SEARCH · PubMed Health

Results for “Fenthion”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1994

Fenthion produces a persistent decrease in muscarinic receptor function in the adult rat retina.

Several reports have suggested that exposure to organophosphate pesticides damages the visual system. The prolonged effects of an acute dose of fenthion (dimethyl 3-methyl-4-methylthiophenyl phosphorothionate) were studied on the cholinergic system of the rat retina. Fenthion was administered in a single dose of 0 or 100 mg/kg (sc, in corn oil) to adult, male, Long-Evans rats. The animals were killed 4, 14, or 56 days after treatment and cholinesterase (ChE) activity as well as muscarinic receptor (mChR) function measured in the retina and frontal cortex. Fenthion produced 89% inhibition of ChE activity in both tissues at 4 days, and, although there was recovery, slight (15%) inhibition of the enzyme activity was still observed at 56 days in both tissues. A long-lasting decrease in carbachol-stimulated inositolphosphate (IP) release was observed following fenthion treatment in the retina: IP release was depressed at 4 days and this depression persisted up to 56 days after dosing. The density of mChR in the retina as well as in the cortex was decreased by 14-20% at 4 days and returned to control levels by 56 days. Fenthion had no effect on the metabolism of phospholipids in the retina following intraocular injections of labeled precursors [3H]myo-inositol, [methyl-14C]choline, or [2-3H]glycerol 4 days after fenthion treatment. These prolonged effects of fenthion on mChR function (signal transduction) appear to be specific to the retina as the cortex showed no change in receptor-stimulated IP release even in the presence of significant mChR down-regulation and ChE inhibition. This dose of fenthion did not produce overt morphological changes in the retina or in the cortex, as observed with light microscopy, although an increase in glial fibrillary acidic protein immunoreactivity (GFAP IR) extending from the internal limiting membrane to the external limiting membrane of the retina was noted. This increase in GFAP IR was observed at 14 days and persisted as long as 56 days post-treatment in the retina, but was not noted in the cortex at any of the time points studied. Thus, this long-lasting perturbation in the retinal cholinergic second messenger system induced by fenthion may occur independently of depressed ChE activity and down-regulation of mChR.

Animals↗

PubMed1991

Secondary poisoning hazard of fenthion to American kestrels.

The possibility that fenthion, an organophosphorus pesticide, could represent a secondary poisoning hazard to birds of prey was tested, using American kestrels (Falco sparverius) and house sparrows (Passer domesticus) as representative models of a naturally occurring predator-prey interaction. Fourteen kestrels were presented with live sparrows exposed previously to perches containing Rid-A-Bird 1100 solution (11% fenthion active ingredient). Eleven kestrels died within twenty-four h after consuming one fenthion-exposed sparrow. Two kestrels died after consumption of a second fenthion-exposed sparrow on day 2, and a final kestrel died after partially consuming a third fenthion-exposed sparrow on day 3. Brain cholinesterase (ChE) activity in kestrels was depressed to levels diagnostic of poisoning by a ChE-inhibiting compound. The majority of fenthion contamination of sparrows was external, with the highest amounts measured on the feet. The detection of fenthion residues in kestrel gastro-intestinal tracts confirmed secondary fenthion poisoning.

Animals↗

PubMed1984

Potentiation of acute toxicity of 2-sec-butylphenyl N-methylcarbamate (BPMC) by fenthion in mice.

