Ameliorative Effects of Honey, Propolis, Pollen, and Royal Jelly Mixture against Chronic Toxicity of Sumithion Insecticide in White Albino Rats.

Sumithion (Fenitrothion) (SUM) is an organophosphorus insecticide used to combat a wide variety of plant pests. Exposure to SUM causes significant toxicity to the brain, liver, kidney, and reproductive organs through, for example, binding to DNA, and it induces DNA damage, which ends with oxidative stress. Therefore, the present study aimed to examine the protective role of bee products: a mixture of honey, propolis, palm pollen, and royal jelly (HPPJ) against SUM-induced toxicity. Twenty-four male albino rats (Rattus norvegicus) were classified into four groups, each containing six rats: control (corn oil), SUM (85 mg/kg; 1/20 LD50), HPPJ, and SUM + HPPJ once daily for 28 consecutive days. Blood samples were gently collected in sterilized ethylenediaminetetraacetic acid (EDTA) tubes for blood picture analyses and tubes without anticoagulant for serum isolation. Serum was used for assays of enzymatic and biochemical characteristics. The results revealed that SUM increased the weights of the liver, kidney, and brain as well as the enzymatic activity of glutathione peroxidase (GP), serum superoxide dismutase (SOD), and glutathione-S-transferase (GST). Additionally, SUM significantly increased the activity of lactate dehydrogenase (LDH), alkaline phosphatase (ALP), and γ-glutamyltransferase (γ-GT) and glucose, uric acid, and creatinine contents, while decreasing the acetylcholine esterase (AChE) activity and total lipids and total protein content. Furthermore, because of the inclusion of phenolic, flavonoids, terpenoids, and sugars, the HPPJ mixture counteracted the hematological, renal, and hepatic toxicity of SUM exposure.

Amelioration of fenitrothion induced oxidative DNA damage and inactivation of caspase-3 in the brain and spleen tissues of male rats by N-acetylcysteine.

N-acetylcysteine (NAC) has largely been used as an effective chemo- protective agent owing to their beneficial effect in restoring several physiological parameters and relieving oxidative stress. Interestingly, it has been suggested that NAC mechanisms of action extend beyond being a precursor to the antioxidant glutathione and that they may involve several neurotropic and inflammatory pathways. Exposure to fenitrothion, an organophosphorus insecticide, promotes oxidative stress and induces several deleterious changes in the immune response and various tissues including cerebrum and spleen. The main objective of our study was to investigate ameliorative efficacy of N-acetylcysteine for immunological and neurological alterations and oxidative DNA damage induced by fenitrothion toxicity in cerebrum and spleen tissues of male rats. Our results revealed that oral exposure to fenitrothion for 30 days caused a reduction in the erythrocyte count in addition to leukocytosis, lymphocytosis, and neutrophilia. Also, this route of administration increased the serum levels of LDH, TNF-α, and IL-2 with reduction in serum immunoglobulins (IgG & IgM) concentrations. Furthermore, a significant downregulation in the antioxidant markers (GSH & SOD) with an elevation of free radical (MDA) levels were noticed. Regarding the brain, fenitrothion administration inhibited AchE activity and increased brain GABA, serotonin and dopamine levels. Moreover, it induced an elevation in oxidative DNA damage indicated by 8-hydroxy 2-deoxyguanosine (8OH2dG) and mRNA expression of pro-apoptotic genes, including Bax, and p53, but Bcl-2 expression was reduced. N-acetylcysteine co-treatment restored the normal physiological tone in most of these parameters. Immunostaining for GFAP and Caspase-3 markers in the brain and spleen tissues were increased respectively. In conclusion, N-acetylcysteine supplementation has an ameliorative effect against immunotoxic, neurotoxic and oxidative DNA damage induced by fenitrothion exposure.

The ameliorating effects of selenium and vitamin C against fenitrothion-induced blood toxicity in Wistar rats.

Fenitrothion is widely used organophosphate pesticide in agriculture and health programs, but besides, it causes several toxic effects. The present study was designed to evaluate the possible protective effects of selenium (0.5mg/kg b.w.) and vitamin C (100mg/kg b.w) on altered haematological, biochemical and oxidative stress parameters in the blood of rats orally treated with fenitrothion (20mg/kg b.w) for 30days. Fenitrothion caused changes in body weight, food and water intake, and some haematological and biochemical parameters. Fenitrothion altered the glutathione redox status (GSH and GSSG) and decreased activity of antioxidant enzymes (GSH-Px, GST, SOD and CAT), leading to a lipid peroxidation. Selenium and vitamin C, by improving the activity of antioxidants, reduced oxidative stress and a lipid peroxidation, maintaining the values of examined parameters to optimal levels. Therefore, selenium and vitamin C could be useful in providing protection of exposed non-target organisms including people from fenitrothion.

