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.     

Protective role of propolis against reproductive toxicity of chlorpyrifos in male rats

Chlorpyrifos (CPF) is causing different toxicity and propolis has been reported to be an effective antioxidant. Therefore, the present study is aimed to elucidate the possible protective effects of propolis in alleviating the toxicity of chlorpyrifos on reproductive performance, testosterone levels, enzyme activities and lipids profile in serum of male rats. Animals were divided into four groups; one orally administered (o.d.) CPF at a dose of 9 mg/kg b.w. for consecutive 70-days, propolis group (50 mg/kg b.w.), propolis and chlorpyrifos group and a control group. Results showed that there was a correlation between CPF administration and the significant decrease of the sperm counts, spermatozoon survival and testosterone level as well as increase of sperm aberrations. CPF increased significantly the lipid profile and the levels of various serum liver marker enzymes. In contrast, co-administration of propolis to CPF-treated rats restored almost most of these biochemical parameters to normal levels. On the other hand, CPF resulted in histopathological alterations in testes of male rats. However, pre-administration of propolis to CPF-treated animals improved the testicular damage and alleviates the toxic effects of CPF on reproductive functions in male rats.     

Chlorpyrifos-induced oxidative stress and histological changes in retinas and kidney in rats: Protective role of ascorbic acid and alpha tocopherol

This study was undertaken to evaluate the antioxidant effect of vitamins C and E against oxidative stress, apoptosis and histological changes of kidney and retina in CPF-treated rats. Forty male Sprague-Dawley rats were divided into four groups including the control group, the group treated orally with a single dose of CPF (63 mg/kg b.w.), the group injected intramuscularly (i.m.) with vitamin C (250 mg/kg b.w.), and intraperitonealy (i.p.) with vitamin E (150 mg/kg b.w.) daily for 7 days and the group treated with CPF (single dose) and injected with vitamins (for 7 days). The results showed that CPF induced apoptosis and severe oxidative stress as indicated by the significant increase in MDA and sFasL concentration and the significant decrease in GSH concentration in serum. Co-administration of vitamins C and E ameliorate these toxic effects and improved the histological pictures of kidneys and retinas. It could be concluded that combined administration of vitamins C and E is useful in the routine therapy for the protection against tissue damage induced by CPF.     

Metabolic and histological parameters of silver catfish (Rhamdia quelen) exposed to commercial formulation of 2,4-dichlorophenoxiacetic acid (2,4-D) herbicide

The objective of this study was to investigate the effects of commercial formulation of herbicide 2,4-D on metabolic parameters, acetylcholinesterase (AChE) activity and liver histological evaluation of silver catfish (Rhamdia quelen) exposed for 96 h. AChE activity increased in brain (600 and 700 mg L⁻¹) and decreased in all concentrations tested in muscle tissue. Hepatic glycogen was reduced after 2,4-D exposure ranging from 47.67% (400 mg L⁻¹) until 59.3% (700 mg L⁻¹). Hepatic tissue showed lactate reduction at all 2,4-D concentrations tested and glucose was reduced only at 700 mg L⁻¹. In the highest concentration tested hepatic glycogen and glucose reduced instead plasma glucose levels increased. White muscle tissue showed glycogen reduction in fingerlings exposed to all herbicide concentrations and glucose reduction at 700 mg L⁻¹. Muscle lactate levels increase at all 2,4-D concentrations tested. Vacuolation of hepatocytes and changes in its arrangement cords were observed by histologic analysis in group treated with 700 mg/L of 2,4-D. These results suggest that silver catfish exposed to concentrations of 2,4-D near of CL₅₀ showed metabolic and histological response to compensate some stress caused by herbicide exposure. Taken together parameters measured can be used as biomarkers to monitor herbicide contaminated water.     

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.     

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

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

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.     

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.     

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.     

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.     

