Protective effect of vitamin C against chlorpyrifos oxidative stress in male mice

Pesticides may induce oxidative stress leading to generate free radicals and alternate antioxidant or oxygen free radical scavenging enzyme system. This study was conducted to investigate the acute toxicity of chlorpyrifos toward male mice and the oxidative stress of the sub-lethal dose (1/10 LD₅₀) on the lipid peroxidation level (LPO), reduced glutathione content (GSH) and antioxidant enzymes; catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PD), and glutathione-S-transferase (GST) activities. Also, the protective effects of vitamin C (200 mg/kg body weight, bw) 30 min before or after administration of chlorpyrifos were investigated. The results demonstrated that the LD₅₀ value of chlorpyrifos was 134.95 mg/kg bw. The oral administration of 13.495 mg/kg chlorpyrifos significantly caused elevation in LPO level and the activities of antioxidant enzymes including CAT, SOD and GST. However, GPx activity remained unchanged, while the level of GSH and G6PD activity were decreased. Vitamin C treatment to chlorpyrifos intoxicated mice decreased LPO level and GST activity, normalized CAT, SOD and G6PD activities, while GSH content was increased. We conclude that vitamin C significantly reduces chlorpyrifos-induced oxidative stress in mice liver and the protective effect of the pre-treatment with vitamin C is better than the post-treatment.     

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.     

In vivo chlorpyrifos induced oxidative stress: Attenuation by antioxidant vitamins

Chlorpyrifos (O,O′-diethyl O-3,5,6-trichloro-2-pyridyl phosphorothionate, CPF) exposure in rats causes elevation in the levels of thiobarbituric acid reactive substances (TBARS) and inhibition of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT), and glucose-6-phosphate dehydrogenase (G6PDH) activities in the liver, kidney, spleen, and brain of rats. The sublethal exposure of CPF also causes decrease in the levels of reduced glutathione (GSH) and consequent increase in oxidized glutathione (GSSG) levels, resulting in a significant decrease in GSH/GSSG ratio in all the rat tissues tested. These results clearly indicate that CPF exposure causes oxidative stress in rat tissues. However, CPF exposure to rats fed with antioxidant vitamins (vitamin A, E, and C) for 1 month, prevented derangement of these antioxidant parameters. The accumulation of TBARS was also not seen in tissues of rats fed with antioxidant vitamins on CPF exposure. AChE activity, which is sensitive to OP pesticides, was also not significantly inhibited in these rats on CPF exposure. The present findings clearly show that oral intake of a mixture of vitamin A, E, and C, protects the rats from CPF induced oxidative stress and suggesting that this treatment alleviates the toxicity of this pesticide.     

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.     

Effect of combined exposure of commonly used organophosphate pesticides on lipid peroxidation and antioxidant enzymes in rat tissues

Organophosphate compounds are among the most widely used synthetic chemicals for controlling a wide variety of pests. Organophosphate (OP) poisoning continues to be major cause of morbidity and mortality in the third world countries. Indiscriminate use of these pesticides tends to leave residues on the objects of the environment. Present study is aimed to compare the potential of three commonly used OP pesticides, chlorpyrifos (CPF), methyl parathion (MPT) and malathion (MLT), to generate oxidative stress in rat tissues and to evaluate whether the combined exposure of these pesticides exerts synergistic or antagonistic effects. Results of the present study showed that CPF, MPT and MLT exposure to rats caused accumulation of malondialdehyde (MDA) and 4-hydroxynonanal (4HNE), the two major end products of lipid peroxidation, in liver, kidney, brain and spleen of rats. Combined exposure of these pesticides also resulted in accumulation of MDA and 4HNE in rat tissues but the increase was almost of the same order as observed in rat tissues given these pesticides singly. Exposure with CPF, MPT and MLT singly or in mixture, caused dose-dependent decrease in the activities of antioxidant enzymes namely, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx), in rat tissues when compared with control, and the decrease observed was of the same order in all the groups. Acetylcholinesterase (AChE) activity, an indicator of OP poisoning, was also decreased in rat tissues in dose-dependent manner in CPF, MPT, MLT and mixture treated group. Differential increase in the levels of cytochrome P450 (cyt P450) in hepatic and extra-hepatic tissues of rats given CPF, MPT or MLT singly or in mixture, indicate different rates of metabolism of these pesticides. Results of the present study clearly show that CPF, MPT and MLT exposure singly or in mixture, induced oxidative stress in rat tissues which may be the major contributor of the overall toxicity of the OP pesticides. Combined exposure of these pesticides does not seem to potentiate the toxicity of each other and their toxic effects are not additive.     