EFFICACY OF THREE INSECTICIDES ON RAT FLEA (XENOPSYLLA CHEOPIS) INFESTING RODENTS IN GIZA GOVERNORATE, EGYPT.

The extensive use of insecticides in public health and agriculture sectors is the main reason for development of resistance in fleas associated in domestic rodents. The present work was planned to investigate the insecticidal efficacy of Lambda-cyhalothrin, Chlorpyrifos and Fenitrothion against rat flea (Xenopsylla cheopis) infesting rodent species in Giza Governorate, Egypt. The lethal concentration Lc50 and Lc90 of population percent were obtained from the established regression log concentrate-response lines. Data indicated that the values of lethal concentration (Lc50) were 0.293, 1.725 & 2.328% for Lambda-cyhalothrin, chlorpyrifos and Fenitrothion, respectively. The values of lethal concentration (Lc90) were 0.467, 2.839 & 5.197% for Lambda-cyhalothrin, chlorpyrifos and Fenitrothion, respectively.

Evaluation of urinary corticosterone as a biomarker of stress in rats using fenitrothion as a chemical stressor.

Regulatory guidelines for pharmaceutical toxicity studies recommend using one dose near the maximum tolerated. At that level significant toxicities may occur, leading to systemic stress and secondary immune suppression which can be difficult to differentiate from a primary drug effect. Therefore, there is a need for a biomarker of stress applicable to toxicity studies. This study evaluated urinary corticosterone as a biomarker, using as a pharmacologic stressor fenitrothion, which was previously shown not to cause primary immune suppression. Rats were administered fenitrothion orally at 20 and 30 mg/kg daily for 2 or 8 days, with matched vehicle controls (n = 6/group). Urine was collected for 6 and 24 h, before treatment and on Day 2 and Day 8. Urine was assayed for corticosterone, separately for the first 6 h of collection and for the whole 24 h sample. Animals were euthanized on Day 3 or Day 9 and lymphoid tissue samples were collected, weighed and examined histologically. Treated rats showed neurologic signs following treatment. Findings also included time- and dose-dependent decreases in body weight and spleen and thymus weight decreases supra-proportional to body weight on Day 9. Histologic changes were mild at a dose of 20 mg/kg, but significant at 30 mg/kg, consisting of lymphocytolysis at Day 3 and lymphoid depletion at Day 9. Urine corticosterone levels were increased on Day 2 and Day 8, in the 6-h samples, but not the 24-h ones, at both dose levels. Based on the results, urine corticosterone appears to be a sensitive biomarker of systemic stress caused by fenitrothion. Other chemical stressors should be evaluated in a similar manner in order to fully validate urine corticosterone measurement as a stress biomarker.

Fenitrothion alters sperm characteristics in rats: ameliorating effects of palm oil tocotrienol-rich fraction.

Exposure to organophosphate insecticides such as fenitrothion (FNT) in agriculture and public health has been reported to affect sperm quality. Antioxidants may have a potential to reduce spermatotoxic effects induced by organophosphate. The present study was carried out to evaluate the effects of palm oil tocotrienol-rich fraction (TRF) in reducing the detrimental effects occurring in spermatozoa of FNT-treated rats. Adult male Sprague-Dawley rats were divided into four equal groups: a control group and groups of rats treated orally with palm oil TRF (200 mg/kg), FNT (20 mg/kg) and palm oil TRF (200 mg/kg) combined with FNT (20 mg/kg). The sperm characteristics, DNA damage, superoxide dismutase (SOD) activity, and levels of reduced glutathione (GSH), malondialdehyde (MDA), and protein carbonyl (PC) were evaluated. Supplementation with TRF attenuated the detrimental effects of FNT by significantly increasing the sperm counts, motility, and viability and decreased the abnormal sperm morphology. The SOD activity and GSH level were significantly increased, whereas the MDA and PC levels were significantly decreased in the TRF+FNT group compared with the rats receiving FNT alone. TRF significantly decreased the DNA damage in the sperm of FNT-treated rats. A significant correlation between abnormal sperm morphology and DNA damage was found in all groups. TRF showed the potential to reduce the detrimental effects occurring in spermatozoa of FNT-treated rats.