Effects of the organophosphate pesticide Folidol 600® on the freshwater fish, Nile Tilapia (Oreochromis niloticus)

Nile Tilapia (Oreochromis niloticus) juveniles were exposed to different concentrations of Folidol 600® in static toxicity tests. The 24, 48, 72 and 96 h LC₅₀ values of Folidol 600® to O. niloticus were 17.82, 8.91, 4.00 and 2.70 mg L⁻¹, respectively. The values of hematological parameters increased, and inhibition of cholinesterases activity (AChE, BChE and PChE) in plasma of fish exposed to the higher concentrations of pesticide reached 94%. Furthermore, the exposure of Tilapia to Folidol 600® caused an increase of 4%, 20% and 38.4% in oxygen consumption at 0.1, 0.5 and 1.0 mg L⁻¹, respectively. However, exposure to 2.5, 5.0 and 10 mg L⁻¹ caused a decrease of 33.6%, 35.2% and 42.4% in oxygen consumption relative to the control. The ammonium excretion of fish exposed to 0.0, 0.1, 0.5, 1.0, 2.5, 5.0 and 10.0 mg Folidol 600®/L was 0.12, 0.18, 0.30, 0.33, 0.37, 0.36 and 0.33 μg/g/min, i.e., 50%, 150%, 175%, 208%, 200% and 175% increase, respectively, relative to the control.     

Neurotoxic effects of subacute exposure of dichlorvos and methyl parathion at sublethal dosages in rats

The present study was designed to understand the effects of sublethal dosages of dichlorvos (DIC) and methyl parathion (MP) on acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) in various tissues of rats exposed to 5 and 10 ppm of DIC and MP in drinking water ad libitum for 28 days continuously. According to the results, AChE activity was significantly decreased in all the tissues of rats treated with both dosages of DIC and MP except for in the lungs treated with both dosages of DIC. With regard to the BChE, MP caused a significant decrease in the liver, heart and lungs with 5 ppm dosage whereas it did not change the BChE activity in the other tissues with two dosages. Also, DIC caused a significant decrease in BChE activity in the heart tissue treated with both dosages and in the brain of rats treated with 5 ppm. The observations presented led us to conclude that the administrations of MP and DIC at sublethal concentrations inhibited AChE and BChE activities in the rats. These results suggest that inhibition of AChE may be a better biomarker for the assessment of neurotoxic effects in the living.     

Prallethrin induced serum biochemical changes in Wistar rats

The present study was designed as a repeated dose 28-day oral toxicity study in rodent. All the rats were randomly divided into five groups (C1, C2, T1, T2 and T3) each containing 10 Wistar rats (5 male and 5 female). Group C1 served as control as no treatment was administered. Group C2 was administered groundnut oil (1 ml/100 g b.wt) and served as vehicle control. Group T1 was put on high dose 153.33 mg/kg b.wt (LD50/3), while group T2 received intermediate dose of 92 mg/kg b.wt (LD50/5), and group T3 was administered low dose of 46 mg/kg b.wt (LD50/10) of Prallethrin suspended in 1 ml/100 g b.wt of groundnut oil. Blood samples were collected from all groups on the 7th, 14th, 21st and 28th day of the experiment for measurement of serum glucose, serum urea, serum triglyceride, serum cholesterol, serum aspartate aminotransferase (AST), serum alanine aminotransferase (ALT) and serum alkaline phosphatase (ALP). According to data obtained on the 7th day of the study, no statistically significant change in any of the treatment groups was observed as compared to the control group. On the 14th day of the study, in comparison to the control group, triglyceride level and ALP activity were found to be significantly increased in the group T1 female and group T1 male rats respectively. On the 21st day of the study, compared to the controls, significant increase in cholesterol and ALP levels were present in both T1 and T2 females and in addition to this total protein and triglycerides levels were also significantly increased in group T1 female rats. In group T1 male total protein, triglycerides, ALT and ALP activity was found to be increased significantly as compared to healthy control group. On the 28th day, all the recorded biochemical parameters were found to be significantly increased, except BUN and AST in group T1 female rats. In group T2 female rats, significantly increased cholesterol, ALT and ALP levels were observed. In group T3 female rats, none of the parameters were found to be significantly affected. Among male rats, only total protein level was found to be increased in groups T2 and T3. Whereas, total protein, triglyceride, ALT and ALP were significantly elevated in group T1 male rats at the end of the study. In conclusion, the results of this study demonstrate that subacute oral administration of Prallethrin; at dose levels of 1/3 LD50 and 1/5 LD50 for 28 days induces moderate toxic effects on different biochemical parameters.     