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.     

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.     

The growth and antioxidant defense responses of wheat seedlings to omethoate stress

Omethoate is one of the most powerful insecticides in China. Despite its high risks of human health and environmental safety, omethoate is still hard to be replaced because of its low price and high efficiency. To better understand physiological and biochemical responses to omethoate, we examined plant growth and antioxidative defense responses as well as omethoate uptake in wheat seedlings grown hydroponically with omethoate. Fresh and dry shoot weights were significantly higher at low concentrations (e.g. 0.1 g/L) than at high concentrations (e.g. 5.0 g/L). The same is true for the soluble protein content. On the contrary, contents of malondialdehyde, proline and omethoate, and activities of superoxide dismutase, peroxidase and ascorbate peroxidase in shoots increased linearly with increasing concentration of omethoate and with exposure time as well. However, catalase activity was increased dramatically at 0.1 g/L but sharply decreased by omethoate added at 1.0 g/L and above compared with that of the control. Taken together, these results support our hypothesis that antioxidative defense response is an important component of plant responses to omethoate and oxidative damage is the major cause for growth reduction of wheat exposed to higher concentrations of omethoate.     

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.     

Comparative studies on chlorpyrifos and methyl parathion induced oxidative stress in different parts of rat brain: Attenuation by antioxidant vitamins

Organophosphate (OP) pesticides are among the most widely used synthetic chemicals for controlling a wide variety of pests. Chlorpyrifos (o,o′-diethyl-o-3,5,6-trichloro-2-pyridyl phosphorothionate, CPF) is among the leading OP pesticides used extensively throughout the world including India while methyl parathion (o,o-di methyl-o-p-nitrophenyl phosphorothioate, MPT) another OP compound, widely used as insecticide and acaricide to control many biting or sucking pests of agricultural crops. Present study was carried out to compare the chronic toxicity of CPF and MPT, their potential to generate oxidative stress and ameliorating effects of antioxidant vitamins in brain of rats. Results of the present study clearly demonstrated that the oral exposure of CPF or MPT, generated oxidative stress in different parts of rat brain consequently accumulating malondialdehyde (MDA) and 4-hydroxynonanal (4HNE), the two major end products of lipid peroxidation, in all the three brain regions i.e. fore-, mid- and hind-brain. The levels of hydrogen peroxide (H₂O₂) were also increased in all the three brain regions when compared with control. CPF and MPT exposure caused decrease in the levels of reduced glutathione (GSH) and increase in the levels of oxidized glutathione (GSSG) in all the three brain regions. The increase in the levels of MDA, 4HNE, H₂O₂ and GSSG was less pronounced when CPF or MPT was given to the rats fed with a mixture of vitamin A, E and C. The present findings clearly show that oral intake of a mixture of vitamin A, E and C protects the rats from MPT or CPF induced oxidative stress and suggest that this treatment alleviates the toxicity of these pesticides to a greater extent.     

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.     

Toxicological effects of oxyfluorfen on oxidative stress enzymes in tilapia Oreochromis niloticus

Several environmental pollutants enhance the intracellular formation of reactive oxygen species, and can lead to the damage of macromolecules and a decrease in oxidant defences levels in fish. The effects of the herbicide oxyfluorfen on the activities of antioxidant enzymes such as catalase, superoxide dismutase, glutathione reductase, and glutathione S-transferase were evaluated in freshwater fish Oreochromis niloticus. These were determined in tilapia liver exposed to sublethal concentrations (0.3 and 0.6 mg/L at 7, 14, and 21 days of exposure. This study also analyzed the effects of oxyfluorfen on the total fatty acid profile. The results showed that CAT activity was higher in tilapia exposed to oxyfluorfen at the sampling days, except at the highest concentration after 21 days. Similarly, the enhancing effect of the herbicide was observed on the GR activity. However, its effect was moderate at the highest dose. On the contrary, fish treated with oxyfluorfen at both doses displayed a decrease in the SOD activity. After 7 days of treatment at both concentrations tilapia showed a significant increase in GST levels, although the enzymatic activity decreased at 14 and 21 days of exposition when compared with the control. The major saturated fatty acids measured in tilapia liver were the palmitic acid (C16:0; 17.9%) and stearic acid (C18:0; 8.7%). The exposure to oxyfluorfen caused a significant increase of the oleic acid (C18:1), whereas the amount of nervonic acid (C24:1) increased at all sampling data. The results of the present study should be taken in account when using tilapia as an environmental indicator species in studies of xenobiotic biotransformation and biomarker response, as well as in monitoring programmes.     

