Selenium and vitamin E, natural antioxidants, protect rat cerebral cortex against dimethoate-induced neurotoxicity

Pesticides have been used in agriculture to enhance food production by eradicating unwanted insects and controlling disease vectors, nevertheless occupational exposure to high levels of these compounds can lead to neurodegenerative disorders, characterized by serious oxidative and neurotoxic effects. However, there is a lack of consensus as to which determinations are best used to quantify future risks arising from xenobiotic exposure and natural antioxidant interventions. Our study aims to determine the potential ability of selenium and/or vitamin E, used as nutritional supplements, to alleviate oxidative stress in cerebral cortex tissue induced by dimethoate, an organophosphorus pesticide. Adult Wistar rats were exposed either to dimethoate (0.2 g/L of drinking water), dimethoate + selenium (0.5 mg/kg of diet), dimethoate + vitamin E (100 mg/kg of diet), or dimethoate + selenium + vitamin E, for 30 days. Exposure to dimethoate increased malondialdehyde levels, protein carbonyl groups and advanced oxidation protein products, while Na⁺K⁺-ATPase, acetylcholinesterase and butyrylcholinesterase activities decreased in the cerebral cortex. An increase in glutathione peroxidase, superoxide dismutase and catalase activities and a decrease in glutathione, non-protein thiols and vitamin C levels were observed. Administration of selenium and/or vitamin E through the diet in dimethoate treated rats ameliorated the biochemical parameters cited above. The histological findings confirmed the biochemical results. The model of this study that we employed characterized the relationships between dimethoate-induced neurotoxicity and its alleviation by natural antioxidants like selenium and vitamin E. These elements may be considered beneficial for the protection of cerebral cortex against injury induced by dimethoate.     

Effect of short-time malathion administration on glucose homeostasis in Wistar rat

The main objective of this study is to investigate the 24 h kinetic effect of acute administration of malathion, an organophosphorus insecticide, on glucose homeostasis in adult rats. A single dose of malathion (400 mg/kg, 1/5 of LD₅₀) was administered orally to rats, blood glucose was measured, liver and pancreas were removed to determine the level of hepatic glycogen, the activity of pancreatic acetylcholinesterase and butyrylcholinesterase, as well as the level of TBARs. Blood glucose increased in rats treated with a single dose of malathion. This effect was observed in the first hours of treatment, reached a 2.2 fold peak after 2 h, and then decreased after 4 h, followed by a decrease in the level of hepatic glycogen. The storage of glycogen starts from 6 to 12 h of administration. A decrease in cholinesterase activities was noted. The level of TBARs increased considerably in liver and pancreas. Results of this study can be explain by a stimulation of glycogenolysis and gluconeogenesis by liver, with a temporarily loss of endocrine functions of pancreas leading to hyperglycemia.     

Effects of dimethoate (O,O-dimethyl S-methyl carbamoyl methyl phosphorodithioate) and Ethanol in antioxidant status of liver and kidney of experimental mice

Organophosphorus insecticides and ethanol individually cause free radical production induced by oxidative stress and alter the antioxidants and scavengers of free radicals. The present study indicates the effect caused by dimethoate in combination with ethanol on antioxidant status in mice. Daily, dimethoate at a dose of 18 mg/kg body weight and ethanol at 1 g/kg body weight were orally administered concurrently in a subacute study for 14 days. After the experimental period, the liver and kidney homogenates were analysed for various antioxidant enzymes. The results compared with dimethoate alone treated control indicated an increase in hepatic cytochrome P450 and lipid peroxidation. Decrease in superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and glutathione in liver was observed. In kidney, decrease in CAT, SOD, GR, GST, and GSH was observed. Acetyl cholinesterase activity of RBC was increased. No significant change was observed in catalase in liver and glutathione peroxidase in kidney. The results of the study allow us to hypothesize that dimethoate along with ethanol disturbs the antioxidant status.     

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.     

