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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↗

PubMed2004

Dieldrin promotes proteolytic cleavage of poly(ADP-ribose) polymerase and apoptosis in dopaminergic cells: protective effect of mitochondrial anti-apoptotic protein Bcl-2.

Previously, we demonstrated that the organochlorine pesticide dieldrin induces mitochondrial depolarization, caspase-3 activation and apoptosis in dopaminergic PC12 cells. We also demonstrated that protein kinase Cdelta (PKCdelta), a member of a novel PKC family of proteins, is proteolytically activated by caspase-3 to mediate apoptotic cell death processes. In the present study, we have further characterized the protective effect of the major mitochondrial anti-apoptotic protein Bcl-2 against dieldrin-induced apoptotic events in dopaminergic cells. Exposure to dieldrin (30-100 microM) produced significant cytotoxicity and caspase-3 activation within 3h in vector-transfected PC12 cells, whereas human Bcl-2-transfected PC12 cells were almost completely resistant to dieldrin-induced cytotoxicity and caspase-3 activation. Also, dieldrin (30-300 microM) treatment induced proteolytic cleavage of poly(ADP-ribose) polymerase (PARP), which was blocked by pretreatment with caspase-3 inhibitors Z-DEVD-FMK and Z-VAD-FMK. Additionally, dieldrin-induced chromatin condensation and DNA fragmentation were completely blocked in Bcl-2-overexpressed PC12 cells as compared to vector control cells. Together, these results clearly indicate that overexpression of mitochondrial anti-apoptotic protein protects against dieldrin-induced apoptotic cell death and further suggest that dieldrin primarily alters mitochondrial function to initiate apoptotic cell death in dopaminergic cells.

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↗

PubMed2000

Spatial and temporal regulation of the pesticide dieldrin within industrial catchments

The river catchments of south Yorkshire support a very high density of wool processing industries. Dieldrin was once used as a moth proofing agent, as a sheep dip, and as a pesticide to protect wool fleeces during storage and transport, all of which caused pollution of these catchments due to textile processing. Weekly sampling of four of these rivers revealed two classes of dieldrin contamination: the Aire and Calder (the rivers which support very high concentrations of wool processing industries) had higher concentrations (averaging approximately 3 ng/l) than the Don and Trent (approximately 1 ng/l). The average flux of dieldrin from these rivers into the Humber estuary was 9.8 g/day, with the Aire (of which the Calder is a tributary) and the Trent contributing almost equally, with a smaller contribution from the Don. The Trent has the highest average flow, explaining its large contribution to dieldrin flux. Less detailed sampling of rivers from the north Humber catchment which drain predominantly rural areas had dieldrin concentrations similar to the heavily industrialized southern catchment rivers. This suggests that dieldrin from agronomic and domestic usage may be more persistent than the pollution caused by textile processing industries. Evidence is presented to suggest that the principle dieldrin sources to the Humber catchments are sewage treatment plants, and that the dieldrin sources are in rapid equilibrium with the water column.

Journal Article↗

PubMed1964

DDT ANTAGONISM TO DIELDRIN STORAGE IN ADIPOSE TISSUE OF RATS.

Storage of dieldrin in the adipose tissue of female rats was markedly depressed when DDT and dieldrin were fed simultaneously. The amount of dieldrin present in the tissues of rats fed 1 and 10 parts of dieldrin per million was significantly reduced by the addition of 5 ppm DDT to the feed. The addition of 50 ppm DDT to the feed caused a 15-fold reduction in the amount of dieldrin stored in rats fed 1 ppm dieldrin, and a 6-fold reduction in rats fed 10 ppm dieldrin. This antagonistic effect of DDT suggests that the criteria used in predicting the pharmacological effects of combined residues of related insecticides need some revision.

Adipose Tissue↗

PubMed1964

THE MONOFACTORIAL INHERITANCE OF RESISTANCE TO DIELDRIN IN LARVAL AND ADULT CULEX QUINQUEFASCIATUS SAY.

