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PubMedDate not supplied

Gas chromatographic method for determination of fenitrothion in fenitrothion technical and in formulated products: collaborative study.

A gas chromatographic (GC) method for determination of fenitrothion in fenitrothion technical and formulated products has been subjected to a collaborative study with 7 participating laboratories. Formulations are extracted with chloroform containing dibutyl sebacate as an internal standard and are analyzed by gas chromatography using an OV-210 column. Collaborators were furnished matched pairs of technical product and water-dispersible powder and emulsifiable concentrate formulations. Relative standard deviations for reproducibility (RSDR) for the paired samples were 0.54, 1.00, and 1.56%, respectively, for technical fenitrothion, water-dispersible powders, and emulsifiable concentrates. The method has been approved interim official first action as an alternative to the present official first action AOAC method 6.A19-6.A24, which uses a polyphenyl ether, 6 ring (PPE-6R) column packing and fluoranthene as internal standard.

Chromatography, Gas↗
PubMed1976

Resistance to fenitrothion in Danish houseflies, Musca domestica.

Resistance to fenitrothion was investigated in housefly populations in Danish farms 1964--72 in connection with trials of fenitrothion, dimethoate and other organophosphorus compounds for fly control. Resistance was tested by topical application and expressed as resistance ratios, R/S, relative to normal susceptible strains. In 1964--70 fly populations on farms sprayed with fenitrothion (one year each) only developed mode-rate fenitrothion-resistance, R/S at LD 95 below 21 and fly control was generally satisfactory. However, in 1972 high fenitrothion-resistance, R/S 100--400 at LD 95, was found in several fly populations, both on farms treated with fenitrothion and on farms treated with dimethoate, fenitrothion, or bromophos. In all cases the high fenitrothion-resistance was associated with high resistance to dimethoate. Some characteristics of this, apparently complex, resistance are discussed including the effect of certain synergists. Resistance to fenitrothion in Danish flies is only partly reduced by pretreatment with high dosages of sesamex, which inhibits microsomal detoxication, and very little by TBTP (S, S, S tributyl phosphorotrithioate), which inhibits other types of break-down of organophosphorus compounds, e.g. by ali-esterases. The occurrence of fenitrothion- resistance in field populations of houseflies in other regions is briefly reviewed. Widespread, partly very high, resistance has recently been reported from Japan.

Animals↗
PubMed1976

Resistance to fenitrothion in Danish houseflies, Musca domestica.

Resistance to fenitrothion was investigated in housefly populations in Danish farms 1964--72 in connection with trials of fenitrothion, dimethoate and other organophosphorus compounds for fly control. Resistance was tested by topical application and expressed as resistance ratios, R/S, relative to normal susceptible strains. In 1964--70 fly populations on farms sprayed with fenitrothion (one year each) only developed mode-rate fenitrothion-resistance, R/S at LD 95 below 21 and fly control was generally satisfactory. However, in 1972 high fenitrothion-resistance, R/S 100--400 at LD 95, was found in several fly populations, both on farms treated with fenitrothion and on farms treated with dimethoate, fenitrothion, or bromophos. In all cases the high fenitrothion-resistance was associated with high resistance to dimethoate. Some characteristics of this, apparently complex, resistance are discussed including the effect of certain synergists. Resistance to fenitrothion in Danish flies is only partly reduced by pretreatment with high dosages of sesamex, which inhibits microsomal detoxication, and very little by TBTP (S, S, S tributyl phosphorotrithioate), which inhibits other types of break-down of organophosphorus compounds, e.g. by ali-esterases. The occurrence of fenitrothion- resistance in field populations of houseflied in other regions is briefly reviewed. Widespread, partly very high, resistance has recently been reported from Japan.

Agriculture↗
PubMed1996

Immunotoxicological insignificance of fenitrothion in mice and rats.

