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PubMed1985

The effects of phenobarbital, atropine, L-alpha-methyldopa, and DL-propranolol on dieldrin-induced hyperglycemia in the adult rat.

The hyperglycemic response of adult male Wistar rats given dieldrin (63 mg/kg, po) and either phenobarbital (40 mg/kg, ip), atropine (4 mg/kg, sc), L-alpha-methyldopa (200 mg/kg, ip), or DL-propranolol (8 mg/kg, sc) was studied. The hyperglycemia was maximal (73% above control values) 2 hr after exposure to dieldrin alone. Phenobarbital reduced the hyperglycemia by 41% and abolished dieldrin-induced convulsions. It also prevented the increases that dieldrin causes in hepatic phosphoenolpyruvate carboxykinase (PEPCK) activity. These results suggest that the dieldrin-induced hyperglycemia is mediated via the CNS. Atropine prevented the hyperglycemia for 2 hr and delayed the attainment of maximal glucose concentrations for another 2 hr. However, additional atropine 4, 8, 12, and 18 hr after the dieldrin had no effect. Atropine also increased (125%) the time to the onset of dieldrin-induced convulsions. It did not alter hepatic PEPCK activity. L-alpha-Methyldopa decreased (24%) the hyperglycemic response in the first 2 hr after dieldrin treatment. It caused similar reductions in blood glucose when given during the peak hyperglycemic response. L-alpha-Methyldopa also reduced (49%) the dieldrin-effected increase in hepatic PEPCK activity. DL-Propranolol did not alter the effects of dieldrin. Thus these data suggest that the dieldrin-induced hyperglycemia is mediated by the CNS, primarily via enhanced cholinergic activity and secondarily by increased alpha-adrenergic activity. It is suggested that the pancreas responds to the cholinergic outflow by increasing the secretion of glucagon while simultaneously responding to the alpha-adrenergic outflow by decreasing insulin secretion.

Administration, Oral↗
PubMed1991

Metabolism of aldrin to dieldrin by rat skin following topical application.

Metabolism of the pesticide aldrin to dieldrin in the rat was studied following topical and ip administration of 0.1-10 mg aldrin/kg body weight. When aldrin was applied topically to the dorsal skin at a dose of 10 mg/kg body weight, absorption was less efficient than after ip administration; lower blood levels of aldrin and dieldrin were seen and peak dieldrin levels were delayed. After ip administration of 1 or 10 mg aldrin/kg body weight, dieldrin was found at similar concentrations in the dorsal and ventral skin 7 hr later, whereas 7 hr after topical administration of 10 mg aldrin/kg, the dieldrin concentration in the skin at the dorsal site of application was four times higher than that at a ventral skin site. Similar differences in dieldrin concentrations between dorsal and ventral skin persisted throughout the 7-hr period following topical application. The results indicate that topically applied aldrin is metabolized to dieldrin in the skin during absorption, but the overall proportion of metabolism that takes place in the skin is small compared with the contribution of the liver. Dieldrin was not detected in the ventral skin remote from the application site 1 hr after topical application of aldrin, whereas a dieldrin concentration of 2.2 nmol/g was detected in the skin of the application site at this time; more than 99% of this dieldrin was probably formed locally by dermal metabolism of percutaneously absorbed aldrin. The efficiency of conversion of applied aldrin to dieldrin decreased with increasing aldrin dose in the range 0.1 to 10 mg/kg.

Administration, Topical↗
PubMed1980

Overview of human exposure to dieldrin residues in the environment and current trends of residue levels in tissue.

An overview of available literature indicates that dieldrin residues are still found routinely in soil, air, water, and food, despite the 1974 U.S. Environmental Protection Agency ban on the use of aldrin and dieldrin. Dieldrin residue levels in environmental substrates, which are indicative of aldrin or dieldrin use, have decreased significantly since the mid-1960s, the peak usage years. However, human tissue studies do not show a corresponding decline in dieldrin residue levels. Thirteen studies, conducted between 1963 and 1976, show that average dieldrin levels in human adipose tissue and human milk fat remain between 0.160 ppm and 0.220 ppm. Other studies suggest that an equilibrium exists in the distribution of dieldrin among various tissues in humans, including blood, fat, brain, and liver. This relationship indicates that the concentration of dieldrin in any tissue may be used as an index of total body burden. Thus it appears that the concentration of dieldrin in the human body has reached a constant level at which the amount ingested and absorbed equals the amount metabolized and excreted. The mechanism of the stable concentrations is unknown, as are the possible health effects of chronic, low-level exposure to dieldrin.