Nephrotoxicity induced by dimethoate in adult rats and their suckling pups

The purpose of this study was to investigate the effect of dimethoate (DM), an organophosphorus insecticide, on oxidative stress in kidneys of adult rats and their suckling pups. Female Wistar rats were given daily DM in drinking water 0.2 g/L equivalent to 40 mg/kg bw from day zero until day 10 after delivery. A significant increase was found in relative kidney weights of treated adult rats and their offspring. DM administration affected strongly specific markers of kidney function such as the 24-h urine volume which was higher than in the controls. In test group we have found higher plasma levels and lower urinary levels of creatinine, a specific indicator of glomerular function, and urea than in the controls. Significant increase in creatinine clearance was also found in treated mothers and their suckling pups. These results indicated that DM exposure provoked low glomerular filtration rate in treated group. Interestingly, these biochemical modifications were accompanied by a marked enhancement of lipid peroxidation in kidney indicating significant induction of oxidative damage and alterations of enzymatic antioxidant defences in test group. Impairment of renal function corresponds histologically. In fact, histological changes, seen in the kidney of mothers and their pups treated with DM are characterized by a narrowed Bowman’s space, degenerative of tubular epithelial cells and widened tubular lumen. Moreover in mothers, extensive vascular congestion was observed.We concluded that the effect of DM treatment in lactation period of mothers was fairly reflected in the offspring in all parameters analysed.     

Subacute oral toxicity of chlorpyriphos and protective effect of green tea extract

This paper reports the effect of green tea administration following subacute toxicity caused by exposure to organophosphorus pesticide chlorpyriphos in liver of rats. Four groups containing five male Sprague-Dawley rats each were selected. Group I served as control. Group II rats were permitted free access to solubilised crude extract of green tea (1.5%w/v in water) as the sole drinking fluid. Group III rats were given a single daily oral dose of chlorpyriphos (30 mg/kg bodyweight in corn oil). Group IV rats received oral dose of pesticide and green tea extract simultaneously. All rats were sacrificed after 15 days. Significant damage to liver was observed via increased serum levels of transaminases and alkaline phosphatase. Lipid peroxidation showed a 5-fold increase in pesticide exposed rats compared to control. In contrast, levels of antioxidant GSH, glutathione-dependent enzymes like glutathione peroxidase (GPx), glutathione S-transferase (GST) and free radical scavengers like catalase (CAT) and superoxide dismutase (SOD) were significantly lower than those of the control group reinforcing oxidative damage. The use of green tea extract appeared to be beneficial to rats, although not to a great extent in significantly reducing and reversing the damage sustained by pesticide exposure and favors recovery.     

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.     

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.     

Induction of insulin resistance by malathion: Evidence for disrupted islets cells metabolism and mitochondrial dysfunction

Hyperglycemia is observed with exposure to organophosphorus (OP) pesticides. The aim of this study was to investigate the effects of malathion on secretion of insulin from rat pancreatic islets in vitro and in vivo. Malathion was administered through food for 4 weeks at concentrations of 100, 200, and 400 ppm. For in vivo experiment, at the end of treatment, blood sample was obtained and plasma was separated. For in vitro experiment, the treated rats were anesthetized and underwent a laparatomy. The common bile duct was cannulated and the pancreas distended by injecting of cold collagenase V using peristaltic infusion pump. Islets were then hand picked under a stereomicroscope and cultured in the presence of various doses of glucose and KCl. Malathion at doses of 200 and 400 ppm increased plasma glucose and insulin concentrations and lowered activity of erythrocyte acetylcholinesterase. The isolated islets from pretreated animals with malathion 200 and 400 ppm showed lower glucose-stimulated insulin secretion while no change was observed in the presence of KCl. Light microscopic examination revealed that malathion causes patchy degenerative changes in pancreatic islets. Combination of in vivo and in vitro findings suggests that malathion induces a kind of insulin resistance that cannot overwhelm hyperglycemia. This action of malathion is mediated through disruption of islets mitochondrial function.     