Pesticide-contaminated feeds in integrated grass carp aquaculture: toxicology and bioaccumulation.

Effects of dissolved pesticides on fish are widely described, but little is known about effects of pesticide-contaminated feeds taken up orally by fish. In integrated farms, pesticides used on crops may affect grass carp that feed on plants from these fields. In northern Vietnam, grass carp suffer seasonal mass mortalities which may be caused by pesticide-contaminated plants. To test effects of pesticide-contaminated feeds on health and bioaccumulation in grass carp, a net-cage trial was conducted with 5 differently contaminated grasses. Grass was spiked with 2 levels of trichlorfon/fenitrothion and fenobucarb. Unspiked grass was used as a control. Fish were fed at a daily rate of 20% of body mass for 10 d. The concentrations of fenitrothion and fenobucarb in pond water increased over time. Effects on fish mortality were not found. Fenobucarb in feed showed the strongest effects on fish by lowering feed uptake, deforming the liver, increasing blood glucose and reducing cholinesterase activity in blood serum, depending on feed uptake. Fenobucarb showed increased levels in flesh in all treatments, suggesting bio-concentration. Trichlorfon and fenitrothion did not significantly affect feed uptake but showed concentration-dependent reduction of cholinesterase activity and liver changes. Fenitrothion showed bioaccumulation in flesh which was dependant on feed uptake, whereas trichlorfon was only detected in very low concentrations in all treatments. Pesticide levels were all detected below the maximum residue levels in food. The pesticide-contaminated feeds tested did not cause mortality in grass carp but were associated with negative physiological responses and may increase susceptibility to diseases.

Alteration of carbohydrates metabolism and midgut glucose absorption in Gromphadorhina portentosa after subchronic exposure to imidacloprid and fenitrothion.

This study was undertaken to test the hypothesis that following exposure to insecticides, changes take place in the metabolism of carbohydrates and absorption in the midgut of insects. The Madagascar hissing cockroach (Gromphadorhina portentosa) was chosen for the experiment as a model organism, due to it being easy to breed and its relatively large alimentary tract, which was important when preparing the microperfusion midgut bioassay. In each group of cockroaches treated with imidacloprid and fenitrothion, absorption of glucose, expressed as the area under the curve (AUC), was elevated compared to the control group. Glucose in the hemolymph of the examined insects was present in a vestigial amount, often below the threshold of determination, so the determinable carbohydrate indices were: hemolymph trehalose concentration and fat body glycogen content. The level of trehalose found in the hemolymph of insects when exposed to fenitrothion, and irrespective of the level of concentration mixed into food, were significantly lower when comparing to the control samples. Imidacloprid acted analogically with one exception at the concentration of 10 mg·kg(-1) dry food where trehalose concentration did not differ from the control values. Coupling with fat body glycogen concentration was less visible and appeared only at the concentrations of 5 and 10 mg imidacloprid·kg(-1) dry food. As described in this study changes in the sugar distribution and midgut glucose absorption indicate that insects cover the increased energy needs induced by insecticides; also at the gastrointestinal tract level. The result indicates that the midgut glucose absorption parameters could be considered as a non-specific biomarker of insecticide toxicity.

Acute oral toxicity of the organophosphorus pesticide fenitrothion to fat-tailed and stripe-faced dunnarts and its relevance for pesticide risk assessments in Australia.

The scarcity of information on the effects of pesticides on native Australian vertebrates constrains the development of biologically relevant risk assessments in Australia for the registration of pesticides. The concern that endemically old and unique Australian vertebrate fauna might display high sensitivity to pesticides used for locust control provoked examination of the acute oral toxicity of the organophosphorus pesticide fenitrothion for the fat-tailed dunnart, Sminthopsis crassicaudata (Gould 1844), and the stripe-faced dunnart, S. macroura (Gould 1845). By using the up-and-down method for determining acute oral toxicity, S. crassicaudata and S. macroura were found to have estimated median lethal doses (LD50s) of 129 mg/kg (95% confidence interval [CI] = 74.2-159.0) and 97 mg/kg (95% CI = 88.3-120.0), respectively. These values are 10 to 14 times lower than the reported LD50 values for a similar-sized eutherian mammal, Mus musculus (L. 1758; LD50 = 1,100-1,400 mg/kg) and lower than all other reported mammalian LD50 values. Such wide interspecific variation in sensitivity to fenitrothion may be a consequence of underlying differences in the metabolic pathway for fenitrothion detoxification in mammals and a possible explanation for the increased toxicity of fenitrothion to dunnarts, compared with other mammals, is proposed. The unexpectedly high sensitivity of these Australian marsupials to fenitrothion emphasises the importance of adequately evaluating the risks of pesticides to endemic Australian fauna.