Adipose Tissue↗
PubMed1991

Teratogenesis, toxicity, and bioconcentration in frogs exposed to dieldrin.

Teratogenesis, acute and chronic toxicity, growth and bioconcentration were investigated in various life stages (embryos, tadpoles, juveniles, adults) of the frogs Xenopus laevis (African clawed frog), Rana catesbeiana (bullfrog) and Rana pipiens (leopard frog) exposed to aqueous dieldrin in static-renewal and flow-through systems in a study on the development of wildlife-based water quality criteria. R. catesbeiana was the most sensitive tadpole in acute tests; X. laevis was the most sensitive in embryo-larval and chronic tadpole tests. Tadpole 96-h LC50s ranged from 40.4 to 49.5 micrograms/L dieldrin for X. laevis, from 8.7 to 30.3 micrograms/L for R. catesbeiana and was 71.3 micrograms/L for R. pipiens. The 24-day LC50 for X. laevis tadpoles was 5.5 micrograms/L dieldrin; the 28-day LC50 for R. pipiens tadpoles was 8.3 micrograms/L. Adult R. pipiens had a 28-day LC50 of 53.4 micrograms/L dieldrin. Gross spinal deformities in embryo-larval tests were observed at dieldrin concentrations as low as 1.3 micrograms/L after 10-days exposure to X. laevis and at 25.4 micrograms/L for a 21-day exposure to R. catesbeiana. Mean X. laevis 14 to 21-day LOAEL (Lowest Observed Adverse Effect Level) and NOAEL (No Observed Adverse Effect Level) values for embryo-larval tests (25.5 and 11.0 micrograms/L dieldrin, respectively) were virtually the same as the 21-day single test values obtained for R. catesbeiana (25.1 and 11.0 micrograms/L dieldrin). Mean 14 to 24-day X. laevis LOAEL and NOAEL values for tadpole chronic tests (1.6 and less than 1.4 micrograms/L dieldrin, respectively) were lower than the 28-day single test values obtained for R. pipiens (4.1 and 1.9 micrograms/L, respectively). Tissue dieldrin levels at the LC50, LOAEL and NOAEL in the tadpole acute tests were fairly similar between X. laevis (11, 24 and 7 micrograms/g, respectively) and R. catesbeiana (means of 8.6, 12.0 and 1.2 micrograms/g, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Dual action of the cyclodiene insecticide dieldrin on the gamma-aminobutyric acid receptor-chloride channel complex of rat dorsal root ganglion neurons.

The gamma-aminobutyric acidA (GABAA) receptor-chloride channel complex is known to be the target site of dieldrin, a cyclodiene insecticide, and lindane. In order to elucidate the mechanisms of dieldrin interaction with the GABA system, whole-cell patch clamp experiments were performed with rat dorsal root ganglion neurons in primary culture. When co-applied with GABA, dieldrin exerted a dual effect on the GABA-induced chloride current. The chloride current induced by 10 microM GABA was greatly enhanced by the first 20-sec co-application with 1 microM dieldrin, but the enhancement subsided during repeated co-applications, and the current was eventually suppressed below the control level. No recovery occurred after a prolonged washing with dieldrin-free solution. Desensitization of the chloride current was accelerated by dieldrin. However, when the period of co-application was limited to 2 sec, which was short enought to avoid desensitization, no suppression of current was observed during repeated co-applications and recovery occurred after washing. The desensitization and suppression occurred with an EC50 of 92 nM, whereas the enhancement required a higher EC50 at 754 nM. The GABA-induced chloride current comprised two components, one with a high sensitivity to dieldrin suppression with an EC50 of 5 nM and the other with a lower sensitivity with an EC50 of 92 nM. Dieldrin exerted its inhibitory effect on the GABA-induced current regardless of the presence or absence of pentobarbital and chlordiazepoxide. However, its effect was attenuated by the presence of picrotoxin. Furthermore, dieldrin suppressed the GABA-induced chloride current in a noncompetitive manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Regulation of GABA(A) receptor subunit mRNA expression by the pesticide dieldrin in embryonic brainstem cultures: a quantitative, competitive reverse transcription-polymerase chain reaction study.

