The effects of Saw palmetto on flumethrin-induced lipid peroxidation in rats

In the present study, 40 male Wistar albino rats were used and divided into 4 groups. The first group served as the control group; the second group was administered Saw palmetto extract at the dose of 20 mg/kg/bw; the third group was administered flumethrin at the dose of 15 mg/kg/bw; and the fourth group was administered a combination of 20 mg/kg/bw Saw palmetto extract and 15 mg/kg/bw flumethrin, for 21 days, orally. After the trial period, blood and tissue (liver, kidney and brain) samples were taken from the rats. Saw palmetto extract did not cause significant alterations in plasma and tissue malondialdehyde (MDA) levels, serum and tissue nitric oxide (NO) levels, erythrocyte and tissue superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities when compared to the controls (p > 0.05). Flumethrin led to increased plasma and tissue MDA levels, serum and tissue NO levels, tissue GSH-Px activities and decreased erythrocyte and tissue SOD and CAT activities, and erythrocyte GSH-Px activity, compared to the controls (p < 0.05). The flumethrin and Saw palmetto extract combination increased erythrocyte SOD activity and decreased brain GSH-Px activity as compared to flumethrin (p < 0.05). In conclusion, it was determined that Saw palmetto extract did not cause any negative effect on the prooxidant-antioxidant balance. While flumethrin stimulated lipid peroxidation; Saw palmetto extract at the dose of 20 mg/kg/bw did not exhibit enough antioxidant effect in rats.     

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

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

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.     

Comparative effects of lindane and deltamethrin on mortality, growth, and cellulase activity in earthworms (Eisenia fetida)

Laboratory tests were conducted to compare the effects of various concentrations of lindane and deltamethrin on mature earthworms (Eisenia fetida) cultured in artificial soil during typical acute (14d) and subchronic (42d) exposure periods. The effects of the two pesticides on earthworm mortality, growth inhibition, and cellulase activity were determined for different exposure durations. The toxicity order for earthworm mortality from the 14-day exposure was lindane > deltamethrin, with median lethal concentrations (LC₅₀) of 162.1 and 432.9 mg kg⁻¹, respectively. Earthworms exposed to deltamethrin showed dose-dependent toxic effects on growth and cellulase activity only from the acute exposures, whereas lindane’s effects on these activities were seen correlated with both the acute and subchronic doses. Also, changes in biomass and cellulase activity during the subchronic exposure period appear to be a more sensitive parameter than the LC₅₀ value in assessing pesticidal injury.     

Effects of dichlorvos on lipid peroxidation in mice on subacute and subchronic periods

In this study, the effects of dichlorvos to lipid peroxidation were investigated at subacute and subchronic periods. Dichlorvos was given with drinking water to Swiss Albino male mice in three dosage levels as 10, 20, and 40 mg/kg b.w. Lipid peroxidation was evaluated by determining the malondialdehyde (MDA) levels in plasma, determining the superoxide dismutase and catalase activities in erythrocytes. The analysis of these enzymes was done in blood samples collected from mice on the days 15 and 45. The results showed that MDA levels increased in dichlorvos treated groups. Actually MDA levels in control and dichlorvos treated groups were determined (as nmol/ml) 10.49, 13.83, 14.30, and 14.50, respectively, at subacute period; 7.77, 8.15, 10.88, and 12.33, respectively, at subchronic period. Catalase activity in erythrocytes decreased at subacute and subchronic periods in dichlorvos treated groups. At subacute period CAT activities were determined (as k/mg Hb) in control and dichlorvos treated groups, 563.45, 532.11, 524.76, and 497.08, respectively; 660.53, 588.84, 525.85, and 512.01, respectively, at subchronic period. When subacute and subchronic periods were compared with each other; it was shown that SOD and CAT activities increased at subchronic period.     