Fenitrothion was administered orally to mice or rats in daily doses of up to 1/25 of the LD50 for 14 days, and numbers of splenic plaque-forming cells against sheep red blood cells (SRBC-PFC), one of the most common immune parameters, were measured. Splenic SRBC-PFC number was suppressed by fenitrothion only in rats which received 30 mg/kg body weight (bw) of the compound. Other immune parameters, including the arthus reaction, delayed-type hypersensitivity, and activities of macrophages and natural killer cells in rats, were not influenced by fenitrothion. Adrenal hyperfunction manifesting as increased organ weight and elevated plasma corticosterone level was noted along with strong cholinergic signs in rats which received 30 mg/kg bw of fenitrothion. At lower doses such as 3 or 0.3 mg/kg bw of fenitrothion, rats had no strong cholinergic signs, adrenal hyperfunction, or evidence of immunosuppression despite significant suppression of systemic cholinesterase (ChE) activities. In mice, no suppression of SRBC-PFC number or mixed lymphocyte reaction was noted even at the highest dose (40 mg/kg bw) of fenitrothion, at which significant suppression of systemic ChE activities but no cholinergic signs were noted. These findings strongly suggest that the immunosuppressive effect of fenitrothion noted in rats was due to systemic, potent cholinergic stress and that fenitrothion has no immunotoxicity in mice and rats.

Animals↗
PubMed1986

An assessment of the neurotoxic potential of fenitrothion in the hen.

The potential of single, toxic doses of fenitrothion (O,O-dimethyl O-(4-nitro-m-tolyl)phosphorothioate) to elicit delayed neurotoxicity in the adult White Leghorn hen was compared to the effects produced following similar treatment with the known neurotoxin, tri-o-tolyl phosphate (TOTP). Hens (2.0-2.5 kg body wt) received single oral doses of fenitrothion (500 mg/kg) or TOTP (500 mg/kg), the resulting toxicity being assessed by measuring biochemical (brain and spinal cord acetylcholinesterase (AChE) and neurotoxic esterase (NTE), physiological (motor function) and morphological (cross- and longitudinally-sectioned and stained preparations) parameters of the brains, spinal cords and sciatic nerves of groups (n = 5) of hens at 24 h, 7, 14, 28, 42 and 56 days post-treatment. At 24 h after treatment, fenitrothion caused a marked inhibition of neuronal AChE while TOTP had no effect. In contrast, TOTP caused a significant inhibition of NTE whereas fenitrothion was without effect. At 7 days after treatment, the NTE was still significantly reduced in TOTP-treated hens but normal levels of activity were detected at 14 days post-treatment. No alternation in NTE activity was found in any fenitrothion-treated hens. A characteristic, central-peripheral, distal axonopathy was observed following treatment with TOTP, mild signs appeared 7-14 days post-treatment and increased in severity up to 28 days after treatment, concomitant with morphological changes primarily in the sciatic nerves and spinal cords. Minimal morphological changes were elicited by fenitrothion at this dosage, the tissues appearing no different than those seen in vehicle-treated control hens. The results demonstrated that fenitrothion was distinctly different from TOTP in the biochemical, physiological and morphological effects produced in acutely treated hens and that fenitrothion could not be considered to be neuropathic in the classical manner of TOTP.

Acetylcholinesterase↗
PubMed2000

Evaluation of a 5-day Hershberger assay using young mature male rats: methyltestosterone and p,p'-DDE, but not fenitrothion, exhibited androgenic or antiandrogenic activity in vivo.