Cyclodiene organochlorine pesticides, such as dieldrin, inhibit gamma-aminobutyric acid (GABA)ergic neurotransmission by blocking the Cl- channel of GABA(A) receptors. This action may make the developing nervous system especially vulnerable to these neurotoxins, which could interfere with the trophic actions of GABA on developing neurons and alter expression of GABA(A) receptors. We have used an in vitro model to determine whether exposure to dieldrin alters developmental expression of GABA(A) receptor subunit mRNA transcripts. Dissociated cell cultures were prepared from embryonic day 14 (E14) brainstem and cultured in serum-containing medium for 1 day in vitro (DIV), then treated for 2 DIV with 10 microM dieldrin in serum-free medium. This dose was based on preliminary experiments and previous studies (Nagata et al.: Brain Res 645:19-26, 1994; Pomes et al.: J Pharmacol Exp Ther 271:1616-1623, 1994). Absolute amounts of alpha1, beta3, gamma1, gamma2S and gamma2L mRNA transcripts were quantified in these cultures by quantitative, competitive reverse transcription-polymerase chain reaction (RT-PCR) using subunit-selective internal standards. The most abundant GABA(A) subunit transcript was beta3, which was much more highly expressed than gamma2S, gamma1, gamma2L, or alpha1 subunit mRNAs. Dieldrin differentially regulated expression of these transcripts. Levels of beta3 subunit transcripts were significantly increased (by 300%) by dieldrin, whereas expression of gamma2S and gamma2L transcripts were decreased (by 50% and 40%, respectively). However, dieldrin did not alter the ratio of gamma2S to gamma2L transcripts, indicating that it did not affect alternative splicing of gamma2 transcripts. Dieldrin appeared to increase expression of alpha1 subunit transcripts, but this effect was not statistically significant. Dieldrin did not significantly alter expression of gamma1 subunit transcripts. These results support the hypothesis that in utero exposure to cyclodiene pesticides could pose a risk to the developing brain by virtue of their ability to alter gene expression of GABA(A) receptor subunits, which could produce GABA(A) receptors with altered functional properties.

Animals↗
PubMed1998

Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures.

Dieldrin can be retained for decades in lipid-rich tissue and has been measured in some postmortem PD brains. Dieldrin has been reported to deplete brain monoamines in several species and has been shown to inhibit mitochondrial respiration. To further investigate the possibility that it may be involved in the pathogenesis of parkinsonism, its toxicity for dopaminergic (DA) neurons was assessed in a mesencephalic cell culture model. Primary neuronal cultures of mesencephalic neurons were prepared from fetal rats or fetal mice, grown for 1 week and incubated with Dieldrin (0.01-100 microM) for 24 or 48 h. Toxicity for DA neurons was determined by measuring density of surviving tyrosine hydroxylase immunoreactive (TH-ir) cells. Toxicity for gamma-aminobutyric acid (GABA)-ergic neurons was determined by measuring survival of glutamate decarboxylase (GAD)-ir neurons. General, nonselective cytotoxicity was determined by counting cells visualized by phase contrast microscopy or by DAPI-stained cells with fluorescence microscopy. Dieldrin exposure for 24 h resulted in a dose-dependent decrease in survival of TH-IR cells (DA neurons) with a 50% decrease (EC50) produced by 12 microM in rat mesencephalic cultures. Dieldrin also produced a dose- and time-dependent decrease in mouse DA-ergic and GABA-ergic neurons in mouse mesencephalic cultures. GABA-ergic neurons were less sensitive to the toxin compared to DA-ergic neurons. Cellular uptake of 3H-DA was also affected by lower concentrations of Dieldrin (EC50 = 7.98 microM) than uptake of 3H-GABA (EC50 = 43 microM). Thus, Dieldrin appears to be a relatively selective DA-ergic neurotoxin in mesencephalic cultures. Dieldrin, which may be ubiquitous in the environment, is proposed as an agent which can initiate and promote dopaminergic neurodegeneration in susceptible individuals.

Animals↗
PubMed1996

Subchronic effects of dieldrin and phenobarbital on hepatic DNA synthesis in mice and rats.