Toxico-pathological effects of cypermethrin upon male reproductive system in rabbits

The objective of this work was to identify the reproductive toxico-pathological effects of cypermethrin (CY) in mature male rabbits. Apparently healthy adult age- and weight-matched rabbits (n = 40) were procured from the local market, kept under similar management conditions and divided into four equal groups. Different doses of CY (50, 100 and 150 mg kg⁻¹ body mass) mixed in mustard oil were injected intraperitonealy at weekly intervals in male rabbits (groups B-D) prior to mating. Group A served as control and each animal in this group received equivalent volume of mustard oil. Treatment was continued for 71 days. Decreased testicular and epididymal sperm counts were recorded mostly in dose and time dependent manner in CY-treated rabbits. The serum testosterone concentrations in CY-treated rabbits were significantly lower than those of control group. Degeneration, arrested spermatogenesis and connective tissue (CT) proliferation in testes, while sperm-less seminal plasma and tailless spermatozoa in epididymis of CY-treated rabbits were observed. It was inferred that CY-induced defects in sperms and pathological alterations in testes and epididymis.     

Binding of phenthoate to bovine serum albumin and reduced inhibition on acetylcholinesterase

Organophosphorus pesticides (OPs) are of environmental significance due to their high toxicity to animals. Binding to plasma proteins may effective influence the toxicological properties of xenobiotics. In an attempt to evaluate the affinity of phenthoate (PTA) to bovine serum albumin (BSA) and inhibitory ability of bound PTA to acetylcholinesterase (AChE), we investigated the interactions between phenthoate (PTA) and bovine serum albumin (BSA) using tryptophan fluorescence quenching and subsequent inhibition on AChE activity by PTA. The results showed that PTA caused the fluorescence quenching of BSA because of the formation of a PTA-BSA complex. Quenching constants (K_sv), determined using the Sterns-Volmer equation to provide a measure of the binding affinity between PTA and BSA at 303, 306, 310 and 313 K were (3.4295 ± 0.0763) × 10⁻⁴, (3.2446 ± 0.0635) × 10⁻⁴, (3.0434 ± 0.0856) × 10⁻⁴ and (2.8262 ± 0.0569) × 10⁻⁴ M⁻¹, respectively. The thermodynamic parameters, ΔH and ΔS were −25.04 kJ mol⁻¹ and 168.94 J mol⁻¹ K⁻¹, respectively, which indicated that the electrostatic interactions played a major role in PTA-BSA association. The presence of BSA consistently reduced the inhibitory ability of PTA on AChE, with the relative activity being increased from 46.98 to 61.71% for the concentration range of BSA between 0 and 4.0 g L⁻¹.     

Toxic effects of novel organophosphorus insecticide (RPR-V) on certain biochemical parameters of euryhaline fish, Oreochromis mossambicus

The euryhaline fish, Oreochromis mossambicus was exposed to sub-lethal concentration (0.017 mg L⁻¹) of a novel phosphorothionate, 2-butenoic acid-3-(diethoxy phosphinothionyl) ethyl ester (RPR-V) for 30 days and allowed to recover for 7 days. Important biomarker enzymes were assayed in plasma, brain, gill, liver, kidney, and muscle during exposure tenures of day-3, -7, -15, -30, and also at 7 days (withdrawal) after stopping treatment. Acetylcholinesterase (AChE) activities of brain, gill, and muscle were strongly inhibited by 67, 75, and 66%, respectively, on day-30. Exposure (time) dependent increases in alanine aminotransferase (ALAT), and aspartate aminotransferase (ASAT), acid phosphatase (AcP), and alkaline phosphatase (AkP), activities in plasma and kidney; AcP and AkP activities in gill were noticed. However, significant decrease in ALAT, ASAT, AcP, and AkP activities in liver was observed. The depletion of glycogen was observed in liver, brain, and gill tissues, an indication of typical stress related response of the fish with pesticide. A significant increase in lactate dehydrogenase (LDH) activity in gill and brain was observed and decreased in liver and muscle, indicating tissue damage and muscular harm. Depletion of glutathione (GSH) was observed in the above tissues, there by enhancing the lipid peroxidation resulting in cell damage. The induction in hepatic glutathione-S-transferase (GST) levels indicates the protection against the toxicity of xenobiotic-induced lipid peroxidation. There was a significant recovery in all the above biochemical parameters, in all the tissues of fish after a recovery period of 7 days. These results revealed that RPR-V affects the intermediary metabolism of O. mossambicus and the increase of biomarker enzymes in plasma, might be due to the necrosis of liver.     