This study was undertaken to determine whether interactions of toxicologic importance might occur during combined exposure of male mice to 2-sec-butylphenyl N-methylcarbamate (BPMC) and O,O-dimethyl O-(3-methyl-4-methylthiophenyl)phosphorothioate (fenthion). The equitoxic coadministration of BPMC and fenthion resulted in only a 1.6-fold potentiation compared to the expected LD50. However, 1 hr oral pretreatment with 3 (1/100 LD50), 7.5, 15, and 30 mg/kg of fenthion resulted in 5-, 9-, 12-, and 15-fold potentiation of the acute oral toxicity of BPMC, respectively. This fenthion pretreatment caused significant increases in the BPMC plasma concentrations and in the area under the concentration-time curve. The increase of the plasma concentrations of BPMC depended upon the fenthion dose and was associated with that of the potency ratio. The pretreatment of fenthion prolonged the hexobarbital sleeping time. The plasma concentrations of BPMC after the administration of a dose of LD2.5 (20 mg/kg) in fenthion-pretreated mice were clearly lower than those of a dose of LD2.5 (195 mg/kg) in nontreated mice. These results suggested that fenthion pretreatment caused the potentiation of the acute toxicity of BPMC partially by the inhibition of detoxification of BPMC.

Administration, Oral↗

PubMed1996

Effect of fenthion treatment on larval densities of insecticide-resistant Culex quinquefasciatus in an urban area of Sri Lanka.

In Sri Lanka the national Anti-Filaria Campaign (AFC) has routinely employed fenthion since 1974 for larvicidal control of Culex quinquefasciatus, the vector of Bancroftian filariasis in urban areas, where this mosquito breeds prolifically in polluted waters. During 1994 the efficacy of AFC fenthion treatment against organophosphate-resistant Cx quinquefasciatus was investigated at Dehiwela, near Colombo. The AFC target rate of fenthion application was 1 mg a.i./l, but the actual concentrations of fenthion in freshly treated pits ranged from 0.64 to 63.2 mg a.i./l. There was significant suppression of larval densities in treated soakage pits, the predominant breeding site of Cx quinquefasciatus, although the mosquito population was 6-fold resistant to fenthion at the LC50 level. Production of pupae was almost completely prevented in soakage pits which were sprayed weekly with fenthion, indicating that adult mosquito emergence from this source was minimal. The rapid decline in concentration of fenthion detected in the water of soakage pits indicated that a weekly treatment schedule is essential for effective control. With the rapid recolonization of treated sites, the weekly schedule must be strictly implemented in order to achieve control of resistant larvae. Fenthion activity levels detected in treated pits suggest that a 7-10 day schedule of retreatment would completely suppress susceptible Cx quinquefasciatus.

Animals↗

PubMed1995

An aquatic toxicological evaluation of fenthion in the context of finch control in South Africa.

Queletox, containing fenthion as active ingredient, is the avicide formulation used in South Africa to control red-billed finches (Quelea quelea). Control measures involve night spraying of roosting areas with a light aircraft. Since roosting areas often include reedbeds along riversides and on islands, proper control is difficult without exposing the aquatic environment to some risk of contamination. This study tested the acute effects of fenthion, in association with the queletox formulation, on the cladocerans Daphnia pulex and Ceriodaphnia dubia and the fish species Poecilia reticulata, Tilapia rendalli, Cyprinus carpio, and Oreochromis mossambicus. The chronic effects of fenthion on D. pulex were evaluated in a 14-day reproduction test. Mean 48-hr LC50 values estimated for D. pulex and C. dubia were 1.30 and 1.72 micrograms liter-1 respectively. For the fish estimated 96-hr LC50 values were as follows: 2.12 (P. reticulata), 2.53 (C. carpio), 2.92 (T. rendalli) and 1.71 micrograms liter-1 (O. mossambicus). In the chronic test reproduction of the exposed population was stimulated at the lowest two fenthion concentrations (0.1 and 0.6 ng liter-1), while a reproductive impairment was recorded at concentrations varying from 1 to 10 ng liter-1. Concentrations of fenthion measured in dams after spraying are given to indicate the levels of contamination that may occur. QSAR was used to estimate the toxicity of some fenthion metabolites. The results of this study reveal that fenthion, at the concentrations occurring in the environment after aerial spraying, can have marked effects on the survival and reproduction of D. pulex for long periods after spraying.

Animals↗

PubMed1994

A member of the tomato Pto gene family confers sensitivity to fenthion resulting in rapid cell death.