A 5-day Hershberger assay using young mature male rats to detect compounds interfering with androgen receptor (AR)-mediated mechanisms was evaluated for ability to identify p,p'-DDE (a weak AR antagonist) and methyltestosterone (MT, an AR agonist). Fenitrothion, an organophosphate pesticide, was also evaluated in this validated assay. Castrated male Crj:CD(SD)IGS rats (1 week after castration, 11 weeks of age) were subjected to experiments. To determine a suitable value of testosterone propionate (TP) as a reference androgen for detection of antiandrogenic chemicals, castrated male rats were treated daily with TP (0, 0.06, 0.25, 1, 4, or 16 mg/kg/day, s.c.). TP produced increases in weights of ventral prostate, seminal vesicles and levator ani plus bulbocavernosus muscles. Serum androgen level measured by RIA kit (mostly TP) were elevated in a dose-related manner, while the weights of organs with 1 mg/kg/day of TP were nearly equivalent to the maximum responses (i.e., sub-maximal). One hundred mg/kg/day of p,p'-DDE significantly attenuated TP 0.1 mg/kg-induced increases in weights of seminal vesicles and muscles, and TP 1 mg/kg-induced increases in weights of ventral prostate, seminal vesicles and muscles, but did not affect the weight of these organs in either TP 16 mg/kg-treated or intact rats, demonstrating that the dose range of 0.1-1 mg/kg TP is suitable for reference androgen. Oral treatment with 100 mg/kg of MT increased the weights of ventral prostate, seminal vesicles and muscles as strongly as did subcutaneous injection of 1 mg/kg of TP. These findings demonstrate that the 5-day Hershberger assay using young mature as well as immature male rats is a sensitive and valid short-term screening method for the detection of chemicals interfering with AR-mediated mechanisms. To determine whether fenitrothion interferes with AR-mediated mechanisms in vivo, fenitrothion (0, 0.75, 1.5 or 3 mg/kg/day) was administered by gavage for 5 days to castrated rats for androgenicity, or to castrated rats treated with 1 mg/kg TP for antiandrogenicity. Treatment with fenitrothion had no adverse effects on clinical signs, body weight, or liver or kidney weights, but cholinesterase activities in the brain and erythrocytes were significantly suppressed by fenitrothion to, respectively, 77-81% and 66-67% of control levels. In the antiandrogenicity experiment, serum androgen levels of TP-treated, castrated rats did not differ among groups. Treatment with 100 mg/kg of p,p'-DDE as a positive control again significantly attenuated TP-induced increases in weights of the ventral prostate and seminal vesicles, while fenitrothion had no effect on the weights of any organs. In the androgenicity experiment, treatment with 100 mg/kg of MT significantly increased weights of ventral prostate, seminal vesicles and muscles, but fenitrothion had no effects on the weights of any of these organs. These findings yield no evidence that fenitrothion interferes with AR-mediated mechanisms in vivo, consistent with the result of several toxicological bioassays.

Androgen Antagonists↗
PubMed1999

Toxicity of cypermethrin and fenitrothion on the hemolymph carbohydrates, head acetylcholinesterase, and thoracic muscle Na+, K+-ATPase of emerging honeybees (Apis mellifera mellifera. L).

Comparative effects of sublethal doses (0, 0.1, 0.2. 0.4, 0.8, and 1 nmol/bee) of cypermethrin and fenitrothion have been studied on emerging honeybees. The insecticides were injected intrathoracially between the third and the fourth segment. Biochemical effects were determined over a 3-h period. Both cypermethrin and fenitrothion led to a significant hypoglucosemia and hypotrehalosemia 15 min after injection, but cypermethrin seemed more active than fenitrothion at the same doses. A recovery phase appeared for glucosemia and trehalosemia, 60 min after injection. The higher toxicity of cypermethrin than fenitrothion also appeared in this period, where it took a longer time for honeybees to reestablish carbohydrate levels following cypermethrin than fenitrothion injections. The low values of the correlation coefficients (r) for glucose versus trehalose levels led to the supposition that no typical functional interaction between glucose and trehalose could be considered to be involved in this experience. Na+, K+-ATPases activity was significantly inhibited (P< 0.05) by cypermethrin and maximum percentage inhibition was reached (45%) at 1 nmol/bee. The kinetic analysis of honeybee's acetylcholinesterase inhibition by fenitrothion, indicated that this insecticide acts (P< 0.05) on acetylcholinesterase activity. The percentage inhibition exceeded 60% at 0.2 nmol/bee. This result revealed that in general cypermethrin and fenitrothion share common biochemical effects on carbohydrates, although their neurotoxic effects on honeybees might be different.

