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.     

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.     

Impact of phosphine exposure on development in Caenorhabditis elegans: Involvement of oxidative stress and the role of glutathione

Phosphine (PH₃) is a widely used and ideal fumigant employed to control insect pests in stored grains and other commodities. Chemically, PH₃ is a strong reducing agent and mainly affects the mitochondrial transport system in insects. PH₃ toxicity to insects is also associated with oxidative imbalances. Besides inducing mortality, PH₃ is shown to delay hatching and adversely affect fecundity/fertility of several stored product insect pests. Recent studies have demonstrated the utility of Caenorhabditis elegans as a model organism to obtain basic insights on the toxic implications of PH₃. In the present study, we have examined the impact of PH₃ on the development of C. elegans and the involvement of glutathione (GSH) in its developmental toxicity. We exposed eggs of C. elegans to two concentrations of PH₃ (0.04 and 0.06 mg/L) either in the presence or absence of a GSH depleting agent, diethyl maleate (DEM, 5 mM) for 72 h. PH₃ exposure caused significant delay in the post embryonic development among worms as characterized by the inability of hatched worms to attain gravid adult stage by the end of 72 h. Interestingly, among worms co-exposed to DEM + PH₃, the decrease in GSH levels was associated with more pronounced developmental delay compared to that of worms exposed to PH₃per se. Concomitantly, PH₃-induced depletion of glutathione was associated with significant alterations in activities of key antioxidant enzymes. Our data demonstrate the vital role of GSH and antioxidant defenses among worms developing under PH₃ exposure. Interestingly, this finding also unfolds newer possibilities for developing strategies to disrupt antioxidant defenses in insect pests to enhance the efficacy of PH₃ treatment for the control of stored product insects.     

Biochemical and histological hepatic changes of Nile tilapia Oreochromis niloticus exposed to carbaryl

The purpose of this study was to evaluate biochemical and morphological responses induced by carbaryl in the liver of Nile tilapia (Oreochromis niloticus) exposed during 21 days to sublethal concentrations (0.25 and 0.5 mg L⁻¹), testing also recover for 14 days in clean water, after 14 days exposure. The activities of the following enzymes were measured: superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), glutathione reductase (GR), and reduced (GSH) and oxidized glutathione (GSSG). Globally, our data showed that exposure to carbaryl decreased the SOD, CAT, GR, and GST activities, except for the SOD and GST activities after 14 days exposure to 0.25 mg L⁻¹. In contrast, after 14 days exposure the GR activity of the hepatic tissue from carbaryl-treated fish showed significant elevation in relation to the control. When fish were left to recover, a positive response was seen in the GSH and GSSG contents. The results of the recovery group suggest that the toxicity produced by carbaryl is reversible to some extent within 15 days. The liver histological analysis showed differences between fish concerning the cellular vacuolization degree (VD) of the hepatocytes. In fish exposed to carbaryl it was observed an increasing hepatocellular basophilia. No other histological alterations were observed when fish was exposed to carbaryl, except a few necrotic foci at day 7. The sections stained with PAS reaction showed that the vacuolization was always not due to glycogen deposits, thus suggesting lipid accumulation. The combined increased basophilia and glycogen depletion is a common, although non-specific, liver response to many toxicants. In short, this work shows a relation between histological and biochemical changes in liver and carbaryl exposure. The effects of carbaryl were observed at different concentrations.     

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.     

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.     

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.     

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.     

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.     

Effect of 4-chloro-2-methylphenoxyacetic acid and 2,4-dimethylphenol on human erythrocytes

The effects of exposure of human erythrocytes to different concentrations of 4-chloro-2-methylphenoxyacetic acid (MCPA) and its metabolite—2,4-dimethylphenol (2,4-DMP) were studied. The investigations concerned mainly the content of glutathione (GSH and GSSG), glutathione peroxidase (GSH-Px), glutathione transferase (GST), and the level of adenine energy charge (AEC). Reactive oxygen species (ROS) such as hydroxyl radical, superoxide anion, hydrogen peroxide, and nitric oxide are produced during normal processes in the cell. Under normal conditions, antioxidant systems of the cell minimize damage caused by ROS. When ROS generation increases to an extent that it overcomes the cellular antioxidant systems, the result is oxidative stress. We observed that MCPA and 2,4-DMP decreased the level of GSH in erythrocytes in comparison with control. MCPA did not affect glutathione peroxidase and glutathione transferase activity, while 2,4-DMP increased their activity. 2,4-DMP decreased the level of ATP and increased the content of ADP and AMP, leading to the fall of the level of AEC. MCPA and 2,4-DMP transform hemoglobin into methemoglobin, thus preventing oxygen transport. Comparison of the toxicity of MCPA and 2,4-DMP revealed that the most prominent changes occurred in human erythrocytes incubated with 2,4-DMP.     

Compost enhances plant resistance against the bacterial wilt pathogen Ralstonia solanacearum via up-regulation of ascorbate-glutathione redox cycle