Effect of oral administration of fenitrothion on biochemical and hematological parameters in rats.

The aim of this study was to evaluate the effects of acute exposure to various doses of fenitrothion (FNT) on level of serum glucose, total protein, triglycerides (TG), total cholesterol (TC) and some hematological parameters. The study was conducted on 8-week-old male Wistar rats that divided into four groups (three experimental groups and one control group), were treated orally with different doses (25, 50 and 100 mg kg(-1)) of fenitrothion for 28 consecutive day. After treatment, blood samples were collected for biochemical and hematological studies. Present results demonstrated that exposed groups led to significant dose-dependent increase in serum glucose and cholesterol levels. Significant decrease was observed in some hematological parameters [Red Blood Cell (RBC) counts, Hemoglobin (Hb), Haematocrite (Ht) and Mean Corpuscular Hemoglobin (MCH) values]. Serum total protein and triglycerides were also decreased not significantly in exposed groups when compared with control. Generally, the degrees of observed variations were found to be dose dependent.

Preliminary investigation of changes in the sexually dimorphic nucleus of the rat medial preoptic area following prenatal exposure to fenitrothion.

In vitro, the organophosphate insecticide fenitrothion is a potent competitive androgen receptor antagonist, whereas in vivo it affects the development of the male rat reproductive system. The purpose of this pilot study was to determine whether prenatal exposure to fenitrothion affects development of the rat sexually dimorphic nucleus of the medial preoptic area (SDN-POA). Pregnant rats (n = 5-6 litters/group) were orally dosed with corn oil (vehicle) or fenitrothion (20 or 25 mg kg(-1) day(-1)) from gestation day (GD) 12-21. Offspring were euthanized after reaching sexual maturity (females 60-65 days old and males 96-105 days old) and the SDN-POA volumes determined for two rats/sex/litter. Tremors, increased lacrimation and decreased body weight gain were observed in dams from both fenitrothion exposure groups. Reproductive effects in male offspring, including reduced anogenital distance on postnatal day (PND) 1 and increased retention of areolae (PND 13) were observed following fenitrothion exposure at these dose levels. These effects did not persist into adulthood. There was a dose-related increase in the SDN-POA volume in males and a dose-related decrease in SDN-POA volume in females exposed to fenitrothion. These SDN-POA volume changes contrast with those seen with flutamide, another potent anti-androgen, and suggest that fenitrothion may have mixed endocrine effects on the developing brain.

Inhibition and recovery of maternal and foetal cholinesterase enzymes following fenitrothion administration in CD rats.

The purpose of this study was to characterize tissue esterase activity and blood fenitrothion concentrations in the rat dam and foetus following in-utero exposure to the organophosphate insecticide fenitrothion. Time-mated, 8-week-old rats were gavaged on gestation day 19 with 0, 5, or 25 mg fenitrothion kg-1. Fenitrothion was absorbed rapidly from the gastrointestinal tract, with peak maternal and foetal blood levels observed 0.5-1.0 h after dosing. Fenitrothion concentrations in maternal and foetal blood were virtually identical and demonstrated a non-linear dose-response relationship. Acetylcholinesterase and carboxylesterase activities in maternal liver and blood and in foetal liver and brain decreased within 30-60 min of fenitrothion exposure. Esterase inhibition occurred at a fenitrothion dose (5 mg kg-1) that has not been previously associated with reproductive toxicity, suggesting that esterase inhibition should be considered as the critical effect in risk assessments for this pesticide.

Fenitrothion: toxicokinetics and toxicologic evaluation in human volunteers.