Protective effects of garlic (Allium sativum) extract upon lindane-induced oxidative stress and related damages in testes and brain of male rats

The purpose of this study, carried out on male Wistar rats, was to evaluate the beneficial effects of garlic (Allium sativum) extract injections upon lindane-induced damages in testes, brain and thyroid function. Under our experimental conditions, lindane poisoning (in drinking water for 30 days, supplying about 50 mg/kg body weight per day) resulted in a decreased weight of testes, epididymides, prostate gland and seminal vesicles (−52%, −42%, −50% and −5%, respectively), a decrease of spermatozoa count and motility (−56%, −37%, respectively), an increased level of free thyroxin (+84%) and decreased levels of TSH and FSH in serum (−74%, −77%, respectively). In addition, lindane treatment triggered an oxidative stress in testes and brain as revealed by an increased level of lipids peroxidation (TBARS) (+96%,+92%), an increase of superoxide-dismutase activity in testes (+69%) and a decrease of glutathione-peroxidase and catalase activities in testes and brain (−52%, −34% and −49%, −45%, respectively). These lindane-induced changes were almost reversed to normal in animals injected with a garlic extract (an amount corresponding to 300 mg fresh garlic/kg/day), what confirms a beneficial effect of this vegetal source of anti-oxidants.     

Biochemical and histopathological studies to assess chronic toxicity of triazophos in blood, liver and brain tissue of rats

Triazophos, O,O-diethyl-1-H-1,2,4-triazol-3-yl phosphorothioate, (TZ) is an organophosphorus pesticide which is extensively used in agriculture for controlling insect pests. Except a FAO/WHO report no study has investigated its short-term toxicity with respect to its potential to cause biochemical and histopathological alterations. The present study was designed to identify the effect of TZ at different doses (1.64, 3.2 and 8.2 mg/kg) on the oxidative stress parameters in blood as well as organs involved in xenobiotic metabolism (liver and brain) following chronic exposure for 90 days. Moreover, the study also delineates the effect of TZ on the histo-architecture of these organs. The results indicated a dose dependent induction (p < 0.001) of oxidative stress, as evident by increased malondialdehyde (MDA) level and compromised antioxidant defense including glutathione S transferase (GST) activity, glutathione (GSH) content and ferric reducing ability of plasma (FRAP) in blood, and increased MDA level with concomitantly decreased GSH content in tissues, following chronic exposure to TZ. The ratio of MDA: FRAP in blood was found to be increased following chronic exposure to TZ and may serve as a suitable indicator of severity of oxidative damage. Onset of such biochemical alterations is one of the early adaptive responses to TZ exposure which leads to histopathological alterations in terms of diffuse fatty changes expanding from mid-zonal area to whole lobule in liver. However, increased oxidative stress did not bring any morphological alteration in brain. The present study concludes that induction of oxidative stress, leading to subsequent histopathological alterations in liver, is an important mechanism underlying the TZ induced chronic toxicity.     

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.     

Tissue-specific antioxidative and neurotoxic responses to diazinon in Oreochromis niloticus

The purpose of this study was to evaluate oxidative stress and neurotoxic potential of organophosphorus (OP) insecticide diazinon in the sentinel freshwater fish, Oreochromis niloticus. Antioxidant and acetylcholinesterase (AChE) enzyme activities and malondialdehyde (MDA) and protein levels were measured spectrophotometrically in gill, kidney, alimentary tract, and muscle tissues of fish treated with sub-lethal diazinon concentrations for 1, 7, 15, and 30 days. Dose-dependent inhibitions of AChE were observed in all the experimental fish. On the contrary of alimentary tract, MDA levels were elevated in kidney and muscle and gill was not affected. AChE and MDA levels intercorrelated in kidney and muscle tissues. Diazinon had increased superoxide dismutase (SOD) activities in all the tissues, while kidney was the most affected tissue. Tissue-specific alterations were observed on catalase (CAT) and glutathione peroxidase (GPx) activities; however, the activities were not changed in gill and muscle tissues for GPx and in gill, muscle, and kidney tissues for CAT. Protein levels decreased in kidney, muscle, and alimentary tract, while increased in gill and alimentary tract in 15 days. With respect to these results, diazinon has oxidative and neurotoxic potentials in O. niloticus. Observed changes with diazinon treatment were generally tissue-specific and dose-dependent.     