A susceptible and a resistant strain were isolated from an originally heterogeneous laboratory colony of Culex quinquefasciatus Say (= Culex pipiens fatigans Wiedemann) by use of discriminating concentrations of dieldrin on fourth-instar larvae. By cross-breeding, hybrids of intermediate susceptibility were obtained. By repeated cross-breeding and elimination of susceptibles the authors have shown that resistance to dieldrin is controlled by a single inheritable factor which is neither fully recessive nor dominant in the hybrid genotype, since the ratios of the LC(50) values were 1:19:196. Cross-resistance was shown to lindane but not to malathion or to any of three carbamates.Similar tests were made with adult females exposed to papers impregnated with n-dioctyl phthalate as solvent to secure high concentrations of dieldrin. Resistance in this stage also was neither fully recessive nor dominant, but it can be calculated quantitatively only for the hydrid (approximately 15-fold) since longer exposure was required with the resistant genotype. Determination of dieldrin pick-up showed that this cannot account for the differences in susceptibility of the genotypes. Analysis of resistant females surviving exposure to dieldrin papers showed slow loss of dieldrin and thus added confirmation to the hypothesis that metabolism is not the controlling process in dieldrin-resistance.

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↗

PubMed2001

Comparative effects of dieldrin on hepatic ploidy, cell proliferation, and apoptosis in rodent liver.

Dieldrin-induced hepatocarcinogenesis, which is seen only in the mouse, apparently occurs through a nongenotoxic mechanism. Previous studies have demonstrated that dieldrin induces hepatic DNA synthesis in mouse, but not rat liver. A number of nongenotoxic hepatocarcinogens have been shown to increase hepatocyte nuclear ploidy following acute and subchronic treatment in rodents, suggesting that an induction of hepatocyte DNA synthesis may occur without a concomitant increase in cell division. The current study examined the effects of dieldrin on changes in hepatocyte DNA synthesis, mitosis, apoptosis, and ploidy in mouse liver (the sensitive strain and target tissue for dieldrin-induced carcinogenicity) and the rat liver (an insensitive species). Male F344 rats and B6C3F1 mice were treated with 0, 1, 3, or 10 mg dieldrin/kg diet and were sampled after 7, 14, 28, or 90 d on diet. Liver from mice fed 10 mg dieldrin/kg diet exhibited significantly increased DNA synthesis and mitosis at 14, 28, or 90 d on diet. In rats, no increase in DNA synthesis or mitotic index was observed. The apoptotic index in liver of mice and rats did not change over the 90-d study period. Exposure of mice to only the highest dose of dieldrin produced a significant increase in octaploid (8N) hepatocytes and a decrease in diploid (2N) hepatocytes, which were restricted primarily to centrilobular hepatocytes, with the periportal region showing little or no change from control. No changes in hepatocyte nuclear ploidy were observed in the rat. This study demonstrates that exposure to high concentrations of dieldrin is accompanied by increased nuclear ploidy and mitosis in mouse, but not rat, liver. It is proposed that the observed increase in nuclear ploidy in the mouse may reflect an adaptive response to dieldrin exposure.

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↗

PubMed1979

Strategies, systems, value judgements and dieldrin in control of locust hoppers.

The physiology and field biology of locusts have been extensively studied, and ecological control of Red Locusts has been investigated by field experiment. No fruitful or even promising non-insecticidal method of control has emerged. An effective and economical system requires an insecticide that is: (i) effective at very small area dosages, as a stomach poison placed on the natural vegetation can be, if it is also cumulative; (ii) persistent enough in sunshine and rain to retain effectiveness over the locust's non-feeding periods; (iii) capable of being well distributed by well-tried methods; and (iv) not dangerous to users or consumers and posing a minimal overall risk. Only one insecticide, dieldrin, satisfies all these requirements. Dieldrin is not in the small class of insecticides that are dangerous to man by skin absorption (such as parathion, arsenicals, DNC) and, at the area dosages needed for locust control, is not dangerous to stock. The Sayer exhaust sprayer in a Land Rover, with work rates of the order of square kilometres per hour is excellent for many situations; aircraft spraying at he rate of square kilometres per minute is quicker and less subject to difficulties of terrain, but requires trained and appropriately directed aircrew. Apart from checking, aircraft methods require no party on the ground to find, assess and control locust hoppers. Several ideas about dieldrin are found to be based on insufficient evidence and are probably not true: for example that dieldrin in the atmosphere at a few parts in a million million (10(12)) becomes concentrated in a food web and harmful to man, or that dieldrin is carcinogenic in man. It is noteworthy, however, that one species of antelope in South Africa is exceptionally susceptible to dieldrin poisoning, though harm occurs at area dosages considerably greater than are required in the method of aircraft spraying of Courshee & McDonald (1963). To attack tsetse flies, emissions two orders of magnitude greater have been used. Care must be taken with any insecticide, but the risks of using dieldrin as properly used in locust hopper control have been exaggerated by propaganda. If harm is to be expected, then a quantitative comparison of that with the undoubted benefits of locust control is required to enable one to make a value judgement.

Aircraft↗