In vitro and in vivo effects of some pesticides on carbonic anhydrase enzyme from rainbow trout (Oncorhynchus mykiss) gills

Here we investigated the in vitro and in vivo effects of the pesticides, deltamethrin, diazinon, propoxur and cypermethrin, on the activity of rainbow trout (rt) gill carbonic anhydrase (CA). The enzyme was purified from rainbow trout gills using Sepharose 4B-aniline-sulfanilamide affinity chromatography method. The overall purification was approx. 214-fold. SDS-polyacrylamide gel electrophoresis showed a single band corresponding to a molecular weight of approx. 29 kDa. The four pesticides dose-dependently inhibited in vitro CA activity. IC₅₀ values for deltamethrin, diazinon, propoxur and cypermethrin were 0.137, 0.267, 0.420 and 0.460 μM, respectively. In vitro results showed that pesticides inhibit rtCA activity with rank order of deltamethrin > diazinon > propoxur > cypermethrin. Besides, in vivo studies of deltamethrin were performed on CA activity of rainbow trout gill. rtCA was significantly inhibited at three concentrations (0.25, 1.0 and 2.5 μg/L) at 24 and 48 h.     

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 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.     

Efficacy of insecticides against the Rice Stem-borer,Chilo suppressalis (Walker) (Lepidoptera: Crambidae), and use of sex pheromones to time accurately the yearly application

Larvae of the Rice Stem-borer, Chilo suppressalis (Walker), cause extensive crop losses worldwide. Since pesticide application is the major management tactic in China, judicious timing of a minimal dose of insecticides is important in developing an IPM program for that pest. Pheromone trap captures of male moths were used to time the single insecticide application in two seasons (2010 and 2011). In 2010, six pesticides – deltamethrin, cygon, chlorpyrifos, cartap, fipronil, and esfenvalerate – gave >90% control of stem-borers, and reduced damage to less than 5.0%. In 2011, control exceeding 90% and a damage level of <5.0% and was achieved with 0.35 kg/ha deltamethrin and chlorpyrifos. Cygon, at either 0.30 or 0.35 kg/ha, provided control exceeding 90% and a damage level of <4.0%. With the proviso that the impact of insecticides on biological control agents remains to be investigated, these three insecticides are recommended for use by Chinese rice farmers.     

Chimeric mice with humanized liver as a model for testing organophosphate and carbamate pesticide exposure

BACKGROUND

Diagnosis of acute intoxication with organophosphate (OP) or carbamate (CM) pesticides in humans is achieved by measuring plasma butyrylcholinesterase (BuChE) activity. However, BuChE activity is not an ideal biomarker in experimental animal models. The aim of this study was to establish an experimental mouse model for evaluating exposure to OP and CM pesticides by monitoring BuChE activity using chimeric mice in which the liver was reconstituted with human hepatocytes.

RESULTS

A single oral administration of acephate (300 mg/kg), chlorpyrifos (10 mg/kg), fenobucarb (300 mg/kg) or molinate (250 mg/kg) in chimeric mice led to inhibition of >95%, > 95%, 28% and 60% of plasma BuChE activity after 7, 0.5, 0.5 and 7 h, respectively. Dose‐dependent decreases in plasma BuChE activity were also observed for acephate and chlorpyrifos. A 5‐day repeated‐dose study with 10 or 30 mg/kg acephate found a constitutive reduction in plasma BuChE activity to 80% and 70% of pre‐dose levels, respectively.

CONCLUSION

Changes in plasma BuChE activity in chimeric mice with humanized liver clearly reflected the exposure levels of OP and CM pesticides. These results suggest that the humanized‐liver mouse model may be suitable for estimating levels of exposure to these pesticides in humans. © 2017 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.     

Protection by cAMP and cGMP phosphodiesterase inhibitors of diazinon-induced hyperglycemia and oxidative/nitrosative stress in rat Langerhans islets cells: Molecular evidence for involvement of non-cholinergic mechanisms

The objective of this study was to study the effects of acute administration of diazinon alone or in combination with two phosphodiesterase (PDE) inhibitors with selectivity to cAMP and cGMP (theophylline and sildenafil, respectively) on oxidative/nitrosative stress biomarkers, including nitric oxide (NO), lipid peroxides (TBARS), total antioxidant power (TAP), and concentration of tumor necrosis factor (TNF-α) in isolated Langerhans islets, plasma glucose and insulin levels, and the activity of plasma cholinesterase (ChE). Examination by different doses of diazinon (15, 30, and 60 mg/kg) in single administration lead us to choose diazinon (30 mg/kg) in combination therapies. Theophylline and sildenafil were used at doses of 25 and 5 mg/kg, respectively. In all diazinon-treated groups, plasma ChE activity and plasma insulin level were significantly decreased and plasma glucose concentration and Langerhans islets TNF-α, TBARS, and NO levels were significantly increased in comparison to controls. The TAP did not change in comparison to control. In combination therapy, both theophylline and sildenafil restored diazinon-induced changes in plasma glucose concentration, Langerhans islets TNF-α, NO, and TBARS concentrations but Langerhans islets TAP, plasma insulin, and ChE levels. It is concluded that diazinon stimulates oxidative/nitrosative stress in Langerhans islets that results in hyperglycemia due to insufficiency of insulin. Altered glucagons/insulin ratio, activated hepatic glucose production/release, and insulin resistance are possible mechanisms. The protective effects of cAMP and cGMP PDE inhibitors in restoration of diazinon-induced oxidative/nitrosative stress and hyperglycemia stress back to their antioxidant potentials that seem to be independent of ChE inhibition.     