Dieldrin, an organochlorine pesticide, has been shown to be hepatocarcinogenic in mice but not rats. Phenobarbital, in contrast, induces hepatic tumors in both mice and rats. Previous studies have shown that acute dietary exposure of rats or mice to either dieldrin or phenobarbital produces several liver changes, including centrilobular hypertrophy, induction of hepatic cytochrome P450, and increased liver weight. The present study examined the subchronic effect of dieldrin (0.1, 1.0, 3.0, 10.0 mg dieldrin/kg diet) and phenobarbital (10, 50, 100, 500 mg phenobarbital/kg diet) on the induction of hepatic DNA synthesis and hepatocyte lethality in male B6C3F1 mice and male F344 rats. Eight-week-old animals were treated as above and evaluated for hepatic DNA synthesis after 7, 14, 21, 28, and 90 days of continual treatment to dieldrin or phenobarbital. Maximal induction of hepatic DNA synthesis in mice was seen at the 14-, 21-, and 28-day sampling times. In rats, no significant increase in hepatic DNA synthesis or hepatocyte lethality was observed at any dose of dieldrin investigated. Phenobarbital produced a significant increase in hepatic DNA synthesis in both rat and mouse liver following 7 days of treatment. The induction of DNA synthesis in rat liver was transient, with the labeling index returning to control levels by 14 days of treatment. In contrast, mice treated with phenobarbital showed a significant increase in hepatic DNA synthesis throughout the treatment. In both mice and rats, dieldrin and phenobarbital induced hepatic DNA synthesis selectively in the centrilobular region of the hepatic lobule. The lack of an increase in serum enzymes indicative of hepatic damage and the absence of liver histopathology in mice or rats fed dieldrin or phenobarbital indicate that the induction of DNA synthesis was not mediated by a cytolethal, compensatory hyperplastic response, suggesting a mitogenic mechanism. Therefore, the species-specific induction of hepatic DNA synthesis by either dieldrin or phenobarbital correlated with the previously observed species-specific induction of hepatic cancer by these two compounds.

Analysis of Variance↗
PubMed1994

Selective effects of dieldrin on the GABAA receptor-channel subunits expressed in human embryonic kidney cells.

We have recently demonstrated that the cyclodiene insecticide dieldrin modulates the kinetics of the GABAA receptor-chloride channel complex of rat dorsal root ganglion neurons in a complex manner, causing both stimulatory and inhibitory effects. We now report that the differential effects of dieldrin on the GABA-induced chloride current of human embryonic kidney cells expressing three different combinations of alpha, beta and gamma subunits. The EC50 values for GABA induction of current were estimated to be 9.8 microM for the alpha 1 beta 2 gamma 2s combination, 2.0 microM for the alpha 1 beta 2 combination and 3.0 microM for the alpha 6 beta 2 gamma 2s combination. When co-applied with GABA, dieldrin exerted a dual effect, enhancement and suppression, on the GABA-induced chloride currents in the alpha 1 beta 2 gamma 2s and alpha 6 beta 2 gamma 2s combinations. However, only suppression was observed in the alpha 1 beta 2 combination, indicating that the gamma subunit is necessary for dieldrin's enhancing effect. Dieldrin was more efficacious in enhancing the current in the alpha 6 beta 2 gamma 2s combination than in the alpha 1 beta 2 gamma 2s combination, indicating some specific role of alpha subunits in the dieldrin enhancement of current. Dieldrin suppressed the GABA-induced current in a non-competitive manner, with an EC50 value of 2.1 microM for alpha 1 beta 2 gamma 2s, 2.8 microM for alpha 1 beta 2 and 1.0 microM for alpha 6 beta 2 gamma 2s combination. These results indicated that dieldrin suppression did not require specific subunit combinations among the three tested.

Cell Line↗
PubMed1985

Increased susceptibility to mouse hepatitis virus 3 of peritoneal macrophages exposed to dieldrin.

Interaction of a single dose (36 mg/kg body wt) of the organochlorine pesticide dieldrin with mouse peritoneal macrophages was examined in C57Bl/6, (C57Bl/6 X A/J)F1, and A/J strains of different genetic resistance to mouse hepatitis virus 3 (MHV3) infection. In vivo studies showed increased susceptibility to MHV3 acute disease of C57Bl/6 and (C57Bl/6 X A/J)F1 animals challenged with the pesticide. Significant decrease of mean time of death in dieldrin-exposed, MHV3-infected susceptible C57Bl/6 mice was observed similarly upon po or ip administration of a single, sublethal dose of dieldrin. In addition, decrease of humoral response to the virus was quantified by determination of anti-MHV3 IgG antibodies in spleen cell supernatant fractions and in blood sera of dieldrin-exposed C57Bl/6 mice. A single dose of dieldrin did not alter the in vivo resistance of A/J animals to acute MHV3 disease. The resistant A/J mice, however, showed increased mortality upon two subsequent exposures to dieldrin followed by infection with high lethal doses of MHV3. Phagocytic activity, cell adherence capacity, and attachment and uptake of 3H-radiolabeled MHV3 by C57Bl/6 peritoneal macrophages were determined by in vitro studies. These affector activities of peritoneal macrophages were slightly decreased or unchanged in cells originating from animals exposed to the pesticide. However, the intrinsic activity of MHV3 restriction appeared to be affected in macrophages derived from dieldrin-treated animals: (i) peritoneal C57Bl/6 macrophages collected from the early phase of acute MHV3 disease contained increased MHV3 antigen and (ii) increased cytolysis was observed after in vitro MHV3 infection of macrophages originating from dieldrin-exposed C57Bl/6 mice.

