effects of streptomycin in the midgut tissues of greater wax moth, Galleria mellonella (L.) seventh-instar larvae by measuring content of the oxidative stress indicator, malondialdehyde (MDA), and antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST) and glutathione peroxidase (GPx)] and transaminases [alanine aminotransferase (ALT), aspartate aminotransferase (AST)] activities. The insects were reared from first-instar larvae on artificial diets containing 0.001, 0.01, 0.1 or 1.0 g streptomycin per 100 g of diets. The supplementation of streptomycin at high concentrations to the diets caused oxidative stress as evidenced by the elevation of MDA content, SOD and GPx activities, accompanied by the concurrent depletion of CAT and GST activities. The streptomycin-induced oxidative stress was also accompanied by decreases of transaminases activities in midgut tissues. We found a significant negative correlation of MDA contents with GST activities in the larval midgut tissues. These results suggest that exposure to dietary streptomycin resulted in oxidative stress which could impact midgut digestive physiology at the expense of impairment of antioxidant and transaminases enzymes in G. mellonella larvae.     

Biochemical evidence on positive effects of rolipram a phosphodiesterase-4 inhibitor in malathion-induced toxic stress in rat blood and brain mitochondria

Malathion is an organophosphate (OP) pesticide that has been shown to induce oxidative stress in brain through the generation of free radicals and alteration of the cellular antioxidant defense system independent of its anticholinesterase effects. The aim of this study was to investigate the possible protective role of rolipram as a selective phosphodiesterase (PDE) type 4 inhibitor, on toxicity of malathion, by measuring the activities of brain mitochondrial and plasma peroxynitrite (ONOO⁻), glutathione peroxidase (GPx), superoxide dismutase (SOD), Mn-SOD, catalase (CAT), and lipid peroxidation (LPO) in rats. Effective doses of malathion (200 mg/kg/day) and rolipram (200 μg/kg/day) were administered alone or in combination for 7 days by intraperitoneal injection. At the end of the experiment, the brain mitochondria and plasma of the animals were separated. In the brain cells mitochondria and blood plasma, the LPO, ONOO⁻, and GPx were higher in the malathion group as compared with controls. Rolipram ameliorated all of malathion-induced changes. Plasma CAT decreased in malathion-treated animals while it increased in brain mitochondria comparing with controls. Co-administration of rolipram with malathion improved CAT in both brain mitochondria and plasma. Malathion and rolipram did not alter total SOD or Mn-SOD in the plasma while both caused a significant elevation in brain mitochondria. In conclusion, this model of study that we employed, in a large extent, characterized the relationships among malathion-induced neurotoxicity, mitochondrial dysfunction, and significant increase in systemic and local oxidative/nitrosative stress in plasma and brain, respectively. Intracellular cAMP-elevating agents like rolipram, may be considered beneficial for the protection or recovery of malathion-induced toxic damage in brain mitochondria and blood.     

Effects of indoleacetic acid and kinetin on lipid peroxidation and antioxidant defense in various tissues of rats

This study aims to investigate the effects of indoleacetic acid (IAA) and kinetin (Kn), which are plant growth regulators (PGRs), on antioxidant defense systems [reduced glutathione (GSH), glutathione-S-transferase (GST), catalase (CAT)], and lipid peroxidation level (malondialdehyde, MDA) various tissues of rats. Rats (Sprague-Dawley albino) were exposed to 100 ppm IAA and Kn. One hundred parts per million of PGRs was administered orally to rats ad libitum for 21 days continuously. The PGRs treatments caused different effects on the content of MDA and antioxidant defense system in comparison to those of control rats. According to the results, the subchronic treatments of IAA caused significant decrease in the GSH concentration and CAT activity in erythrocyte. Kn decreased GSH concentration in erythrocyte too. While the MDA concentration in brain was increased significantly by IAA and Kn, Kn decreased significantly brain CAT and GST activity. The liver GST activity was decreased by IAA and Kn. But, liver CAT activity was increased by IAA. On the other hand, while IAA treatment caused a significant decrease kidney GST activity, Kn caused a significant decrease both kidney GST and CAT activity. Also, while heart CAT activity was decreased by IAA, heart GST activity was decreased by both IAA and Kn. Moreover, MDA concentration in heart was increased by Kn treatment. It was concluded that IAA might effect MDA and antioxidant defense on the animals at subchronic treatment.     