七种新烟碱类杀虫剂对韭菜迟眼蕈蚊幼虫及蚯蚓的选择毒力

为筛选出高效安全的韭蛆防治药剂,室内采用胃毒触杀联合毒力法比较了吡虫啉、啶虫脒、噻虫嗪、噻虫胺、呋虫胺、烯啶虫胺、噻虫啉与毒死蜱和高效氯氟氰菊酯等6种对照药剂对韭菜迟眼蕈蚊幼虫的毒力,同时用人工土壤法测定了13种药剂对蚯蚓的急性毒性,并通过盆栽试验验证了其对韭蛆和蚯蚓的选择毒力。结果表明,吡虫啉、噻虫胺、呋虫胺、噻虫啉、噻虫嗪对韭菜迟眼蕈蚊4龄幼虫的毒力明显高于6种对照药剂,对虫酰肼的相对毒力倍数分别为101.6、55.0、32.9、27.2、13.6;13种供试药剂中,除吡虫啉、啶虫脒、噻虫胺、呋虫胺对蚯蚓中等毒性外,其余均为低毒;盆栽试验中,吡虫啉、噻虫嗪、毒死蜱、噻唑膦、高效氯氟氰菊酯的防虫效果和保苗效果均分别高于其它药剂,但其中只有噻虫嗪对蚯蚓没有明显致死作用。     

Effects of diazinon on the activity and gene expression of mitochondrial glutamate dehydrogenase from rat pancreatic Langerhans islets

The main propose of the present study was to determine the effects of diazinon on the activity and gene expression of glutamate dehydrogenase (GDH) as the key enzyme of Langerhans islet for secretion of insulin. Diazinon was administered intraperitoneally at doses of 15, 30, and 60 mg/kg. Langerhans islets were isolated from the pancreas of rats by a standard collagenase digestion, separation by centrifugation, and hand-picking technique. The activity and gene expression of the mitochondrial GDH was determined in the islets homogenates. Glutamate, C-peptide, and insulin were determined in plasma.Diazinon at all tested doses (15, 30, and 60 mg/kg) significantly (p < 0.01) decreased plasma insulin after 1 h while the values did not differ from control when examined after 18 h. Diazinon at all tested doses (15, 30, and 60 mg/kg) significantly (p < 0.01) increased concentration of C-peptide both 1 and 18 h post-administration. Diazinon at all tested doses (15, 30, and 60 mg/kg) significantly (p < 0.05) increased production of glutamate while the values did not differ from control when tested after 18 h. Administration of diazinon at doses of 30 and 60 mg/kg significantly (p < 0.001) increased activity of GDH after 1 h while all doses of diazinon increased GDH activity when measured after 18 h. Diazinon at dose of 60 mg/kg significantly (p < 0.01) decreased expression of GDH gene 18 h post-administration.It is concluded that GDH is a component of diazinon-induced changes in release of improper insulin.     

Dimethoate induced biochemical perturbations in rat pancreas and its attenuation by cashew nut skin extract