Animals↗
PubMed1998

Modulation of 7,12-dimethylbenz[a]anthracene disposition and hepatocarcinogenesis by dieldrin and chlordecone in rainbow trout.

The present study examined whether modified xenobiotic transport, resulting from chlordecone (CD) or dieldrin pretreatment, would alter polycyclic aromatic hydrocarbon (PAH) or organochlorine (OC) target organ doses and subsequent tumor organospecificity or incidence rates in rainbow trout. Additionally, the potential for exposure to dieldrin or CD, following PAH exposure, to enhance tumor incidence was assessed. Evaluation of CD pretreatment effects on [14C]CD disposition in trout was conducted following two i.p. (0-15 mg/kg) and two dietary (0-0.4 mg/kg/d) pretreatment regimes. To assess the influence of OC pretreatment on cancer induced by the PAH 7,12-dimethylbenz[a]anthracene (DMBA), juvenile trout were fed control, CD (0.1, 0.4 mg/kg/d), or dieldrin (0.1, 0.3 mg/kg/d) diets for 9 wk, received a waterborne [3H]DMBA exposure (1 mg/L, 20 h), and resumed control, CD, or dieldrin diets for 33 wk. [3H]DMBA disposition and hepatic [3H]DMBA binding were examined immediately and 24 h after exposure. Hepatic and stomach tumor incidences were determined 33 wk after DMBA exposure. CD pretreatment did not influence [14C]CD or [3H]DMBA hepatic concentrations, hepatic [3H]DMBA DNA binding, or hepatic/stomach tumor incidence. It did, however, elevate bile [14C]CD and [3H]DMBA concentrations. Postinitiation exposure to CD weakly enhanced DMBA-induced hepatic tumor incidence at the low but not the high CD dose. Dieldrin pretreatment did not influence stomach [3H]DMBA equivalents or stomach tumor incidence but did cause an elevation in biliary and hepatic concentrations of [3H]DMBA equivalents. [3H]DMBA binding to liver DNA was significantly increased and hepatic tumor incidence was elevated by dieldrin pretreatment. Dieldrin treatment following DMBA initiation did not enhance hepatic or stomach tumor incidence. Ecoepidemiology studies, to date, have reported correlations between the co-occurrence of PAHs and OCs and elevated tumor incidence in feral fish, but cause-and-effect relationships have been difficult to establish. The results of the present study confirm that OCs, such as dieldrin and CD, play a role in modifying PAH-induced carcinogenesis in fish.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1976

Effect of dieldrin and calcium on the performance of adult Japanese quail (Coturnix coturnix japonica).

Two experiments were conducted to determine the effects of dieldrin and calcium on reproductive performance of quail. At 25% egg production the quail received diets containing 0,10 or 25 p.p.m. of dieldrin for 6, 28-day periods in experiment 1 and 0, 5, or 25 p.p.m. of dieldrin for 4, 28-day periods in experiment 2. Pesticide treatments were employed with diets containing 0.5% and 3.0% calcium. The results show that egg shell thickness, cracked eggs, egg production, feed consumption, egg weights, fertility, hatchability and body weights were not affected by dieldrin treatments. However, egg shell thickness, cracked eggs, egg production and hatchability were adversely affected by the lower calcium level. Female body weights were consistently heavier for the low calcium diet. Mortality increased in the presence of 10 and especially 25 p.p.m. of dieldrin. Livability of chicks from hens receiving rations with 10 and 25 p.p.m. of dieldrin was significantly lower than those fed no dieldrin. In summary, dieldrin was without effect on egg shell quality or other reproductive factors but did exert a detrimental effect on adult mortality and livability of progeny.