Acetylcholinesterase↗
PubMed1983

Effect of adrenalectomy, pretreatment with SKF 525-A, phenobarbital and diethyl maleate on the acute toxicity of fenitrothion in male rats.

The effect of adrenalectomy (Adx), SKF 525-A, phenobarbital (PB), and diethyl maleate (DEM) on the acute toxicity of fenitrothion was investigated in male rats by assessing the degree of plasma cholinesterase activity. PB, 60 mg/kg/day for 3 days, exerted no protective effect on the toxicity of fenitrothion (100 mg/kg, p.o.) given 24 h after the last injection. In adrenalectomized and SKF 525-A-pretreated rats, the toxicity of fenitrothion was lower than that of the controls. Fenitrothion toxicity was increased by administration of DEM (1 ml/kg), which depletes hepatic glutathione (GSH) levels. In vitro, the rates of fenitrothion decomposition and fenitrooxon formation by microsomes were markedly affected by PB, SKF 525-A and Adx. The decomposition of fenitrooxon by the microsomal fraction and GSH-dependent decomposition of fenitrooxon by the soluble fraction were not affected by PB, SKF 525-A and Adx pretreatment. The GSH-dependent decomposition of fenitrothion and fenitrooxon was increased by addition of GSH to the incubation mixture. The present results indicate that the GSH-dependent metabolic pathway plays an important role in the detoxication of fenitrothion.

Adrenalectomy↗
PubMed1984

Pharmacokinetic analysis of increased toxicity of 2-sec-butylphenyl methylcarbamate (BPMC) by fenitrothion pretreatment in mice.

The potentiating effect of O,O-dimethyl O-(3-methyl-4-nitrophenyl) phosphorothioate (fenitrothion) on the toxicity of 2-sec-butylphenyl methylcarbamate (BPMC) in male mice was analyzed pharmacokinetically. The animals pretreated by dietary administration of 1000 ppm fenitrothion for 1 week (4.4% of the po LD50 daily) did not show toxic symptoms except for a slight decrease in body weight. In the fenitrothion-pretreated mice, toxicity of fenitrothion was not changed but a fivefold potentiation was observed in po and ip acute lethality and a threefold potentiation of iv lethality of BPMC. Toxic signs after BPMC administration were similar regardless of fenitrothion pretreatment or of route of administration. Fenitrothion pretreatment followed by BPMC administration (20 mg/kg po or 8 mg/kg iv, approximate LD5 in the pretreated mice) significantly increased the plasma BPMC concentration and the total area under the plasma concentration versus time curve (AUC0-infinity). The pretreatment increased the oral AUC0-infinity more greatly than the iv AUC0-infinity (for po, 6.3-fold; for iv, 2.0-fold). The oral systemic availability of BPMC (fraction reaching systemic circulation) was increased by fenitrothion treatment to 3.3-fold. These results suggest that a major cause of the potentiation may be the increase in amount of BPMC in the systemic circulation.

Animals↗
PubMed1991

Metabolic activation of the organophosphorus insecticides chlorpyrifos and fenitrothion by perfused rat liver.