The significant antiradical activity of cashew skin extract was previously described. In this investigation, the extent of protection offered by cashew nut skin extract (CSE) against the damage induced in rat pancreas by sub chronic doses dimethoate (DM), an organophosphorous pesticide was studied. Rats were supplemented with CSE at 20 mg/kg b.w./d after a daily dose of DM at 40 mg/kg/d b.w. for 2 months. Weekly random blood glucose, oral glucose tolerance test (OGTT); pancreatic damage markers like amylase and lipase; oxidative damage markers such as reactive oxygen species generated, extent of lipid peroxidation, host antioxidant defenses like reduced glutathione (GSH); GSH-dependent enzyme activities viz., glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR); free radical scavenger enzymes viz., catalase and superoxide dismutase (SOD); xenobiotic metabolizing enzymes like DT-diaphorase and NADPH-diaphorase were measured in the four different groups namely (1) control, (2) DM treated, (3) CSE supplemented, (4) CSE supplements following DM treatment. Random blood glucose levels increased significantly on exposure to DM compared to that in control rats (119 ± 5 mg/dl vs. 92 ± 4 mg/dl), while the blood glucose levels in CSE supplemented rats were comparable to that of controls. DM treated rats exhibited impaired glucose tolerance at the end of two months as indicated by OGTT, while DM treated rats with CSE supplements showed normal glucose tolerance. Pancreatic specific marker enzymes like amylase and lipase in serum were restored to normalcy in rats supplemented with CSE following treatment with DM which otherwise was increased in the DM treated rats. Distinctly lower levels of GSH, increased levels of ROS, higher extent of lipid peroxidation, along with alterations in antioxidant enzymes and increase in xenobiotic metabolizing enzymes were evident in pancreas of DM treated rats. However, CSE supplement ameliorated the biochemical alterations in the pancreatic milieu in DM treated rats. Treatment with CSE significantly protected rat pancreas from injury, thus ameliorating and restoring tissue antioxidant status and also conferring normal glucose tolerance. The active components present in cashew skin extract can perhaps be effective in reducing the extent of pancreatic injury and in overcoming tissue damage caused by exposure to dimethoate.     

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 diazinon at different doses on rat liver and pancreas tissues

Diazinon is one of the most widely used organophosphates in agriculture. Toxic effects of diazinon are due to the inhibition of acetylcholinesterase, an enzyme needed for proper nervous system function. This study was designed to investigate the effects of diazinon at different doses on pancreas and liver tissues and in which dose level diazinon shows its effects. Sixty male Wistar albino rats were included in this study. Animals were initially divided into control and diazinon given groups. There were 10 animals in the control group and 50 animals in diazinon administered group. The latter was divided into five equal subgroups: 25, 50, 100, 200 and 300 mg/kg of diazinon administered groups. Control group was given only saline. All animals in 300 mg/kg diazinon group died. After 24 h, rats were sacrificed under ether anesthesia. Tissue and blood samples were taken for biochemical and histopathological analysis. Sample tissues were examined under light microscope. In biochemical analysis, AST, ALT, LDH, amylase and lipase enzyme activities were measured. One-way ANOVA test was used to compare the groups. In 200 mg/kg diazinon given group, it has been observed some histopathological changes in pancreas and liver tissues. Cholinesterase activities were significantly decreased and alkaline phosphatase levels were increased in all diazinon given groups, when compared with the controls. There was statistically significant difference between the control and diazinon given groups by means of serum amylase, lipase, ALT and AST activities (p < 0.05). LDH activities were significantly increased in 100 and 200 mg diazinon given groups, when compared with the controls (p < 0.05). Histopathological changes were observed only in 200 mg diazinon given group. This evidence suggest that diazinon effect is dose dependent and this is possibly 10-15% of the LD₅₀ dose (200 mg/kg), which cause acute pancreatitis and histopathological changes in liver.     

Protective effects of caffeic acid phenethyl ester on rotenone-induced myocardial oxidative injury

Rotenone, an insecticide, causes toxicity through inhibition of mitochondrial electron transport chain at complex I and oxidative injury to the tissues. The aim of the present study was to determine in vivo effects of rotenone on myocardium and cardio-protective effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, against rotenone toxicity in rats. The rats were divided into three groups: untreated control, rotenone (2.5 mg/kg/day for 60 days, i.p.) and rotenone + CAPE groups. CAPE was administrated i.p. 10 μmol/kg/day for 62 days started two days before first dose rotenone injection. The malondialdehyde, nitric oxide levels and xanthine oxidase activity of rotenone group was significantly higher than control and rotenone + CAPE groups (p < 0.05). However, catalase activity in the rotenone group was decreased in comparison with the other groups (p < 0.05). The superoxide dismutase activity of rotenone group was insignificantly decreased compared to the others. In conclusion, rotenone caused lipid peroxidation in myocardial tissue and CAPE treatment prevented this rotenone-induced lipid peroxidation in rats. CAPE might be a cardio-protective agent against myocardial toxicities.     