Leaves of tomato cultivars that contain the Pto bacterial resistance locus develop small necrotic lesions within 24 hr after exposure to fenthion, an organophosphorous insecticide. Recently, the Pto gene was isolated and shown to be a putative serine/threonine protein kinase. Pto is one member of a multigene family that is clustered within a 400-kb region on chromosome 5. Here, we report that another member of this gene family, termed Fen, is responsible for the sensitivity to fenthion. Fen was isolated by map-based cloning using closely linked DNA markers to identify a yeast artificial chromosome clone that spanned the Pto region. After transformation with the Fen gene under control of the cauliflower mosaic virus (CaMV) 35S promoter, tomato plants that are normally insensitive to fenthion rapidly developed extensive necrotic lesions upon exposure to fenthion. Two related insecticides, fensulfothion and fenitrothion, also elicited necrotic lesions specifically on Fen-transformed plants. Transgenic tomato plants harboring integrated copies of the Pto gene under control of the CaMV 35S promoter displayed sensitivity to fenthion but to a lesser extent than did wild-type fenthion-sensitive plants. The Fen protein shares 80% identity (87% similarity) with Pto but does not confer resistance to Pseudomonas syringae pv tomato. These results suggest that Pto and Fen participate in the same signal transduction pathway.

Amino Acid Sequence↗

PubMed1995

Use of a gene expression system based on potato virus X to rapidly identify and characterize a tomato Pto homolog that controls fenthion sensitivity.

A novel transient gene expression system was used to study both the tomato disease resistance gene Pto and a Pto homolog designated Fen. The gene expression system was based on potato virus X (PVX). Tomato plants that were both susceptible to strains of Pseudomonas syringae pv tomato carrying the corresponding avirulence gene avrPto and insensitive to the insecticide fenthion were infected with in vitro-generated transcripts of PVX derivatives containing either Pto or Fen. Expression of the Pto gene from the virus genome failed to elicit P.s. tomato resistance, indicating that the PVX system is not suitable for the study of Pto. However, expression of the Fen gene resulted in sensitivity to fenthion. The utility of the PVX gene expression system was further demonstrated through structure/function studies of the Fen gene. A correlation was shown between Fen protein kinase activity and the ability of this protein to confer fenthion sensitivity to tomato. Furthermore, it was demonstrated that mutation of a putative N-terminal myristoylation site, proposed to be involved in membrane targeting, rendered the Fen protein inactive. Analysis of a Pto-Fen chimeric gene allowed the fenthion sensitivity domain to be localized to the C-terminal part of the Fen protein. Interestingly, expression of the Fen kinase from the PVX genome in Nicotiana spp resulted in a fenthion-independent necrotic response. Our results support the involvement of the Fen gene in a signal transduction pathway(s).

Amino Acid Sequence↗

PubMed1986

Mechanism of potentiation of BPMC toxicity by fenthion pretreatment in mice.

The mechanism of potentiation of 2-sec-butylphenyl N-methylcarbamate (BPMC) toxicity by O,O-dimethyl O-(3-methyl-4-methylthiophenyl) phosphorothioate (fenthion) in mice was investigated in relation to BPMC metabolism in the liver. Simultaneous administration of BPMC and either one of the thiophosphates (fenthion, its sulfoxide and sulfone) in a dose of 1/40 of its LD50 resulted in a 2- to 3-fold potentiation. On the other hand, one hour pretreatment with these thiophosphates in the same dose resulted in a 7- to 9-fold potentiation of BPMC toxicity, but that with fenthion oxon resulted in only a 2-fold potentiation. Plasma levels of BPMC were significantly increased by pretreatment with the thiophosphates, but not by the oxon. In an in vitro study, an inhibition of hepatic microsomal metabolism of BPMC and a decrease of cytochrome P-450 content by thiophosphates were observed at the concentration of 10 microM, but not by 25 microM of oxon. In an in vivo study, an inhibition of hepatic microsomal metabolism of BPMC, aminopyrine and aniline by the thiophosphates pretreatment were observed in doses of 1/40 of their LD50's, but not by the oxon in doses of up to 4/10 of its LD50. Cytochrome P-450 content was decreased by the thiophosphates in doses of 4/10 of their LD50's, but not by the oxon. These results suggested that the inhibition of BPMC metabolism might be, at least in part, the mechanism for the fenthion-induced potentiation of BPMC toxicity and that desulfuration of fenthion might be responsible for the inhibition of BPMC metabolism.