Effects of thiacloprid, deltamethrin and their combination on oxidative stress in lymphoid organs, polymorphonuclear leukocytes and plasma of rats

Deltamethrin and thiachloprid are an α-cyano class pyrethroid and neonicotinoid insecticide, respectively. Recently, a pesticide combining deltamethrin and thiacloprid has also been released. In the present study, the acute and subacute toxic effects of deltamethrin, thiachlopride, and a combination of these insecticides, on the lymphoid organs (spleen, thymus and bone marrow), polymorphonuclear leukocytes (PMNs) and plasma of rats, were determined to better understand mammalian antioxidant-oxidant and inflammatory system responses. For this purpose, rats were treated orally with different doses of thiacloprid (single acute dose of 112.5 mg/kg); subacute dose of 22.5 mg/kg/day for 30 days; deltamethrin (single acute dose of 15 mg/kg); subacute dose (3 mg/kg/day for 30 days), or a combination of these pesticides. Results were compared with those from a comparable dosing regimen with the known immunosuppressive drug cyclophosphamide. Pesticide treatments caused significant changes in the levels of liver and kidney injury markers. Antioxidant enzyme (catalase and glutathione peroxidase), glutathione and plasma antioxidant levels decreased but lipid peroxidation increased in all lymphoid organs and the plasma. Glutathione-S-transferase and especially DT-diaphorase activity, decreased after thiacloprid treatment. Myeloperoxidase activity, carbonyl content, lipid peroxidation and total nitrite levels increased in PMNs and plasma. When evaluated as a whole, the oxidative and inflammatory stresses seen in the pesticide combination groups were not much more pronounced than in the groups treated with a single pesticide. In terms of the evaluated biochemical parameters, the pesticides showed similar effects to cyclophosphamide.     

Effects of vitamin E and selenium on tissue bio-element status in organophosphate toxicity of rats

The present study was designed to investigate the effects of vitamin E (vit E), selenium (Se) and vit E + Se against organophosphate (OP) toxicity in tissues’ trace and major element levels and erythrocyte antioxidant enzyme activities of rats. Trace and major element concentrations in the tissues were measured by inductively coupled plasma-optical emission spectroscopy. Erythrocyte antioxidant enzyme activities were studied by using spectrophotometer. Antioxidant enzyme activities such as superoxide dismutase, glutathione peroxidase and catalase increased in the fenthion-treated groups (control) more than that of sham group subjects. Heart and pectoral muscle tissue Se and Zn concentrations in the control group were higher than sham group. However, jejunum, kidney, liver and pancreas Se and Zn concentrations in the control group were found to be lower than those in the sham group. The Mn concentrations in the all of the tissues were lower in the control group when compared with the sham group. Brain, heart, jejunum, kidney and pancreas Fe concentrations and heart, jejunum, liver, pectoral muscle and pancreas Cu concentrations were found to be lower in the control group. The treatment of vit E, Se and vit E + Se were increased bio-element levels in the many tissue. In conclusion, the results of the present study demonstrate that the tissue trace and major element concentrations and enzymatic antioxidant system were significantly affected OP toxicity. Furthermore, we have shown an association between bio-elements and antioxidant enzymes in OP toxicity. In addition, administration of vit E, Se and vit E + Se might regulate some trace and major element levels in the many tissues.     