The present study was undertaken to characterize the metabolic activation of the organophosphorus insecticides chlorpyrifos [O,O-diethyl O-(3,5,6-trichloro-2-pyridyl) phosphorothionate] and fenitrothion [O,O-dimethyl O-(3-methyl-p-nitrophenyl) phosphorothionate] by intact rat liver. Single-pass perfusions of rat livers with chlorpyrifos or fenitrothion to steady state conditions resulted in the appearance of their corresponding oxygen analogs in effluent. In addition, detoxification of chlorpyrifos oxon [O,O-diethyl O-(3,5,6-trichloro-2-pyridyl) phosphate] or fenitrooxon [O,O-dimethyl O-(3-methyl-p-nitrophenyl) phosphate] by rat blood did not proceed at a rate rapid enough to prevent passage of at least some of these chemicals from liver to extrahepatic tissues, suggesting that hepatic biotransformation of chlorpyrifos and fenitrothion by rat liver results in their net activation. Although male rat livers produced more chlorpyrifos oxon and fenitrooxon from chlorpyrifos and fenitrothion, respectively, than did livers from female rats, the acute toxicities of chlorpyrifos and fenitrothion were greater in females than in males. Therefore, differences in hepatic activation of chlorpyrifos and fenitrothion in males and females cannot account for the sex differences in their acute toxicities in the rat. Finally, S-methyl glutathione and S-p-nitrophenyl glutathione were not detected in effluent or bile of livers perfused with fenitrothion, suggesting that glutathione-mediated biotransformation of this insecticide does not occur to any significant degree in intact liver.

Animals↗
PubMed1989

Detection of S-methylfenitrothion, aminofenitrothion, aminofenitroxon and acetylaminofenitroxon in the urine of a fenitrothion intoxication case.

A 23-year-old male attempted suicide by ingesting approximately 50 ml of 5% fenitrothion emulsion, and vomited soon afterwards. He was admitted to a hospital about 3 h after ingestion. He recovered and was discharged from hospital 3 days after admission. The serum cholinesterase activity (normal range: 175-440 I.U.) was only 29 at 3 h, 32 at 1 day, 59 at 2 days and 75 at 3 days after ingestion. Fenitrothion and its metabolites in the body fluids were extracted by an Extrelut column extraction method, detected by a gas chromatograph equipped with either a hydrogen flame ionization detector or a flame photometric detector, and confirmed by a gas chromatograph-mass spectrometer. Fenitrothion concentration in the blood was 169.5 ng/g at 3 h after ingestion. The half life of blood fenitrothion concentration was found to be about 4.5 h. Fenitrothion metabolites, 3-methyl-4-nitrophenol, aminofenitrothion, aminofenitroxon, acetylaminofenitroxon and S-methylfenitrothion, were detected in the urine samples. All of them except S-methylfenitrothion were detected in the urine samples collected up to 62 h after ingestion. It would appear therefore that fenitrothion poisoning can be determined by detection and analysis of the metabolites in urine even if fenitrothion has not been detected in the blood.

Adult↗
PubMed2003

Contribution of metabolites to mutagenicity during anaerobic biodegradation of fenitrothion.

The contribution of fenitrothion and its microbial metabolites to the mutagenicity of a fenitrothion-containing solution was investigated during anaerobic biodegradation. Although a mixed culture of bacteria obtained from a paddy field degraded fenitrothion and reduced its concentration from 4.6 to 0.1 mg/l in 6 days, the indirect mutagenicity of the solution in Salmonella strain YG1029 increased. This increase was found to be partially due to amino-fenitrothion generated during the biodegradation. In addition, other unidentified metabolites contributed to the mutagenicity. In contrast, the indirect mutagenicity in strain YG1042, which was initially large because of fenitrothion, then decreased, and increased again. This increase in mutagenicity was also due to amino-fenitrothion and other unidentified metabolites. The mutagenicity in strains YG1029 and YG1042 decreased after day 6. The greatest contribution of amino-fenitrothion to the mutagenicity was calculated to be 73% and 61% in YG1029 and YG1042 on day 3 of incubation, respectively. That of unidentified metabolites was calculated at 49% and 61% on day 20, respectively. Therefore, because not all the toxic metabolites of a compound can be identified, it is important to evaluate the toxicity of a whole solution in a bioassay such as the Ames assay rather than deducing the toxicity of the solution from the combined toxicities of known metabolites.

Anaerobiosis↗
PubMed2003

Metabolism of fenitrothion and conjugation of 3-methyl-4-nitrophenol in tomato plant (Lycopersicon esculentum).