Animals↗
PubMed1988

Dieldrin-induced changes in isoenzyme composition in the livers of CF-1 mice.

The isoenzyme composition of lactic dehydrogenase (LDH), pyruvate kinase (PK) and alanine-aminotransferase was determined in the livers of CF-1 mice exposed to 0, 5 or 10 ppm dieldrin in the diet, over a period of 14 months. This study was carried out to evaluate whether the liver tumor promoter dieldrin advances the biological age of CF-1 mouse liver. Oral dieldrin exposure induced a dose-dependent shift towards the fetal types of lactic dehydrogenase and pyruvate kinase, within 1.5 months of initiation of treatment. After the initial shift, no additional dieldrin-dependent changes were found in CF-1 mouse liver throughout the experimental observation period. Thus, the initial shifts in isoenzyme composition of LDH and PK appear to reflect the adaptation of the liver to increased functional demands imposed by dieldrin treatment. The expression of the cytoplasmic A-alanine-aminotransferase isoenzyme decreased with age in untreated control mice. Dieldrin treatment enhanced this process in a dose-dependent manner. These data suggest that dieldrin treatment can accelerate age-dependent changes in gene expression.

Aging↗
PubMed1999

Effects of dieldrin on life stages of the African catfish, Clarias gariepinus (Burchell).

Early life stages of Clarias gariepinus were found to be less sensitive to acute dieldrin toxicity than were those of Nile tilapia, Oreochromis niloticus; 96-h LC50 values for 37-day-old fry were 11. 7 and 4.95 microg liter-1, respectively. The growth of C. gariepinus fry was unaffected by 30 days of exposure to 2.4 microg liter-1 dieldrin under static conditions with water renewal every 96 h, whereas growth of O. niloticus fry was significantly reduced. Adult C. gariepinus exposed to dieldrin for 30 days, with water changes every 96 h, rapidly absorbed dieldrin from aqueous solution. Dieldrin concentration was measured just before water changes and from an initial concentration of 4.0 microg liter-1, stabilized after 12 days at about 0.075 microg liter-1, indicating that a balance between uptake and excretion and metabolism had been achieved. Dieldrin accumulated in the tissues during these exposures, especially in the liver, where after 30 days the bioconcentration factor relative to initial concentration was about 900. Chronic exposure of C. gariepinus to dieldrin had no effect on blood hematocrit and hemoglobin, but appeared to slow the growth of catfish and had a clear negative effect on the reproductive potential of mature females.

Animals↗
PubMedDate not supplied

Comparative behavior of dieldrin and carbofuran in the field.

To measure the amounts of dieldrin and carbofuran lost to the environment, we incorporated them into soils in small (0.6-1.1 ha) watersheds in separate years. The disappearance of each was monitored by periodically measuring residues in the soil, runoff, maize plants, and overlying air (dieldrin only). Soil residues were nonuniformly distributed. Best estimate for the time for 95% disappearance of dieldrin from the soil was 12.8 years. Carbofuran disappearance conformed to a first-order reaction and gave 95% disappearance times ranging from 145 to 434 days, depending on soil pH, moisture, and temperature. Runoff losses of both pesticides were highest in rainfalls during the first month after application. Over the season, dieldrin losses ranged up to 2.3% of that applied and were concentrated in the solids. Carbofuran losses in runoff occurred largely in the water and comprised up to 1.9% of the application. More than twice as much carbofuran (and metabolites) as dieldrin was accumulated in the maize plants, mainly in the leaves. Volatilization was an important route of dieldrin loss, amounting in the first year to 4.5% of that applied. Volatility of carbofuran, which was only 1/18th that of dieldrin in a laboratory test, was not measured in the field. The data show that use of optimum management practices can substantially reduce the environmental impact of agricultural applications of these pesticides.

Air↗
PubMed1978

Dieldrin-14C elimination from chickens.