A two generation chronic mixture toxicity study of Clophen A60 and diethyl phthalate after gestational and lactational exposure in female Wistar rats

Polychlorinated biphenyls and diethyl phthalate are both lipophilic in nature and are likely to be present in the same environmental compartment or bioaccumalate over a period of time, thus a mixture toxicity study was undertaken to evaluate the type of interaction between polychlorinated biphenyls (Clophen A60) and diethyl phthalate over two generations in female Wistar rats. Healthy male and female albino rats of Wistar strain weighing 75-100 g (6-7 weeks old) were randomly assigned to four groups of six each. Group I male and female rats were fed on normal diet and water ad libitum. Group II male and female rats were maintained on normal diet mixed with corn oil as oil control. GroupS III and IV male and female rats were given Clophen A60 and diethyl phthalate dissolved in corn oil mixed with the diet at 50 mg/kg of the diet individually to each group. Group V male and female rats received a mixture of diethyl phthalate and Clophen A60, each dissolved in corn oil mixed with the diet at 50 mg/kg of the diet. Hundred days after the treatment, females were mated with the males in each group for 10 days. Exposure to diethyl phthalate and Clophen A60 was continued throughout mating, gestation until termination at weaning, which was 150 days of total treatment period of the parental generation female rats. Treatment for F1 generation male and female pups (6 males & 6 females) with Clophen A60 and diethyl phthalate individually and in mixture was continued at doses reduced to 25 mg/kg of the diet after they reached 75-100 g in weight. The treatment was carried out similar to the parental generation for a period of 150 days. Liver and serum aspartate aminotransferase, liver cholesterol and glycogen were significantly increased in the F1 generation Clophen A60 + diethyl phthalate treated group, whereas serum cholesterol, liver glutathione and glutathione reductase showed a significant decrease in the F1 generation Clophen A60 + diethyl phthalate treated group as compared to the parental generation mixture and individually treated groups as well as the individually treated F1 generation groups. A significant increase was observed in the liver and serum aspartate aminotransferase activity of Clophen A60 and serum aspartate aminotransferase levels of diethyl phthalate treated F1 generation rats as compared to the parental generation Clophen A60 and diethyl phthalate individually and mixture treated rats. Liver glutathione levels were significantly decreased in the F1 generation Clophen A60 and diethyl phthalate individually treated rats which was similar to the parental generation individually treated rats as compared to the controls. Liver glutathione reductase level was also significantly declined in the diethyl phthalate treated F1 individual group as compared to diethyl phthalate individually treated parental generation rats. Histology of the liver showed fatty degeneration in the mixture treated F1 generation rats as compared to Clophen A60 and diethyl phthalate individually treated F1 rats and parental generation Clophen A60 and diethyl phthalate individually and mixture treated rats. Thus, in spite of dose reduction and continuous exposure over two generation’s to a mixture of diethyl phthalate and Clophen A60 exposed through gestation, lactation and diet leads to a synergistic toxic effect in the F1 generation.     

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.     

Can diphenhydramine prevent organophosphate-induced acute pancreatitis? An experimental study in rats

Acute pancreatitis (AP) is a well known complication of organophosphate (OP) poisoning and the true incidence is unknown; but, may be more common than clinically suspected. Previous studies suggest that Diphenhydramine (DPH) may be useful as an alternative or adjunctive therapy in OP poisoning. The aim of this experimental study was to investigate whether DPH could prevent or diminish pancreatic damage caused by OP poisoning as defined by histologic findings, and serum interleukin 10 (IL-10) and tumor necrosis factor alpha (TNF-α) levels. Twenty-four Sprague- Dawley rats were divided into equal three groups. Group 1 did not receive any agent during the experiment. Group 2 received 0.8 g/kg fenthion subcutaneously followed by 3 ml/kg normal saline intramuscularly, 30 min later. Group 3 received 0.8 g/kg fenthion subcutaneously, followed by 30 mg/kg DPH intramuscularly, 30 min later. Twenty-four hours later, pancreatic tissues were excised and blood samples were taken. After blood samples were taken by cardiac puncture, the animals were sacrificed. Treatment with DPH significantly decreased the serum TNF-α and increased the serum IL-10 levels. DPH significantly reduced pancreatic damage, including edema, inflammation, vacuolization and necrosis, as determined by pathologic scoring. The present study show that DPH decreased the severity of OP induced AP in rats. This effects may be related to a decrease of TNF-α level and increase of IL-10 level.     