Animals↗

PubMed1993

Inhibitory effect of fenthion and diazinon on the contraction of rat aorta, and its contribution to lethality.

Fenthion and diazinon, P = S type organothiophosphates which are precursors of cholinesterase inhibitors, cause remarkable atropine-insensitive hypotension in rats when administered intravenously in lethal doses. We investigated their effects on isolated rat aorta and atria to reveal the site of action. Fenthion and diazinon inhibited both types of contractions induced by high K+ solution and norepinephrine in aortic preparations from which the endothelium was removed. IC50 values (under [Ca2+] = 1.5 mM) were 2 x 10(-5) M and 7 x 10(-5) M, respectively. However, the atrial preparations were relatively resistant, since fenthion showed no effect up to 10(-3) M and diazinon at 10(-4) M exhibited a slight inhibition which was antagonized by atropine. The hypotensive effect of fenthion or diazinon was therefore attributable to the direct inhibiting action on the arterial muscle tone, which may be independent of the activation of muscarinic receptors. The results suggested that fenthion and diazinon affect movement and/or utilization of calcium in the aortic muscle cells, since an increase in the calcium concentration in the bathing solution antagonized their inhibitory effect.

Acetylcholine↗

PubMed1988

Effects of topical fenthion on blood cholinesterase and vagal tone in dogs.

A 20% fenthion (0,0-dimethyl-0-(3-methyl-4-(methylthio)-phenyl) phosphorothionate) formulation was applied topically to dogs at 8 mg/kg, 2 treatments at 14-day intervals, and 33 mg/kg, 4 treatments at 7-day intervals. Control dogs received 4 treatments at 7-day intervals of the proprietary vehicle. Following the last dose, the dogs were observed for a 14-day period. Plasma cholinesterase (ChE) exhibited a significant dose-related response with maximum inhibition to 52% and 24% of pre-dose activity occurring 4 days after the final fenthion treatment of 8 and 33 mg/kg, respectively. Erythrocyte ChE activity showed a downward trend to 32% of normal activity measured 9 days following the last treatment of fenthion at 33 mg/kg. No cholinomimetic effects were observed. All dogs were challenged with atropine sulfate (0.02 mg/kg, sc) on the last day of the observation period. A 5 min electrocardiogram was analyzed to estimate V as that portion of the variance in the R-R intervals corresponding with the normal respiratory frequency band for dogs. The mean heart period, mean heart period variance, and mean of V had significant change when measured across time in the atropine challenge (0, 25, 70, and 100 min) with a pronounced decrease at 25 min. An attenuation of the V measure in the fenthion-treated groups indicated an altered muscarinic response to atropine from prior subacute fenthion exposure.

Administration, Topical↗

PubMed1987

Effects of aerial thermal fog applications of fenthion on caged pink shrimp, mysids and sheepshead minnows.

Mosquito control applications of fenthion by aerial thermal fog equipment were studied at 2 sites in Collier County, FL, for sprays that occurred on June 20 and 23, 1984. Acute, lethal effects of fenthion deposited in these estuarine habitats were assessed for caged pink shrimp (Penaeus duorarum), mysids (Mysidopsis bahia) and sheepshead minnows (Cyprinodon variegatus). At Site 1, along a bay with substantial dilution and tidal mixing, fenthion concentrations of 1.5 and 0.29 micrograms/liter were measured in samples taken immediately after both sprays. Concentrations decreased to less than or equal to 0.020 microgram/liter 12 h postspray and no mortality was observed for caged pink shrimp and mysids. Site 2 was along a residential canal system that offered limited dilution and mixing. Maximum concentrations were 2.6 and 0.51 micrograms/liter and measurable concentrations (greater than 0.038 microgram/liter) of fenthion persisted at this site for 4 days. Fenthion concentrations in surface waters were toxic to caged pink shrimp and mysids after both sprays. No mortality occurred among caged sheepshead minnows at either site.