An unblinded crossover study of fenitrothion 0.18 mg/kg/day [36 times the acceptable daily intake (ADI)] and 0.36 mg/kg/day (72 X ADI) administered as two daily divided doses for 4 days in 12 human volunteers was designed and undertaken after results from a pilot study. On days 1 and 4, blood and urine samples were collected for analysis of fenitrothion and its major metabolites, as well as plasma and red blood cell cholinesterase activities, and biochemistry and hematology examination. Pharmacokinetic parameters could only be determined at the higher dosage, as there were insufficient measurable fenitrothion blood levels at the lower dosage and the fenitrooxone metabolite could not be measured. There was a wide range of interindividual variability in blood levels, with peak levels achieved between 1 and 4 hr and a half-life for fenitrothion of 0.8-4.5 hr. Although based on the half-life, steady-state levels should have been achieved; the area under the curve (AUC)(0-12 hr) to AUC(0-(infinity) )ratio of 1:3 suggested accumulation of fenitrothion. There was no significant change in plasma or red blood cell cholinesterase activity with repeated dosing at either dosage level of fenitrothion, and there were no significant abnormalities detected on biochemical or hematologic monitoring.

Effects of in utero exposure to the organophosphate insecticide fenitrothion on androgen-dependent reproductive development in the Crl:CD(SD)BR rat.

Fenitrothion [0,0-dimethyl-O-(4-nitro-m-tolyl) phosphorothioate] is an organophosphate insecticide that has been shown to have antiandrogenic activity using in vitro and in vivo screening assays. Studies were performed to evaluate the ability of fenitrothion to disrupt androgen-dependent sexual differentiation in the male rat. Pregnant Crl:CD(SD)BR rats were administered fenitrothion by gavage at 0, 5, 10, 15, 20, or 25 mg/kg/day ( n = 6-11/group) from gestation day (GD) 12 to 21. Maternal toxicity was observed in the dams treated with 20 and 25 mg fenitrothion/kg/day based on muscle tremors and decreases in body weight gain from GD 12 to 21. Fetal death was increased in the 20 and 25 mg/kg/day exposure groups, as evidenced by a decrease in the proportion of pups born alive. Androgen-mediated development of the reproductive tract was altered in male offspring exposed in utero to maternally toxic levels of fenitrothion (25 mg/kg/day), as evidenced by reduction in anogenital distance on postnatal day (PND) 1 and retention of areolae on PND 13. However, these effects were only transient, and there were no indications of abnormal phenotypes or development of androgen-dependent tissues on PND 100. At the dose levels evaluated in this study, fenitrothion was only weakly antiandrogenic in vivo compared with other androgen receptor antagonists such as flutamide, linuron, and vinclozolin. Based on observed fetotoxicity at 20 mg/kg/day, the lowest observed adverse effect level (LOAEL) for developmental effects can be lowered from 25 to 20 mg/kg/day.

Embryonic toxicity of insecticide Sumithion 50 EC and herbicide Fusilade S in pheasants after individual or combined administration.

The purpose of this work was to determine the individual and combined effects of insecticide Sumithion 50 EC (50% fenitrothion) and herbicide Fusilade S (12.5% fluazifop-P-butyl) on the development of pheasant embryos. Eggs were treated by injection of various concentrations of pesticides into the air space on day 12 of incubation. Pathological examination of embryos was carried out on day 23 of the hatching period. Mortality rate, body weight data and morphological alterations were evaluated after the macroscopic examination. The skeletal staining method was used to detect deformities. The two pesticides used in combination moderated the toxic/teratogenic effects of individual treatment.

Antifeeding effect of several insecticidal formulations against Ctenocephalides felis on cats.

Evaluation of insecticidal activity of flea products is generally based on counting live fleas in the animal's coat 24 and 48 hours following artificial infestation. This approach, however, does not allow to specify whether the fleas have had the opportunity to bite and take a bloodmeal prior to their death. To address this question, 30 cats were alloted to six groups of five animals. Each cat was housed in a separate cage. At Day 0, each group of cats received a single treatment as follows: Group 1: spot-on application of imidacloprid: cats < 4 kg: 40 mg/cat, cats > or = 4 kg: 80 mg/cat (Advantage). Group 2: spot-on application of fipronil: 50 mg/cat (Frontline spot-on). Group 3: spray application of fipronil: 7.5 mg/kg b.w. (Frontline spray). Group 4: foam application of permethrin 40/60: 50 mg/kg b.w. (Defencat). Group 5: aerosol spray application of dichlorvos + fenitrothion: one second/kg b.w. (NuvanTop). Group 6: control group: cats were left untreated. One hour after treatment, each cat was infested with 50 unengorged young adult fleas, Ctenocephalides felis, deposited along the dorsal midline. One hour later, each cat was carefully combed using a fine-toothed comb (13 teeth/cm). Collected fleas were swatted to deteci blood in their abdomen. To the manufacturers respective product use instructions and efficacy claims, reeinfestations were made at Days 3, 7, 14 in all groups; at Days 21 and 30 in Groups 1, 2, 4, 6; at Days 35 and 42 in Groups 3 and 6. The cats were combed one hour after each reinfestation. The results indicate that the topical application of imidacloprid or fipronil does not prevent fleas from biting and feeding within the first hour after infestation prior to being killed while the topical application of dichlorvos/fenitrothion and permethrin let to a better than 80% decrease of the number of engorged fleas for three and seven days post treatment, respectively.