Effect of diethyl phthalate on rat testicular antioxidant system: A dose-dependent toxicity study

The experiment was designed to study toxic effects of diethyl phthalate (DEP) on testicular lipid peroxidation and testicular antioxidants in male Wistar rats for long-term exposure periods at varying concentrations. Healthy male rats were randomly assigned to five groups of six each. Group I male rats were fed on normal diet and water. Group II male rats were maintained on normal diet mixed with corn oil as oil control. Group III, IV and V rats were given diethyl phthalate (DEP) dissolved in minimal quantity of corn oil mixed with the diet at 10, 25 and 50 mg/kg of the diet/day, respectively, for 150 days. Body weight, testis weights, epididymis weight and the serum testosterone and androstenedione levels showed a significant decrease in the three treated groups. Testicular lipid peroxidation showed a significant dose-dependent increase, while testicular antioxidant enzymes including superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) were significantly decreased. These results confirm that, continuous administration of DEP at various concentrations on a long-term basis induces increased levels of lipid peroxidation leading to dose-dependent reduction in the testicular antioxidant defense system. Increased free radical production at various doses of DEP would result in impairment of the defense system leading to an enhanced dose-dependent reproductive toxic effect.     

Prophylactic effect of green tea polyphenols against liver and kidney injury induced by fenitrothion insecticide

The ameliorative effect of daily administrated dose of green tea extract (60 mg polyphenols/animal/day) was investigated on albino rats Rattus norvegicus (150-180 gm) intoxicated with 1/30 and 1/60 LD₅₀ fenitrothion organophosphate insecticide for 28 days. Blood samples were taken at 14 and 28 days for further biochemical parameters. Histopathological studies were carried out in the liver and kidney at the end of the experiment. Significant inhibition in plasma cholinesterase (ChE), a biomarker of Ops, was recorded. Damage in the liver and kidney tissues was observed and confirmed with elevation of plasma alanine aminotransferase (ALT), aspartate aminotaransferase (AST), albumin, urea and creatinine, as well as an elevation in the oxidative stress (OS) marker malondialdehyde (MDA). Decrease in total glutathione (GSH) content in erythrocytes and fluctuation in glutathione S-transferase (GST) activity in plasma was also observed. Green tea supplementation (60 mg/animal/day) partially counteracts the toxic effect of fenitrothion on oxidative stress parameters and repairs tissue damage in the liver and kidney, especially when supplemented to 1/60 LD₅₀ intoxicated animals depending on the duration. It seems that enzyme and metabolite markers of these organs need more time to be restored to the control level.     

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.     

Determination of toxicity of trichloroacetic acid in rats: 50 days drinking water study

This study aims to investigate the effects of the trichloroacetic acid (TCA) on serum marker enzymes [aspartate aminotransferase (AST), alanin aminotransferase (ALT), creatine phosphokinase (CPK), acid phosphatase (ACP), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH)], antioxidant defense systems [Reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT)] and lipid peroxidation content (Malondialdehyde, MDA) in various tissues of rats. TCA (2000 ppm) as drinking water was administered orally to rats (Sprague-Dawley albino) ad libitum for 50 days continuously. TCA treatments caused different effects on the serum marker enzymes, antioxidant defense systems and the MDA content in experimented rats compared to controls. Results showed that TCA caused a significant increase in serum AST, ALT, CPK and ACP activity. The lipid peroxidation end product MDA slightly increased in the erythrocytes, liver and kidney of rats treated with TCA, whereas did not change in the brain. In addition, antioxidant enzyme activity such as CAT and SOD significantly increased in the brain, liver and kidney tissues of TCA induced group whereas the ancillary enzyme GR and the drug metabolizing enzyme GST activity did not significantly change in the all tissues. The observations presented led us to conclude that the administration of subchronic TCA promotes lipid peroxidation content, elevates tissue damage serum marker enzymes and fluctuates in the antioxidative systems in rats. Also the rats resisted to oxidative stress via antioxidant mechanism but the antioxidant mechanism could not prevent the increases in lipid peroxidation in rat’s tissues. These data, along with the determined changes suggest that TCA produced substantial systemic organ toxicity in the erythrocyte, liver, brain and kidney during the period of a 50-day subchronic exposure.     