The interactions between the pathogen Ralstonia solanacearum and potato Solanum tuberosum plants were studied to investigate the reactive oxygen species metabolic system and ascorbate (ASC)-glutathione (GSH) redox cycle in response to compost application. Single potato eyepieces were germinated and grown in pots containing sandy soil with or without compost at a rate of 7.5 g kg^?1 soil. Non-compost- and compost-treated plants (CTP) were inoculated with R. solanacearum 25 days after planting and then analyzed after 10 days, unless otherwise stated. The present results revealed that pathogen infection caused a remarkable decrease in plant growth related parameters and productivity and an increase in disease incidence. However, under these conditions compost had substantially improved plant growth and decreased disease incidence and bacterial population. R. solanacearum resulted in significant enhancement in the activities of NADPH oxidase, lipoxygenase, the production rate of superoxide and hydroxyl radicals, levels of hydrogen peroxide, membrane lipid peroxidation, and protein oxidation indicating the induction of oxidative stress in potato roots. However, the pathogen-mediated enhancement in indices of oxidative stress was considerably decreased by compost application, which enhanced the activities of ascorbate peroxidase (APX, EC 1.11.1.11), monodehydroascorbate reductase (MDHAR, EC 1.6.5.4), dehydroascorbate reductase (DHAR, EC 1.8.5.1) and glutathione reductase (GR, EC 1.6.4.2) in infected potato plants, implying a better ROS-scavenging activity. Data also indicated that there were general increases in ASC and GSH content in infected compost treated plants, but non-compost treated ones significantly had lower levels of such redox metabolites. In addition, significantly higher ratios of ASC/DHA (dehydroascorbate) and GSH/GSSG (glutathione disulphide) were generally found in CTP than in non-compost treated-ones. The obtained results suggest that compost provides effective protection against the Ralstonia bacterial pathogen via up-regulation of the capacity of the ASC-GSH cycle and modulation of the cellular redox status, thereby eliminating ROS damage and sustaining membrane stability.     

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.     

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.     

Exogenous Silicon Protects <Emphasis Type="Italic">Brassica napus</Emphasis> Plants from Salinity-Induced Oxidative Stress Through the Modulation of AsA-GSH Pathway,Thiol-Dependent Antioxidant Enzymes and Glyoxalase Systems

Although silicon (Si) has showed its potential role in mitigating abiotic stress-induced damages in many plant species its role in coordinated induction of antioxidant defense is yet to be elucidated. Therefore, we studied rapeseed (Brassica napus) seedlings applied with exogenous Si for changes occurring in antioxidant defense and glyoxalase systems. Seedlings (12-day-old) grown semi-hydroponically were exposed to Si (silicon dioxide, SiO₂; 1?mM) solely and in combination with NaCl (100 and 200?mM) for 48?h. Salinity created oxidative damage by increasing H₂O₂ and malondialdehyde (MDA) contents resulting in disruption of antioxidant defense system and in arousing methylglyoxal (MG) toxicity by the down-regulation of glyoxalase enzyme activities. Exogenous Si treatment showed reduction of both H₂O₂ and MDA contents and up-regulation of antioxidant components including the activities of related enzymes (APX, MDHAR, DHAR, GR, GST, GPX and CAT) and the contents of AsA and GSH. Enhanced activities of glyoxalase I (Gly I) and glyoxalase II (Gly II) detoxified the toxic MG. Thus, this study clearly indicates that Si improved plant tolerance to salinity stress through enhancement of both antioxidant defense and glyoxalase systems that led to reduced oxidative damage and MG toxicity.     

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.     

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.     

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.     

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.     

Effects of N-acetylcysteine on oxidative responses in the liver of fenthion exposed Cyprinus carpio

The aim of this study was to evaluate the effects of different N-acetylcysteine doses on the tolerance to fenthion-induced oxidative stress, alterations in glutathione metabolism and cholinesterase specific activities in the liver by using freshwater fish Cyprinus carpio (Cyprinidae) as a model organism. An acute toxicity study was carried out to determine 96-h median lethal concentration of fenthion for this species (2.16 mg/L) and 80% of this concentration was applied in toxicity studies. Four groups, each containing eight fish were constituted as follows: Control group, fenthion treated group, 0.5 or 400 mg/kg NAC-injected + fenthion-treated groups. Biochemical analyses were carried out spectrophotometrically. Fenthion treatment significantly decreased total glutathione and glutathione levels, glutathione/glutathione disulfide ratio together with glutathione reductase and γ-glutamylcysteine synthetase specific enzyme activities. The higher dose of N-acetylcysteine increased the toxic effects of fenthion and γ-glutamyl transpeptidase specific activity while decreasing glutathione S-transferase specific activity. However, injection of the lower dose provided a limited protection against fenthion toxicity. In all exposure groups, lipid peroxidation increased and total protein levels decreased, while protein depletion was prevented by low dose of N-acetylcysteine application. Acetylcholinesterase and butyrylcholinesterase activities were at similar levels in the liver of C. carpio. A dose-dependent inhibition was observed in butyrylcholinesterase activity by N-acetylcysteine application. The results showed that fenthion had a significant oxidative stress inducing potential through the reduction of glutathione redox capacity. The critical point for overcoming oxidative stress by N-acetylcysteine in fenthion toxicity was the selection of the dose; N-acetylcysteine exerted its toxic effects by means of oxidative stress in fish liver at the higher dose.     

Fate of few pesticide-metabolizing enzymes in the marine cyanobacterium Phormidium valderianum BDU 20041 in perspective with chlorpyrifos exposure

The marine cyanobacterium Phormidium valderianum BDU 20041 is able to dwell and grow in the presence of chlorpyrifos (O,O-diethyl-O-[3,5,6-trichloro-2-pyridyl] phosphorothioate), a phosphorothioate insecticide, at a concentration of 45 ppm. Chlorpyrifos exposure resulted in stunted growth of P. valderianum, and a 48-h exposure revealed increase in activity of pesticide-metabolizing enzymes, such as polyphenol oxidase, catalase, superoxide dismutase, esterase, and glutathione S-transferase. Among the three classes of esterases P. valderianum BDU 20041 was found to use esterases A in the metabolization of chlorpyrifos. Increased activity of catalase and superoxide dismutase clearly depicted the provoked state of oxidative stress, concurrently this circuitously proving the triggered mode of reactive oxygen species mediated degradation of chlorpyrifos.