Animals↗

PubMed1983

Retinal degeneration in rats exposed to an organophosphate pesticide (fenthion).

Pigmented (Long-Evans) and albino (Wistar) rats were chronically exposed to an organophosphate pesticide (fenthion). Fenthion (50 mg/kg) was administered subcutaneously twice a week for 1 year; the total dosage for each animal ranged from 1.6 to 1.8 g. Concurrent with the fenthion administration, the amplitude of the scotopic electroetinogram (ERG) gradually declined, disappearing by the 12th month in all treated pigmented rats. For the albino experimental rats, however, the ERG amplitude disappeared as early as the 6th month in 7 out of 15 treated animals. Funduscopically, degeneration of the retina was observed in all rats when ERG responses had disappeared. Histopathological studies confirmed degeneration of the sensory retina and marked abnormalities in the pigment epithelium cells. Treated pigmented rats also had reduced a rhodopsin concentration in the retina by the 3rd month even though the photoreceptors were structurally normal. Interestingly, the plasma vitamin A levels remained normal and liver stores of vitamin A actually increased during the course of the study. Levels of butylcholinesterase in plasma and liver, on the other hand, were extremely reduced after 3 months of fenthion treatment. In general, the biochemical and functional (ERG) changes appeared before any structural damage could be detected in the retina.

Animals↗

PubMed1969

Mechanisms of resistance to fenthion in Culex pipiens fatigans Wied.

One of the insecticides of choice to control the mosquito Culex pipiens fatigans, a vector of Bancroftian filariasis, is fenthion. The mechanism of resistance to this insecticide which could develop in C. p. fatigans was investigated in a strain from Rangoon, Burma, made 8 times more fenthion-resistant than normal by laboratory selection, by exposing the larvae to (32)P-fenthion and examining the metabolites.Larvae of the resistant strain were found to absorb about half as much fenthion as those of the corresponding normal strain, and they degraded proportionately about twice the amount absorbed to water-soluble metabolites. Thus, the larval content of chloroform-soluble toxicants remaining was only one-third to one-seventh as much in the resistant as in the normal strain. The production of the non-toxic hydrolytic (water-soluble) metabolites was 70% greater in the resistant strain in absolute terms, despite the lower amount absorbed into the larvae. The greatest increase (4-fold) was in the oxonase activity, although the thionase activity was more important in both strains.Esterase zymograms from agar-gel electrophoresis revealed a principal band which was much more intense in the resistant than in the susceptible strain, as judged by its hydrolysis of alpha- and beta-naphthyl acetates and phosphates. This band was comparatively insensitive to the toxicant fenoxon, and could hydrolyse it.

Animals↗

PubMed1985

Determination of the half life of fenthion in New Zealand White rabbits using three routes of administration.

The purpose of this research was to determine if the route of administration influenced the biological half life of fenthion, an organophosphorous insecticide. Twenty mg/kg fenthion was given to groups of New Zealand White Rabbits via the oral, subcutaneous and intravenous routes respectively. The distribution of fenthion in the blood of New Zealand rabbits followed an open two compartment model. There were no significant differences in the kinetic parameters (2, beta, K12, K21, Kel) derived for the three different routes of administration. The biological half life of slightly over 11 hours, did not differ significantly with the route of administration.

Administration, Oral↗

PubMed1988

Effects of multiple dosing of fenthion, fenitrothion, and desbromoleptophos in young chicks.

