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PubMed2002

Distribution of aldrin and its epoxide (dieldrin) in egg-forming tissues and eggs of laying hens following an oral application.

Laying hens were treated orally with a single dose of aldrin (1,2,3,4,10,10-hexachloro-1,4,4a,5,8,8a-hexahydro-1,4:5,8-dimethanonaphthalene, AD) 1 mg kg(-1) bw. Concentrations (microg g(-1)) of AD or its epoxide, dieldrin (1,2,3,4,10,10-hexachloro-6,7-epoxy-1,4,4a,5,6,7,8,8a-octahydroendo-,exo-1,4:5,8-dimetha-nonaphthalene, DD), in the main tissues involved in egg formation (blood, liver, ovary, and oviducts) and egg yolk, collected at 1 day after AD dosing, were determined by normal-phase high-performance liquid chromatography. The limits of determination were 0.07 microg g(-1) for AD and 0.08 microg g(-1) for DD, respectively. In extractable fats from the above tissues and egg yolk, AD was found in the egg yolk; however, no AD was found in tissues involved in egg formation. DD was found in all tissues examined here. The DD level was highest in the liver and was lowest in the blood (P<0.01). These results suggest that the epoxidation of AD to DD occurred rapidly in the hen.

Administration, Oral↗
PubMed2001

Normal-phase high-performance liquid chromatographic determination and identification of aldrin, dieldrin, and DDTs in eggs.

A method for the routine monitoring of residual aldrin, dieldrin, pp'-DDT, op'-DDT, pp'-DDE, and pp'-DDD in eggs by high-performance liquid chromatography (HPLC) with a photo-diode array (PDA) detector is described. The lipids extracted from a whole egg are cleaned by a solid-phase extraction (SPE) ISOLUTE NH2 column with a diethyl ether-hexane (5:95, v/v) eluent. The HPLC separation is carried out using a normal-phase (LiChrosorb NH2) column, a heptane-hexane eluent (97:3, v/v), and a PDA detector. The average recoveries from fortified target compounds (0.1, 0.2, 0.3, and 0.4 microg/g, respectively) are > or = 83%, with standard deviations (SDs) between 2 and 5%. The interassay variabilities and their SDs are < or = 4.8% and < or =0.7%, with intra-assay variabilities of 2.1-3.3%. The limits of determination for these compounds range from 0.04 to 0.08 microg/g.

Aldrin↗
PubMed1990

Isolation of dieldrin resistance from field populations of Drosophila melanogaster (Diptera: Drosophilidae).

High levels (about 4,000-fold) of resistance to dieldrin were isolated by screening field-collected populations of Drosophila melanogaster (Meigen). The resistance was made homozygous following 2-4 generations of selection. A single, major gene mapping to the left arm of chromosome III was solely responsible for resistance. The implications of the recovery of resistant mutants from field populations of D. melanogaster are discussed.

Animals↗
PubMedDate not supplied

Mutagenicity of dieldrin in the Salmonella-microsome test.

Dieldrin was assayed in vitro for its mutagenic activity in several strains of S. typhimurium with and without Aroclor 1254 treated mouse liver homogenate (S-9M). The mutagenicity of the insecticide was expressed maximally in all strains in the presence of liver S-9M and less so in three strains without liver microsomes.

Animals↗
PubMed1996

Actions of picrodendrin antagonists on dieldrin-sensitive and -resistant Drosophila GABA receptors.