The metabolism of (14)C-labeled fenitrothion (Sumithion, [O,O-dimethyl-O-(3-methyl-4-nitrophenyl)phosphorothioate]) in tomato plant (Lycopersicon esculentum Mill., cv. Ponderosa) grown in the greenhouse equipped with quartz glass was conducted to investigate the effect of sunlight on the behavior of fenitrothion and to elucidate the detailed structure of conjugated metabolites. Tomato plants (BBCH 85) were topically treated with (14)C-labeled fenitrothion twice with a 2 week interval between applications. At 15 days after the second application, more than half of the recovered (14)C was detected as unaltered fenitrothion, glucose, and cellobiose esters of 3-methyl-4-nitrophenol (NMC) in extracts from tomato fruit. The photoinduced formation of the S-methyl isomer of fenitrothion via thiono-thiolo rearrangement was detected only in the surface rinse but at trace amounts. In the whole tomato fruit, fenitrothion, the S isomer, NMC-beta-glucoside, and NMC cellobioside were detected at 34.16, 1.28, 7.47, and 15.07% of the recovered (14)C, respectively. Trace amounts of the oxon analogue of fenitrothion were detected only on tomato leaves. The chemical structure of the cellobiose conjugate of NMC, 1-O-beta-d-glucopyranosyl-(1-->4)-beta-d-glucopyranosyl-3-methyl-4-nitrophenol, was determined by spectroscopic analyses (liquid chromatography-mass spectrometry, NMR), using the metabolite obtained from leaves and stems of tomato plant hydroponically grown with (14)C-labeled NMC.

Carbon Radioisotopes↗
PubMed1982

Analysis of fenitrothion and metabolites in stored wheat.

A simple and rapid method for the analysis of fenitrothion and its metabolites, fenitrooxon, S-methyl fenitrothion, demethyl fenitrothion, demethyl S-methyl fenitrothion, 3-methyl-4-nitrophenol, and dimethyl phosphorothioic acid in stored wheat has been developed. Simultaneous analysis of the extract was conducted using FPD-GLC after derivatization with diazoethane except for 3-methyl-4-nitrophenol which was analyzed directly by EC-GLC. Recoveries of all compounds from wheat fortified at the levels from 0.1 to 5.0 ppm were greater than 90%. The developed method was used to quantitatively determine major metabolites found in grain treated with fenitrothion and stored at 20 degrees C for 12 months. Demethyl fenitrothion, 3-methyl-4-nitrophenol, and dimethyl phosphorothioic acid were the major breakdown products of fenitrothion found in stored wheat. Confirmation of these metabolites was carried out by chemical derivatization plus FPD-GLC and by TLC.

Biotransformation↗
PubMed2001

Androgen receptor antagonism by the organophosphate insecticide fenitrothion.

Organophosphate insecticides represent one of the most widely used classes of pesticides with high potential for human exposure in both rural and residential environments. We investigated the interaction of the organophosphothioate pesticide fenitrothion (O,O-dimethyl O-(4-nitro-m-tolyl) phosphorothioate) with the human androgen receptor (AR). Fenitrothion blocked dihydrotestosterone-dependent AR activity in a concentration-dependent and competitive manner in HepG2 human hepatoma liver cells transiently transfected with human AR and an AR-dependent luciferase reporter gene. Schild regression analysis yielded an equilibrium dissociation constant value of 2.18 x 10(-8) M. To determine the antiandrogenic potential of fenitrothion in vivo, 7-week-old castrated Sprague-Dawley rats were dosed once a day for 7 days with testosterone propionate (50 microg/day, sc) plus gavage doses of either corn oil vehicle or fenitrothion (15 or 30 mg/kg/day). An additional group of rats was given testosterone propionate and flutamide (50 mg/kg/day). Motor activity and acetylcholinesterase activity in whole blood and brain were also assessed. Both fenitrothion and the reference antiandrogen flutamide caused significant decreases in the ventral prostate, seminal vesicle, and levator ani plus bulbocavernosus muscles tissue weights. In contrast, blood acetylcholinesterase activity, a standard biomarker of organophosphate poisoning, was only inhibited at the higher dose of fenitrothion (30 mg/kg). Our results demonstrate that fenitrothion is a competitive AR antagonist, comparable in potency to the pharmaceutical antiandrogen flutamide and more potent, based on in vitro assays, than the known environmental antiandrogens linuron and p,p'-, 2,2-bis(p-hydroxyphenyl)-1,1-dichloroethylene ( p,p'-DDE).