Methomyl induced hematological and biochemical alterations - protection by vitamin E

The present study was planned to evaluate the role of vitamin E, if any, in attenuating the methomyl induced hematological and biochemical alterations in blood of male wistar rats. Animals, in the weight range of 130-150 g, were administered methomyl orally in drinking water at a sub-acute dose level of 4 mg/kg body weight on alternate days for a duration of one month, vitamin E was administered intraperitoneally to normal or methomyl treated rats on alternate days as a pretreatment for a week at a dose level of 50 mg/kg body weight and subsequently for a further period of one month. Methomyl treatment resulted in a significant increase in the levels of lipid peroxidation and super oxide dismutase (SOD) activity in erythrocytes. On the contrary, reduced Glutathione levels (GSH) and the activities of catalase, Glutathione-S-transferase (GST) and Glutathione peroxidase (GSHPx) were found to be significantly decreased. Methomyl treatment caused a significant increase in total leukocyte counts (TLC), platelet, neutrophil, eosinophil, and lymphocyte and monocyte counts. Scanning Electron Micrographs showed significant morphological changes, which included spherocytosis and poikilocytosis. However, vitamin E supplementation to methomyl treated rats significantly decreased the raised levels of LPO whereas it caused a significant increase in GSH levels. Also, vitamin E supplementation could significantly elevate the activities of catalase GSHPx, GST and resulted in the normalization of SOD activity. Vitamin E supplementation also proved to be effective in significantly decreasing the already raised values of TLC and lymphocytes counts and almost normalized the platelets, neutrophils, lymphocytes and monocytes counts. Further, vitamin E supplementation improved the morphology of the red blood cells. The study, therefore, concludes that vitamin E can effectively mitigate most of the adverse effects induced by methomyl in rat blood.     

Effects of carbaryl and azinphos methyl on juvenile rainbow trout (Oncorhynchus mykiss) detoxifying enzymes

In this study, the effects of sublethal exposures to the anticholinesterase insecticides azinphos methyl (AzMe) and carbaryl on the detoxifying responses of juvenile rainbow trout Oncorhynchus mykiss were investigated. Juvenile specimen were exposed to sublethal concentrations of AzMe (2.5 and 5 μg/L) and carbaryl (1 and 3 mg/L) for 24, 48 and 96 h. Carboxylesterase (CbE), catalase (CAT) and glutathione S-transferase (GST) activities as well as reduced glutathione (GSH) and cytochrome P450-1A (CYP1A) levels were monitored in liver and/or kidney. In all exposed groups liver CbE was significantly inhibited. Liver and kidney GSH level was reduced after sublethal exposure to both compounds. Carbaryl induced CAT activity during the first 48 h of exposure, followed by a significant decrease, whereas AzMe continuously decreased CAT activity. GST activity and CYP1A were transiently induced at 24 h by carbaryl exposure (3 mg/L) but sublethal exposure to AzMe did not affect GST activity or CYP1A. Our results show that the O. mykiss detoxifying system are a target for carbaryl and AzMe action, probably affecting redox balance. Although the responses showed similar trends in both organs, they were more important in liver than in kidney. The early inhibitory effect in CAT activity and GSH content produced by AzMe may be associated with a high degree of oxidative stress. Early induction of CYP1A, GST and CAT by carbaryl followed by enzyme inhibition suggests a milder or delayed oxidative stress, revealing differences between both pesticides metabolization. CbE inhibition is a good biomarker for AzMe and carbaryl exposure.     