1. A series of terpenoid compounds, recently isolated from Picrodendron baccatum, share a picrotoxane skeleton with picrotoxinin, an antagonist of ionotropic GABA receptors. Referred to as picrodendrins, they inhibit the binding of [35S]-tert-butylbicyclophosphorothionate (TBPS) to rat GABAA receptors. Hitherto, their effects on GABA receptors have not been investigated electrophysiologically. Under two-electrode voltage-clamp, the actions of picrodendrins and related terpenoids have been assayed on homooligomeric GABA receptors formed by the expression of a Drosophila GABA receptor subunit (RDLac) in Xenopus oocytes. 2. All the terpenoids tested, dose-dependently antagonized currents induced by 30 microM (EC50) GABA. 3. Tutin and its analogues (dihydrotutin and isohyenanchin) differ in the structure of their axial C4 substituents. Of these compounds, tutin, which bears an isopropenyl group at this carbon atom, was the most potent antagonist of RDLac homo-oligomers, whereas isohyenanchin, which bears a hydroxyisopropyl group, was the least potent antagonist tested. 4. Picrodendrins differ mainly in the structure of their C9 substituents. The IC50s of picrodendrins ranged from 17 +/- 1.3 nM (picrodendrin-Q) to 1006 +/- 1.3 nM (picrodendrin-O). As such, the most potent picrodendrins (Q, A and B) were approximately equipotent with picrotoxinin as antagonists of RDLac homo-oligomers. 5. Certain picrodendrin compounds effected a use-dependent blockade of RDLac homo-oligomers. Such a biphasic block was not observed with tutin analogues. 6. Picrotoxin-resistant RDLacA3025 homo-oligomers, which have a single amino acid substitution (A302S) in the 2nd transmembrane region, were markedly less sensitive to picrodendrin-O than the wild-type, dieldrin-sensitive, homo-oligomers. 7. The relative potency of tutin analogues demonstrates that the structure-activity relationship of the C4 substituent of picrotoxane-based compounds is conserved in vertebrates and insects. However, the relative order of potency of picrodendrins on RDLac homo-oligomers is distinctly different from that observed in previous radioligand binding studies performed on vertebrate GABAA receptors. As picrodendrin compounds differ in the structure of their C9 substituents, these data suggest that the optimal convulsant pharmacophores of vertebrate GABAA receptors and RDLac homo-oligomers differ with respect to this substituent.

Animals↗
PubMed1966

Dieldrin: extraction of accumulations by root uptake.

Certain forage crops can absorb and translocate the chlorinated hydrocarbon insecticide dieldrin from soil or sand. An extraction technique routinely used for analyses of residues does not quantitatively remove this internal chemical, but a method employing chloroform-methanol extraction leads to essentially quantitative recovery.

Absorption↗
PubMed1967

Dieldrin: degradation by soil microorganism.

An attempt was made to discover microorganisms that degrade dieldrin, an extremely stable chlorinated hydrocarbon insecticide. Examination of more than 500 isolates from soil that had been heavily contaminated with various insecticides revealed the existence of a few microbes that are very active in degrading this compound to various metabolites.

Autoradiography↗
PubMed1968

Hypertrophic, hypoactive smooth endoplasmic reticulum: a sensitive indicator of hepatotoxicity exemplified by dieldrin.

Rats with hypertrophic smooth endoplasmic reticulum (ER) and increased activities of the drug-handling enzymes induced by dieldrin were stressed with larger doses of the pesticide. The activity of the drug-handling enzymes was thus reduced, but liver weight, smooth ER, and P-450 hemoprotein remained elevated. While no changes were apparent by light microscopy, the hypertrophic, hypoactive smooth ER was recognized as tight clusters of tubular membranes associated with abnormalities of the mitochondrial membrane. Similar but not identical morphologic changes were noted in human liver diseases associated with hepatic insufficiency. Hypertrophic, hypoactive smooth ER may indicate transition from adaptation of injury, and can be used as a sensitive parameter of toxicity.

Animals↗
PubMed1971

Carbonic anhydrase interaction with DDT, DDE, and dieldrin.

The active site of various carbonic anhydrases is not blocked by DDT. DDE, or dieldrin. Impairment of catalytic efficiency can only be documented in opalescent test solutions in which the insecticides are present in excess of their solubility limit. These slowly forming precipitates occlude enzyme from solution and furnish a physical explanation of the supposed inhibition. The amounts occluded depend, among other things, on the conformational and topographical characteristics of the particular carbonic anhydrase molecules.

Acetazolamide↗
PubMed1978

Dieldrin-induced mortality in an endangered species, the gray bat (Myotis grisescens).

Brains of juvenile gray bats, Myotis grisescens, found dead beneath maternity roosts in two Missouri caves contained lethal concentrations of dieldrin. One colony appeared to be abnormally small, and more dead bats were found a year after the juvenile bats had been collected. This is the first report to link the field mortality of bats directly to insecticide residues acquired through the food chain.