Acetylcholinesterase↗
PubMed1987

Bioconcentration and metabolism of DDT, fenitrothion and chlorpyrifos by the blue-green algae Anabaena sp. and Aulosira fertilissima.

Anabaena and Aulosira fertilissima showed a marked ability to accumulate DDT, fenitrothion and chlorpyrifos. Although the maximum accumulation of DDT was almost the same in both organisms, there were significant differences in their abilities to accumulate fenitrothion and chlorpyrifos. Patterns of uptake of DDT under different treatments were also similar in both Anabaena and Aulosira, but there were significant differences in the patterns of accumulation of fenitrothion between these two organisms. In Aulosira the maximum accumulation of fenitrothion was observed on the second day, whereas, in Anabaena, maximum accumulation was noticed on the first day. A completely different pattern of accumulation of chlorpyrifos was observed in Aulosira, which continued to accumulate chlorpyrifos throughout the experimental period. Bioconcentration of DDT in Anabaena and Aulosira ranged from 3 to 1568 ppm (microg g(-1)) and 6 to 1429 ppm, respectively. Bioconcentration of fenitrothion and chlorpyrifos in Anabaena varied from 53 to 3467 ppm and 7 to 6779 ppm, respectively. In Aulosira the bioconcentration varied from 100 to 6651 ppm and 53 to 3971 ppm for fenitrothion and chlorpyrifos, respectively. Anabaena and Aulosira metabolised DDT to DDD and DDE. Amounts of these DDT metabolites detected in the organisms were dependent on the concentration of treatment. DDD was the major, and DDE the minor, metabolite. These organisms were not able to metabolise the organophosphorus insecticides, fenitrothion and chlorpyrifos.

Journal Article↗
PubMed1986

The uptake and in vivo metabolism of the organophosphate insecticide fenitrothion by the blue crab, Callinectes sapidus.

Callinectes were exposed to [14C]fenitrothion at a level of 5.2 micrograms/liter in either 22 degrees C, 34 ppt; 22 degrees C, 17 ppt; or 17 degrees C, 34 ppt seawater. Uptake from the water, as measured by a decrease in fenitrothion, and the distribution of radioactivity throughout the Callinectes were determined. The nature of radiolabeled metabolites in the water and hepatopancreas was also determined. Fenitrothion was absorbed more rapidly from the water at the higher salinity and temperature. Radioactivity was detected in all the organs assayed by 24 hr postexposure, though the levels increased in most tissues throughout the experiment. The highest concentrations of radioactivity were found in the hepatopancreas and stomach. The metabolites which were detected in the water and liver indicate that Callinectes metabolize fenitrothion by oxidation of the phosphorothioate to a phosphate to yield fenitrooxon. The presence of aminofenitrothion and 3-methyl-4-aminophenol shows that reduction of the nitro group to an amino group also occurs. The isolation of desmethyl forms of fenitrooxon and fenitrothion as well as 3-methyl-4-nitrophenol indicates that hydrolysis of both the P-O-aryl and P-O-alkyl bonds occurred. Glycoside and sulfate conjugates of both phenols were inferred in the hepatopancreas. Higher levels of fenitrooxon and lower levels of desmethyl fenitrothion were detected in the 34 ppt seawater than in the 17 ppt seawater. The 5 degrees C differential had no significant effect on the nature and concentrations of metabolites detected in the seawater.

Animals↗