A series of experiments was conducted with chickens contaminated with dieldrin-14C to find ways of accelerating the elimination of dieldrin from their bodies. The results of these experiments indicated that charcoal, imbiber beads, and the anion exchanges resins, Dowex XFS-4022 and Dowex SBR-C1, would not be useful agents for increasing the amount of dieldrin eliminated via feces (droppings) of chickens. Further, imbiber beads coalesced in the gizzard of the chickens and reduced their appetites. The anion exchange resin, cholestyramine, might be useful as gastrointestinal absorbant for increasing dieldrin elimination in chickens because it increased carbon-14 elimination in droppings, but its effect on carbon-14 residues in carcasses was not clear. We elected not to investigate this compound further. Probucol, investigated because it might alter gastrointestinal absorption or blood physiology that would affect dieldrin elimination, did not increase dieldrin elimination. Severe starvation was the only method investigated that clearly was useful for increasing dieldrin elimination because it increased carbon-14 elimination in droppings and reduced carbon-14 residues in carcasses.

Animals↗
PubMedDate not supplied

Suppression of avidin processing and presentation by mouse macrophages after sublethal exposure to dieldrin.

The molecular events in macrophage antigen processing and presentation were examined to determine the possible site(s) of cell-xenobiotic interaction. Antigenic processing by mouse peritoneal macrophages of a single protein antigen, avidin, was significantly suppressed following sublethal exposure of animals to an organochlorine pesticide, dieldrin. Exposure of C57B1/6 female mice to dieldrin affected the in vitro uptake of [methyl-14C]avidin by peritoneal macrophages and markedly decreased phagocytosis of fluorescein-labelled microspheres and Salmonella typhimurium. Release of the processed avidin, determined by immunochemical quantification of immunogenic avidin and by bioassay of immunogenicity of the released antigen, was also markedly affected. Dieldrin markedly affected presentation of avidin on the macrophage surface, observed by cytoimmunochemical staining of the antigen with fluorescent antibody and flow cytometry. Inhibition of the release of processed avidin was dieldrin dose- and time-dependent, following single sublethal intraperitoneal (ip) exposure to the pesticide. The antigenic properties of processed avidin, determined by biological assay using lymphocyte cultures of normal C57B1/6 mice primed with avidin, were proportional to the antigen concentration in supernatants of macrophage cultures, for both vehicle controls and dieldrin-exposed animals. This observation and analysis of the kinetics of release of processed avidin by macrophages from control and dieldrin-exposed animals suggested that the release of processed avidin, but not the immunogenicity of the antigen itself, was affected by the pesticide exposure. Generally, impairment of avidin processing and presentation appeared to be more dramatic than other pesticide-related injuries to macrophages, such as the uptake of the antigen. In conclusion, antigen processing could be a sensitive target for dieldrin-related injury of macrophage functional activities, which, in consequence, could produce suppression of the humoral immune response.

Animals↗
PubMed1988

Virus-pesticide interactions with murine cellular immunity after sublethal exposure to dieldrin and aminocarb.

Interaction of two potential immunosuppressive factors, sublethal pesticide exposure and viral inhibition of lymphocyte mitogenesis, was examined in mixed lymphocyte reaction (MLR). Inbred (C57Bl/6 x A/J)F mice, semisusceptible to mouse hepatitis virus 3 (MHV3) infection were exposed to selected pesticides and subsequently infected with the MHV3 virus. The mortality of animals was examined as a function of pesticide exposure. Two pesticides were selected for further studies: the organochlorine pesticide dieldrin, which increased the cumulative mortality of animals, and the carbamate pesticide aminocarb, which did not affect the virus-induced cumulative mortality of animals. Spleen lymphocytes from dieldrin- and aminocarb-exposed C57Bl/6 mice (susceptible to MHV3 infection) were used as responder cells in one-way MLR. A marked immunosuppression of the MLR proliferative response was observed in the dieldrin group, whereas sublethal exposure to aminocarb did not affect the in vitro MLR response. The MLR cultures were subsequently infected in vitro with the MHV3 virus, which resulted in a time-dependent and virus dose-dependent inhibition of lymphocyte proliferation. However, no synergism was observed with the addition of either the MHV3 virus-induced inhibition of in vitro MLR lymphoproliferative response or dieldrin-related immunosuppression, since in vitro MHV3 infection of cells from dieldrin-exposed mice did not aggravate the dieldrin-related immunosuppression. In addition, no "hidden" aminocarb-related damage of the lymphoproliferative response was noted, as the kinetics of the virus-induced inhibition in the aminocarb group were analogous to the control. In conclusion, dieldrin-induced immunosuppression of the cellular immune response, rather than MHV3 virus-induced inhibition of lymphoproliferative activity itself, was the primary factor potentially responsible for the impaired cellular response. Furthermore, the data support the observation that cell-mediated immunity can be a potential target for the adverse effects of pesticide exposure.

Animals↗