Aldrin↗
PubMed1975

Linkage of the genes for DDT and dieldrin resistance in larvae of the mosquito Aedes aegypti.

The DDT resistance gene RDDT1, and the dieldrin resistance gene Rd1 have been mapped on linkage group II with respect to visible markers, in the mosquito Aedes argypti L. The best interpretation of the data gives the order wa - Rdl - ds RDDT1 - s - y but was - Rdl -ds - y - s - RDDT1 is also possible. h is very loosely linked with RDDT1. The length of the linkage group has been considerably extended from previous studies.

Aedes↗
PubMedDate not supplied

Histopathology of carcinomas of the liver in mice ingesting dieldrin or aldrin.

C3HeB/Fe male and female mice, ingesting 10 ppm of the pesticides dieldrin or aldrin in the diet, developed highly significant incidences of carcinomas of the liver. The carcinomas varied from well differentiated to poorly differentiated and undifferentiated and were capable of metastasis.

Adenoma, Bile Duct↗
PubMed2006

IMP PCR primers detect single nucleotide polymorphisms for Anopheles gambiae species identification, Mopti and Savanna rDNA types, and resistance to dieldrin in Anopheles arabiensis.

BACKGROUND: Polymerase chain reactions to distinguish single-nucleotide polymorphisms are commonly used for mosquito identification and identifying insecticide resistance alleles. However, the existing methods used for primer design often result in analyses that are not robust or require additional steps. METHODS: Utilizing oligonucleotides that are unique in having an intentional mismatch to both templates three bases from the SNP at the 3-prime end, three new PCR assays that distinguish SNP targets using standard gel electrophoresis of undigested DNA fragments were developed and tested. These were applied to: (1) an alternative ribosomal DNA PCR assay to distinguish five members of the Anopheles gambiae complex; (2) detection of the Mopti and Savanna rDNA types; and (3) an assay to distinguish resistance to dieldrin (Rdl) alleles in Anopheles arabiensis. RESULTS: Reproducible specific amplification of the target alleles was observed in all three assays. The results were consistent with existing analyses but proved simpler and the results more distinct in our hands. CONCLUSION: The simplicity and effectiveness of the method should be utilized in these and other PCR analyses to increase their specificity and simplicity. These results have the potential to be extended not only to mosquito analyses but also to parasite and human polymorphisms.

Animals↗
PubMed2001

An invertebrate model of the developmental neurotoxicity of insecticides: effects of chlorpyrifos and dieldrin in sea urchin embryos and larvae.

Chlorpyrifos targets mammalian brain development through a combination of effects directed at cholinergic receptors and intracellular signaling cascades that are involved in cell differentiation. We used sea urchin embryos as an invertebrate model system to explore the cellular mechanisms underlying the actions of chlorpyrifos and to delineate the critical period of developmental vulnerability. Sea urchin embryos and larvae were exposed to chlorpyrifos at different stages of development ranging from early cell cleavages through the prism stage. Although early cleavages were unaffected even at high chlorpyrifos concentrations, micromolar concentrations added at the mid-blastula stage evoked a prominent change in cell phenotype and overall larval structure, with appearance of pigmented cells followed by their accumulation in an extralarval cap that was extruded from the animal pole. At higher concentrations (20-40 microM), these abnormal cells constituted over 90% of the total cell number. Studies with cholinergic receptor blocking agents and protein kinase C inhibitors indicated two distinct types of effects, one mediated through stimulation of nicotinic cholinergic receptors and the other targeting intracellular signaling. The effects of chlorpyrifos were not mimicked by chlorpyrifos oxon, the active metabolite that inhibits cholinesterase, nor by nonorganophosphate cholinesterase inhibitors. Dieldrin, an organochlorine that targets GABA(A )receptors, was similarly ineffective. The effects of chlorpyrifos and its underlying cholinergic and signaling-related mechanisms parallel prior findings in mammalian embryonic central nervous system. Invertebrate test systems may thus provide both a screening procedure for potential neuroteratogenesis by organophosphate-related compounds, as well as a system with which to uncover novel mechanisms underlying developmental vulnerability.