Response and recovery of acethylcholinesterase activity in the European eel Anguilla anguilla exposed to fenitrothion.

European eel (Anguilla anguilla) were exposed to sublethal fenitrothion concentrations in a continuous flow-through system for 4 days. Muscle acetylcholinesterase (AChE) activity was evaluated after 2, 8, 12, 24, 32, 48, 56, 72 and 96 hours pesticide exposure. Results showed that AChE activity in eel muscle tissue decreased as concentration of fenitrothion increased. Pesticide induced significant inhibitory effects on the AChE activity of A. anguilla ranging from > 35% inhibition at sublethal concentration of 0.02 ppm to > 44% inhibition at sublethal concentration of 0.04 ppm. Eel were exposed to both fenitrothion concentrations for 96 hours and then allowed a period of recovery in pesticide-free water. Samples were taken out at 8, 12, 24, 48, 72, 96, 144 and 192 hours and eel muscle AChE activity was evaluated. Following 1 week of recovery, the AChE activity for those animals previously exposed to 0.02 and 0.04 ppm fenitrothion was still different from the controls. So, the AChE activity of eel muscle at the end of the recovery phases remained significantly depressed.

A safety study on rat's eye after 13-week oral administration with fenitrothion.

The potential of ocular toxicity of fenitrothion (O,O-dimethyl O-4-nitrom-tolyl phosphorothioate) was assessed in Sprague-Dawley (Crj:CD) rats of both sexes receiving a diet containing the test compound at concentrations of 0, 2.5, 5, 10, or 30 ppm for 13 weeks. The animals were observed daily for clinical signs and their body weights and food consumption were measured weekly during the study. At termination of treatment, surviving animals were subjected to ophthalmoscopy, electroretinography, and biochemical analyses of plasma, erythrocyte, and brain cholinesterase (ChE). Histopathological examinations of ocular tissues were performed on all animals by light microscopy and on two animals/sex/dose by electron microscopy. There were no treatment-related changes in clinical signs, body weights, and food consumption. A significant inhibition of ChE activity was observed in males (plasma and erythrocyte ChE) and females (plasma, erythrocyte, and brain ChE) at 30 ppm and in females (plasma ChE) at 10 ppm. Ophthalmological and histopathological examinations revealed neither functional nor morphological alterations in the visual system at any dose level. Under the conditions of the present study, there was no evidence of ocular toxicity of fenitrothion for male and female rats at dose levels up to 30 ppm (1.70 mg/kg/day for males and 1.96 mg/kg/day for females) where distinct inhibition of ChE activity was observed.

Sublethal effects of an organophosphate insecticide on the European eel, Anguilla anguilla.

The present communication deals with the effects of fenitrothion (0.02 mg/liter) on the energy metabolism of the European eel, Anguilla anguilla, and its recovery from intoxication. Various parameters such as glycogen, lactate, proteins, and glucose levels were measured in different eel tissues after 2, 8, 12, 24, 32, 48, 56, 72, and 96 hr of fenitrothion exposure. Subsequently, the fish were allowed recovery periods of 8, 12, 24, 48, 72, 96, 144, and 192 hr in clean water, and the same parameters were evaluated. Liver glycogen content showed no significant changes during the exposure time, while blood glucose levels increased markedly. Gill, liver, and blood lactate values increased during pesticide exposure, while proteins decreased in comparison to unexposed controls. Most of the metabolic disorders did not persist after eels were allowed to recover in clean water for less than a week. The observed effects of fenitrothion on fish metabolism are discussed in relation to a stress syndrome, as are probable reasons for alterations.