Anti-oxidative and immuno-hematological status of Tilapia (Oreochromis mossambicus) during acute toxicity test of endosulfan

Endosulfan is an organochlorine pesticide widely used in agriculture and hence finds its way into natural water bodies, thus affecting aquatic life. The purpose of this study was to determine LC₅₀ of endosulfan (99%; α:β ratio of 7:3) in Tilapia, Oreochromis mossambicus and study its effect on anti-oxidative enzymes (superoxide dismutase, glutathione-S-transferase and catalase), immuno-hematological profile (RBC, WBC, Hb, serum protein, albumin-A, globulin-G, A/G ratio, phygocytic activity as indicated by nitroblue tetrazolium reduction, serum cortisol and serum lipid peroxidation) and neurotransmitter acetylcholine esterase enzyme activity. The LC₅₀ value at 96 h and 95% confidence limit for tilapia (46.78 g) was estimated as 3.6 μg/L. Activities of anti-oxidative enzymes, immuno-hematological profile, blood glucose and neurotransmitter activity was significantly influenced (P < 0.01) in dose dependent manner. This was reflected in the behavior of fish that was altered from normal during acute toxicity.     

Changes in renal clearance and renal tubular function in albino mice under the influence of Dichlorvos

It is known that organophosphate pesticides and their metabolites are generally eliminated through urine and are likely to affect nephrons. Despite the widespread application of Dichlorvos only limited studies appear to have been done on its toxicity to kidney. Intraperitoneal administration of 400 μg/kg Dichlorvos in mice exhibited maximum reduction in total protein concentration of kidney after exposure to 120 h (52-fold decrease, t-test, P < 0.001). Variations in renal clearance and percent reabsorption of acid phosphatase, alkaline phosphatase and nonspecific esterase enzymes were significant at P < 0.01 and at P < 0.001 (2-way ANOVA), respectively. Maximum significant increase in renal contents of Na⁺ and Ca⁺⁺ was induced by 200 μg/kg dose after 120 and 240 h exposure (P < 0.001), while significantly highest retention of K⁺ and Cl⁻ ions was caused by 400 μg/kg dose after 24 and 72 h exposure (P < 0.01). Histopathological changes in glomeruli, PCTs, DCTs and CTs along with altered renal tubular function and renal clearance of enzymes and various ions indicate the development of acute renal disturbances under the influence of Dichlorvos.     

Acute, subacute and subchronic administration of methyl parathion-induced testicular damage in male rats and protective role of vitamins C and E

Methyl parathion is an organophosphate insecticide that has been used in agriculture and domestic for several years. Vitamin C (200 mg/kg bw per day) + vitamin E (200 mg/kg bw per day), methyl parathion (0.28 mg/kg bw per day) and vitamin C (200 mg/kg bw per day) + vitamin E (200 mg/kg bw per day) + methyl parathion (0.28 mg/kg bw per day) combination were given to rats orally via gavage for 7 weeks. Body and testis weights, sperm counts, sperm motility, sperm morphology and histopathological changes in the testes were investigated at the end of 24 h, 4th and 7th weeks comparatively with control group. No pathological changes were observed in all parameters at the end of 24 h. When methyl parathion-treated group and vitamins C and E + methyl parathion-treated group were compared to control group, body and testis weights decreased significantly at the end of 4th and 7th weeks. It was observed that, at the end of 4th and 7th weeks there was a statistically significant decrease in sperm counts and sperm motility, increase in abnormal sperm morphology when methyl parathion- and vitamins C and E + methyl parathion-treated group were compared to control group. While sperm counts increased at the end of 4th and 7th weeks, sperm motility increased at the end of 7th week when vitamins C and E + methyl parathion-treated group compared with methyl parathion-treated group, no changes were observed in abnormal sperm morphology at the end of 4th and 7th weeks. In our light microscopic investigations, after 4 and 7 weeks of methyl parathion exposure, necrosis and edema were observed in the seminiferous tubules and interstitial tissues. After 4 and 7 weeks of vitamins C and E + methyl parathion exposure, degenerative changes were detected in the seminiferous tubules while no pathological findings were observed in the interstitial tissues. According to the present study, we conclude that vitamins C and E reduces methyl parathion testicular toxicity, but it does not protect completely.