Investigations on Oecophylla longinoda (Latreille) (Hymenoptera: Formicidae) as a biocontrol agent in the protection of cashew plantations

BACKGROUND: Cashew (Anacardium occidentale L.) has become a very important non‐traditional tree crop in Ghana. The crop is, however, attacked by sap‐sucking insects, particularly the mosquito bug, Helopeltis schoutedeni Reuter, the leaf‐footed bug, Pseudotheraptus devastans (Dist.), and the coreid bug, Anoplocnemis curvipes (F.), which feed on shoots, panicles and fruits. Their damage is characterised by withering of the latter. In Ghana, Oecophylla longinoda Latr. occurs in large numbers on cashew and other native plants, but little is known about its relationship with insect pests. The relationship between O. longinoda and shoot and panicle damage by sap‐sucking bugs and the effectiveness of O. longinoda as a biocontrol agent in the protection of cashew as compared with two chemical insecticides, lambda‐cyhalothrin (Karate^®) and cypermethrin + dimethoate (Cyperdim^®), were therefore investigated at Bole in the northern region of Ghana. RESULTS: There was a negative correlation between numbers of O. longinoda nests and pest damage. Trees treated with cypermethrin + dimethoate (969 mg AI mL^?1 tree^?1) and lambda‐cyhalothrin (100 mg AI mL^?1 tree^?1) recorded the smallest bug numbers, followed by O. longinoda. Trees infested by Oecophylla longinoda and trees treated with cypermethrin + dimethoate and with lambda‐cyhalothrin had less than 6% pest damage to shoots, panicles and fruits, while water‐sprayed trees recorded damage as high as 36.8% (shoots) in February, 32.9% (panicles) in February and 37.8% (fruits) in March. Cypermethrin + dimethoate again recorded the highest (485.0 kg ha^?1) nut yield, followed by O. longinoda (431.0 kg ha^?1), with water recording the lowest (93.0 kg ha^?1) nut yield. CONCLUSION: The results indicate that O. longinoda can be used to control some sucking bugs as effectively as some insecticides. Copyright © 2008 Society of Chemical Industry     

Stimulation of insulin and glucagon synthesis in rat Langerhans islets by malathion in vitro: Evidence for mitochondrial interaction and involvement of subcellular non-cholinergic mechanisms

We examined the effects of malathion, an organophosphorus (OP) insecticide, on glucagon, C-peptide, and insulin content or secretion from isolated rat Langerhans islets in vitro. Islets were isolated from the pancreas of rats by standard collagenase digestion, separation by centrifugation, and hand-picking technique. Then islets were cultured in medium and supplemented with various concentrations of malathion (25, 125, and 625 μg/ml) for 1, 3, and 5 h. In vitro exposure to malathion increased insulin and C-peptide contents at doses of 25, 125, and 625 μg/ml following 5 h incubation as compared to control. All doses of malathion increased glucagon content after 3 and 5 h as compared to control. Increase of the glucagon content at all doses in the fifth hour was higher than that of third hour. Malathion also decreased 2.8 and 16.7 mM glucose-stimulated insulin secretion at all doses after 30 min as compared to control.It is concluded that malathion reduce insulin exocytose in a short time (first hour) but after a long time (e.g., 5 h), the content of insulin is increased by compensating mechanisms such as resynthesize of insulin or aggregation of insulin. The present in vitro study for the first time proposes the involvement of subcellular non-cholinergic mechanisms in malathion-induced changes in Langerhans islets insulin and glucagon.