Influences of sub-acute exposure to paraquat on cytochrome P450 3A2 expression in rat liver and lungs

This study was designed to investigate the possible effects of paraquat sub-acute poisoning on cytochrome P450 3A2 expression in the liver and lungs. Twenty adult male rats (150-200 g) were exposed either against saline normal as control group or various doses of paraquat (3.5, 7 and 10 mg/kg, s.c.) as test groups for 7 consecutive days. Paraquat-exposed animals showed loss of body weight and elevation in serum levels of alkaline phosphates and alanine aminotransferase in a dose-dependent fashion. Moreover, animals in the test groups demonstrated a significant (P < 0.05) increase of malondialdehyde content in both the liver and lung tissues. Ultimately, by using RT-PCR method it became clear that 7 days exposure to paraquat resulted in a total suppression of cytochrome P450 3A2 at the mRNA level in the lungs. By contrast, a considerable up regulation of the same gene occurred in the liver. This data suggest that paraquat not only affect the lungs as a main target tissue but also up regulates the predominant cytochrome P450 gene in the liver which may induce detoxification processes.     

Oxidative parameters of Rhamdia quelen in response to commercial herbicide containing clomazone and recovery pattern

In this study, fish Rhamdia quelen, were exposed to different concentrations of herbicide clomazone: 0.0 (control), 0.45 and 0.91 mg L⁻¹. After exposure for 8 days to herbicide, fish were transferred to clean water for a recovery period (8 days). Oxidative stress indicators such as thiobarbituric acid reactive substances (TBARS) levels and protein carbonyl content, as well as antioxidant defenses, such as catalase (CAT), superoxide dismutase (SOD), glutathione S-transferase (GST), ascorbic acid and non-protein thiols levels were studied, using the liver, brain and muscle tissues. Herbicide exposure increased TBARS in muscle and in liver at higher concentration. In liver protein carbonylation increased and catalase activity did not change in fish exposed to herbicide. SOD enhanced in liver at concentration of 0.91 mg L⁻¹. GST, ascorbic acid and non-protein thiols levels increase at both concentrations. At the end of the recovery period the most of the parameters recovered whereas GST and ascorbic acid remain elevated. The present study demonstrates the occurrence of disorders in antioxidant parameters and importance in the assessment of the potential risk of herbicides as clomazone on fish species.     

Improvement by Satureja khuzestanica essential oil of malathion-induced red blood cells acetylcholinesterase inhibition and altered hepatic mitochondrial glycogen phosphorylase and phosphoenolpyruvate carboxykinase activities

The aim of this study was to examine whether Satureja khuzestanica (Lamiaceae) essential oil (SKEO) might have protective effects on toxicity of malathion, a commonly used organophosphorus (OP), by measuring the activities of hepatic cells mitochondrial glycogen phosphorylase (GP) and phosphoenolpyruvate carboxykinase (PEPCK) activities and blood levels of glucose and acetylcholinesterase (AChE) in rats. Malathion (20 mg/kg/day) and SKEO (225 mg/kg/day) were administered alone or in combination by intragastric intubation for 28 days. Treatment by malathion increased blood glucose as measured at days 18 and 28 of treatment. Malathion inhibited erythrocyte AChE and increased hepatic cells GP and PEPCK activities. Coadministration SKEO resulted in restoration of malathion-induced changes in hepatic cells GP and PEPCK activities and levels of blood AChE and glucose. It is concluded that SKEO interferes with malathion-induced stimulation of hepatic cells glycogenolysis and gluconeogenesis through its antioxidant potential and increasing AChE activity.     

Effect of terbutryn at environmental concentrations on early life stages of common carp (Cyprinus carpio L.)

The aim of this study was to assess the toxicity of terbutryn to early developmental stages of common carp (Cyprinus carpio). Based on accumulated mortality in the experimental groups, lethal concentrations of terbutryn were estimated at 36 day LC50 = 3.06 mg l⁻¹ terbutryn. Based on inhibition of growth in the experimental groups, lowest observed-effect concentration (LOEC) = 0.005 mg l⁻¹ terbutryn; and no observed-effect concentration (NOEC) = 0.0007 mg l⁻¹ terbutryn. Fulton’s condition factors were significantly lower in fish exposed to 2 mg l⁻¹ compared with controls. By day 30, fish exposed to 0.00002 mg l⁻¹ - real environmental concentration in Czech rivers - 0.02, 0.2, and 2 mg l⁻¹ terbutryn showed significantly lower mass and total length compared with controls. No significant negative effects on hatching or embryo viability were demonstrated at the concentrations tested, but significant differences in early ontogeny among groups were noted. Fish from the two highest tested concentrations (0.2 and 2 mg l⁻¹) showed a dose-related delay in development compared with the controls. At concentrations of 0.02, 0.2, and 2 mg l⁻¹ damage to caudal kidney tubules when compared to control fish was found.