The effects of multiple doses of desbromoleptophos, fenitrothion, and pure fenthion on brain acetylcholinesterase (AChE), brain neurotoxic esterase (NTE), and walking were investigated in immature chicks, below the age of sensitivity to organophosphorus ester-induced delayed neurotoxicity (OPIDN). Ten milligrams per kilogram per day of delayed neurotoxicant desbromoleptophos (DBL), 15 mg/kg.d of the non-neurotoxicant fenitrothion (FTR), and 3 mg/kg.d of the suspected neurotoxicant fenthion (FEN) were given orally for 7 d to 3-d-old chicks. Behavioral testing was performed for treated and control chicks on various days after treatment. Brain NTE and AChE assays were carried out for treated and control chicks on each day of behavioral testing. DBL altered gait and inhibited both NTE and AChE; FEN altered gait and inhibited AChE but not NTE; and FTR did not affect gait, while inhibiting AChE but not NTE. NTE and AChE inhibition were 70% and 55%, respectively, 24 h after the last treatment, for the chicks treated with DBL. NTE returned to normal levels by around d 25 and AChE by 20 d after the last treatment. FTR caused more than 50% AChE inhibition but no NTE inhibition, 24 h after last treatment. NTE inhibition for the FEN-treated chicks never exceeded 11% during the whole period of the experiment, whereas 54% inhibition of AChE was seen 1 d after last treatment. DBL and FEN significantly altered the gait of treated chicks, but the non-OPIDN-inducing FTR did not. This study confirms that alterations in the gait of young chicks are not direct consequences of either NTE or AChE inhibition, and that fenthion-induced functional deficits can be distinguished from classical OPIDN.

Animals↗

PubMed1992

Observation on a human intentional poisoning case by the organophosphorus insecticide fenthion.

A case of acute poisoning by oral ingestion of fenthion is reported. Plasma cholinesterase activity and fenthion whole blood concentration were thoroughly evaluated during the therapeutic intervention that consisted in administration of atropine, toxogonine and fresh plasma. Correlation studies between clinical signs, cholinesterase activity and fenthion levels revealed that pChE activity was not as helpful as the patient's clinical status in determining when the atropine infusion could be stopped. Moreover pChE was also useless in signaling sudden relapses. It is concluded, based on this case, that supportive care combined with antidotal therapy remains the cornerstone of treatment specially in severe acute poisoning cases.

Adult↗

PubMed1990

A study of the pesticide fenthion: toxicity, mutagenicity, and influence on tissue enzymes.

In this paper results of acute toxicity (oral and dermal), cumulative toxicity, subchronic toxicity, and conjunctiva irritation tests are reported. The mutagenic effects of fenthion, using SCE (in vivo) and UDS (in vitro) as indicators, were also tested. Histochemical changes in enzyme activities (including AChE, ATPase, and AKP) in tissues were observed. The results showed that the acute toxicity of fenthion belongs to highly toxic category. The highly cumulative effect of fenthion was also observed. The subchronic toxicity test, however, did not reveal any abnormal effects except the inhibition of ChE activity in plasma. The dose and ChE activity relationship equation was Y = 0.82x + 4.71. The SCE and UDS tests revealed no mutagenic potential. In histochemical experiments we found that AChE activity in tissues was markedly inhibited. AKP and ATPase activities at the cortex renis were increased in the treated rats.

Acetylcholinesterase↗

PubMed1995

In vitro cytotoxicity of fenthion and related metabolites in human neuroblastoma cell lines.

The aim of our research was the evaluation in vitro of the neurotoxic effects of fenthion and its metabolites on human neuroblastoma cells, as a model for their toxicity in humans. The results indicate that 24 hours exposure was sufficient to produce dose related effects on SK-N-BE and IMR 32 cell viability causing detachment and loss of cells at the effective doses. In the two cell lines fenthion metabolites display an increased cytotoxicity respect to the parent compound with a distinct pattern of toxicity on neurons. Our data suggest that cultured neuronal cells of human origin are discriminating experimental systems, sensitive to minor differences, of correlating in vivo and in vitro neurotoxicants.

Cell Survival↗