Oxidative stress and locomotor behaviour response as biomarkers for assessing recovery status of mosquito fish, Gambusia affinis after lethal effect of an organophosphate pesticide, monocrotophos

Recovery study was performed at regular intervals to establish the time course of 50% and 100% recovery in neurotransmitter enzyme (acetylcholinesterase, AChE, EC 3.1.1.7) and locomotor behaviour response of mosquito fish, Gambusia affinis exposed to lethal concentration (20.49 mg L⁻¹) of an organophosphorous pesticide, monocrotophos (MCP) for 96 h. In vitro AChE activity studies indicated that MCP could cause 50% inhibition (I₅₀) at 10.2 × 10⁻⁵ M. A positive correlation was observed between brain AChE activity and swimming speed during the recovery study. Also, the recovery response of the antioxidant enzymes superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6) and glutathione reductase (GR, EC 1.6.4.2) as well as lipid peroxidation (LPO) as biomarkers of oxidative stress were assessed in viscera of G. affinis. The results showed that the MCP besides its inhibitory effect on target enzyme AChE activity and induction in antioxidant enzyme activities as a characteristic of oxidative stress, which can be used as biomarkers in the pesticide contaminated aquatic streams.     

Allelochemical ethyl 2-methyl acetoacetate (EMA) induces oxidative damage and antioxidant responses in Phaeodactylum tricornutum

Ethyl 2-methyl acetoacetate (EMA) is a novel allelochemical exhibiting inhibitory effects on the growth of marine unicellular alga Phaeodactylum tricornutum (P. tricornutum). Oxidative damage and antioxidant responses in P. tricornutum were investigated to elucidate the mechanism involved in EMA inhibition on algal growth. The increase in reactive oxygen species (ROS) levels and malondialdehyde (MDA) contents following exposure to EMA suggested that alga was suffered from oxidative stress and severely damaged. The decrease in cell activity and cellular inclusions suggested that cell growth was greatly inhibited. The activities of the antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxide (GSH-PX) and glutathione S-transferase (GST) increased with the exposure concentration and decreased with the prolongation of exposure time. Cellular ascorbic acid (AsA) and reduced glutathione (GSH) systems were also involved in resisting oxidative stress of EMA by altering the composition of AsA and GSH pools. EMA exposure increased the contents of AsA, GSH, dehydroascorbate (DAsA) and glutathione (GSSG). However, the regeneration rate of AsA/DAsA did not change obviously between treatments and the control, while that of GSH/GSSG decreased significantly under 14 mmol/L EMA exposure on the 3rd day. These results showed that EMA-induced oxidative damage might be responsible for EMA inhibition on P. tricornutum growth and cellular antioxidant enzymes and non-enzymatic antioxidants were improved to counteract the oxidative stress.     

Oxidative damage, biochemical and histopathological alterations in rats exposed to chlorpyrifos and the antioxidant role of zinc

The protective effects of zinc on liver and kidney injury induced by chlorpyrifos (CPF) were investigated in rats. Male and female rats were orally administered CPF at a dose of 6.75 mg kg⁻¹ body weight for 28 consecutive days. An additional CPF group received zinc (227 mg l⁻¹) in drinking water throughout the experimental duration. Two groups more served as controls. Administration of CPF resulted in a significant increase in serum lipid peroxidation (LPO) level, while induced significant decreases in the activities of plasma superoxide dismutase (SOD), glutathione-S-transferase (GST) and serum acetylcholinesterase (AChE) either in male or female rats. Similarly, a significant increase in the levels of various serum marker enzymes [e.g. aminotransferases (AST and ALT), lactate dehydrogenase (LDH) and gamma glutamyl transferase (GGT)] and increase the level of total protein, uric acid and creatinine. In contrast, co-administration of zinc to CPF-treated animals restored most of these biochemical parameters to within normal levels. In case of AChE, supplementation of zinc showed little alteration in the activity of this enzyme especially in male rats treated with CPF. CPF caused histopathological change in liver and kidneys of male and female rats. However, zinc administration to CPF-treated animals resulted in overall improvement in liver and kidneys damage, emphasizing its antioxidant role. In light of the available data, it can deduce that CPF-induced lipid peroxidation, oxidative stress, liver and kidneys damage in male and female rats, and conjunction supplementation of zinc has resulted in pronounced ameliorating effect.