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.     

Evaluation of aspect of some oxidative stress parameters using vitamin E, proanthocyanidin and N-acetylcysteine against exposure to cyfluthrin in mice

A hundred and sixty female white mice, each weighing 35-40 g, were used in this study. The animals were assigned into eight groups as one control group and 7 experimental groups. Groups 2, 3 and 4 were administered N-acetylcysteine (NAC), proanthocyanidin and vitamin E alone, at doses of 100 mg/kg/body weight/day by intra-peritoneal, oral route and, intramuscular, respectively. Group 5 was administered a single dose of cyfluthrin (100 mg g/kg/body weight ∼1/3LD₅₀) by oral, whereas Groups 6, 7 and 8 were given cyfluthrin+NAC, cyfluthrin+proanthocyanidin and cyfluthrin+vitamin E, at the same dose, respectively. The administration of the drugs was initiated following the administration of cyfluthrin, and continued until the end of the seventh day of the study. Blood samples were collected from each group, 24 h, and 3, 7 and 9 days after the administration of cyfluthrin for the assessment of blood malondialdehyde (MDA) levels and superoxide dismutase (SOD) and catalase (CAT) activities. According to the data obtained, compared to the control group, increase in the plasma MDA level of the group administered cyfluthrin alone, and decrease in erythrocyte SOD activities in some periods and CAT activities in all periods were determined. On the other hand, especially, MDA levels and CAT activities were observed to move closer to values of the control group, in the groups that were administered NAC, proanthocyanidin and vitamin E in addition to cyfluthrin. In other words, in most periods, decrease in plasma MDA levels, and increase in erythrocyte CAT and SOD activities were observed in comparison to the group administered cyfluthrin alone. Statistical analyses demonstrated significant differences to exist between the groups on the third, seventh and ninth days with respect to plasma MDA levels, and the third and ninth days with respect to erythrocyte SOD and CAT activities (P < 0.05). However no significant difference was demonstrated in any of the periods in the groups that were administered NAC, proanthocyanidin and vitamin E alone in comparison to the control group (P > 0.05). In view of the parameters examined, animals were concluded to be affected by cyfluthrin and the administration of the three compounds at the indicated doses and for the indicated periods were considered to alleviate the adverse effects of cyfluthrin partly throughout the study period.     

Dithiocarbamate fungicide zineb induces oxidative stress and apoptosis in Chinese hamster lung fibroblasts

Dithiocarbamate fungicide zineb leads to disturbances in many cellular processes in Chinese hamster fibroblasts (V79 cells). We observed high apoptotic activity and oxidative stress induced in vitro by exposure of V79 cells to zineb demonstrated by statistically significant increase in lipid peroxidation (measured as TBARS - thiobarbituric acid reactive substances) as well as disturbances in glutathione homeostasis. Zineb also inhibited activity of topoisomerase I. Zineb did not show any effect on protein oxidation (measured by protein carbonyls content). N-acetyl-l-cysteine (NAC) suppressed cellular changes induced by this fungicide in V79 cells. NAC pre-treatment prevented TBARS production and significantly decreased the number of apoptotic cells induced by zineb. These results show that zineb can disturb many cellular processes via oxidative damage.     

Role of oxidative stress in organophosphate insecticide toxicity - Short review

The objective of this paper is to present a short review of the state of knowledge regarding oxidative stress and its role in toxicity of organophosphate insecticides. The information has been obtained by searching the relevant literature using chemical abstracts, PubMed, scopus, medline and other data bases. The significance of the problem has been elucidated. Organophosphate insecticides (OP), apart from inhibition of cholinesterase and presence of cholinergic effects, oxidative stress and hyperglycemia has been reported by many authors as one of the adverse effects in poisoning by OP in both humans and animals. Oxidative stress induced by organophosphate leads to disturbances in the function of different organs and tissues. In subchronic or chronic OP exposition induction of oxidative stress has been reported, by many authors, as the main mechanism of its toxicity. Data were categorized according to animal studies (in vitro and in vivo) and clinical studies. On the basis of relevant literature it is concluded, that determination of oxidative stress parameters can be useful for monitoring people exposed to OP professionally. Supplementation with natural or synthetic antioxidant may be beneficial in OP poisoning, however the rat models of OP poisoning used in those studies do not completely reflect clinical situation. For this reason the clinical trials are needed to explore effectiveness of these antioxidants in protection against toxicity of OP.