Animals↗
PubMed2001

Pesticides and breast cancer risk: a review of DDT, DDE, and dieldrin.

Established risk factors for breast cancer explain breast cancer risk only partially. Hence, there has been interest in evaluating what role environmental chemicals, especially those with evidence of being hormonally active agents, play in breast cancer risk. Organochlorine pesticides have received the most attention because of their persistence in the environment, ability to concentrate up the food chain, continued detection in the food supply and breast milk, and ability to be stored in the adipose tissue of animals and humans. Although several early descriptive studies and a cohort study identified a strong positive association with breast cancer risk and adipose or blood levels of the organochlorine pesticide dichlorodiphenyltrichloroethane (DDT) and/or its metabolite dichlorodiphenyldichloroethylene (DDE), most of the more recent case--control and nested case--control studies have not supported this association. In this review I discuss these findings and explore how exposure to different forms of DDT with varying estrogenicities may have affected the results of these studies. I also address how other factors influence the interpretation of the studies on DDT, DDE, and breast cancer risk. These include the effect of analytic methods, dietary factors, menopausal status, use of different types of control populations, lactation history, estrogen receptor status, ethnic/racial subgroups, breast tumor characteristics, and polymorphisms. I also discuss the emerging research on whether serum levels of the persistent organochlorine insecticide dieldrin are related to breast cancer risk in Danish and American women. Further research needs are also identified.

Breast Neoplasms↗
PubMed1994

The pesticides endosulfan, toxaphene, and dieldrin have estrogenic effects on human estrogen-sensitive cells.

Estrogenic pesticides such as DDT and chlordecone generate deleterious reproductive effects. An "in culture" bioassay was used to assess the estrogenicity of several pesticides. The E-screen test uses human breast estrogen-sensitive MCF7 cells and compares the cell yield achieved after 6 days of culture in medium supplemented with 5% charcoal-dextran stripped human serum in the presence (positive control) or absence (negative control) of estradiol and with diverse concentrations of xenobiotics suspected of being estrogenic. Among the organochlorine pesticides tested, toxaphene, dieldrin, and endosulfan had estrogenic properties comparable to those of DDT and chlordecone; the latter are known to be estrogenic in rodent models. The E-screen test also revealed that estrogenic chemicals may act cumulatively; when mixed together they induce estrogenic responses at concentrations lower than those required when each compound is administered alone.

Biological Assay↗
PubMed2001

In vitro hepatic biotransformation of aldrin and dieldrin in food-producing animals.

The hepatic biotransformation of aldrin (AD) and dieldrin (DD) was studied in liver post-mitochondrial supernatants (S-9s) from laying hens, female cattle and swine. S-9s were incubated with 0.03 nmol of AD or DD for 1 h. After 1 h, AD in the samples was almost epoxidated to DD. This formation was found with all the animal S-9s, and the highest rates occurred in pig S-9 (P < 0.01), followed by cow and hen S-9s. No reduction of DD was found with any of the S-9s.

Aldrin↗
PubMed2001

Decreasing half-life of dieldrin in egg yolk following a single oral administration of aldrin to laying hens.

Laying hens were treated orally with a single dose of aldrin (AD) 1 mg/kg body weight. Concentrations (microgram/g) of AD or its epoxide (= dieldrin, DD) in the yolk of eggs laid for 21 days after AD treatment were determined by normal-phase high-performance liquid chromatography. The limits of determination were 0.02 microgram/g for AD and 0.03 microgram/g for DD, respectively. After AD treatment, although the low levels of AD (mean 0.02-0.03 microgram/g) were observed only during a three-day period (from 4th to 6th days), DD (mean 0.15 microgram/g) was found already on the 2nd day, indicating that the epoxidation of AD to DD in the hen's body is rapid. The highest level of DD (mean 0.40 microgram/g) was detected on the 6th day, and then DD levels decreased slowly and were detected up to the 21st day. In this decreasing phase, the half-life of DD in the yolk was estimated to be 25.6 days with a 95% confidence interval from 22.7 to 29.4 days.

Administration, Oral↗