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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↗
PubMed2002

Dieldrin induces human neutrophil superoxide production via protein kinases C and tyrosine kinases.

We have recently found that dieldrin is a potent human neutrophil agonist in vitro and induces neutrophilic inflammation in vivo. Among the responses observed in vitro, dieldrin was found to induce superoxide (O2-) production by a yet unknown mechanism. In the present study, dieldrin- and phorbol 12-myristate 13-acetate (PMA)-induced O2- responses were compared. For this purpose, cells were preincubated with a panel of signal transduction inhibitors including genistein, H-7, HA-1077, pertussis toxin, staurosporine, calphostin C, SB203580, PD098059, and wortmannin. Dieldrin-induced O2- response was significantly reduced with treatment with genistein, H-7, HA-1077, staurosporine, and calphostin C, whereas PMA-induced response was significantly reduced by treatment with H-7, HA-1077, and staurosporine. This indicates that dieldrin mediates its effect via protein kinases C (PKCs) and tyrosine kinases. Involvement of tyrosine kinases in dieldrin-induced human neutrophils was further demonstrated by an increase in tyrosine phosphorylated protein level expression. Finally, we found that treatment with the mitochondrial stabilizer bongkrekic acid and with the inhibitor of vesicular transport brefeldin A did not reverse dieldrin-induced O2- response.

Cell Culture Techniques↗
PubMed2000

Dieldrin induces cytosolic [3H]7, 12-dimethylbenz[a]anthracene binding but not multidrug resistance proteins in rainbow trout liver.

Previously it was demonstrated that biliary excretion of a single dose of [14C]dieldrin or [3H]7, 12-dimethylbenz/alanthracene (DMBA) was stimulated up to 700% and 300%, respectively, in rainbow trout fed 0.3-0.4 mg dieldrin/kg/d for 9-12 wk. This was not explained by increased activities of hepatic microsomal xenobiotic-metabolizing enzymes or increased amounts of any of six cytochrome P-450 isozymes quantitated by Western blots. It was hypothesized that stimulated excretion was explained by induction of (1) cytosolic binding proteins that facilitated intracellular trafficking of DMBA to sites of metabolism, or (2) ATP-dependent proteins that transport xenobiotic metabolites from liver to bile. Binding of 15 and 60 nmol [3H]DMBA/mg protein increased about 200% in hepatic cytosol from dieldrin-fed fish. A 50-fold molar excess of unlabeled DMBA reduced binding of 15 nmol [3H]DMBA/mg protein (nonspecific binding) by the same amount in cytosol from control and dieldrin-fed fish, indicating that dieldrin induced specific binding. Liver sections from control and dieldrin-fed fish were treated with multidrug resistance (MDR) protein monoclonal antibodies C494, C219, and JSB-1, and polyclonal antibody MDR Ab-1. There were no marked differences in optical densities of immunohistochemical staining near bile canaliculi of control and dieldrin-fed fish. Induction of xenobiotic binding capacity in cytosol of dieldrin-fed rainbow trout at least partially explained altered DMBA disposition in fish pretreated with this cyclodiene insecticide.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

Uptake and disposition of aldrin and dieldrin by isolated perfused rabbit lung.

The uptake, metabolism, and release of aldrin and dieldrin by the lungs were studied by use of isolated perfused rabbit lungs that were artificially ventilated and perfused through the pulmonary artery. Both recirculating and single-pass experiments were conducted using an artificial medium as perfusate. Aldrin accumulated in the lung from the perfusate through two distinct phases of uptake: a rapid phase involving simple diffusion and nonspecific binding and a slower phase representing its metabolic turnover as dieldrin. Dieldrin was not metabolized but accumulated in the lungs by a saturable and a nonsaturable process. Single-pass experiments with aldrin indicated that the initial velocity of uptake could be fitted to one component and a constant representing the rate of metabolism. Uptake of dieldrin was biphasic: one phase independent of the perfusate concentration and the other saturable with respect to the perfusate concentration. By the application of Michaelis-Menten kinetics, the maximum amount of dieldrin accumulation attributable to the saturable component was calculated to be 0.64 mumol/lung. Our results indicate that the accumulation of these chlorinated xenobiotics takes place through the processes of simple diffusion followed by nonspecific tissue binding. There was no evidence for irreversible binding of aldrin or dieldrin, its epoxide, in the lung. While the lung plays a role in metabolizing aldrin to dieldrin followed by a transient storage, neither substrate has the potential for long-term storage in the lung.

Aldrin↗
PubMed1972

The morphologic effects of dieldrin and methyl mercuric chloride on pars recta segments of rat kidney proximal tubules.

This investigation was undertaken to evaluate the morphologic effects in rat kidney resulting from chronic exposure to low doses of the pesticide dieldrin, methyl mercuric chloride (CH(3)HgCl) and the combination of dieldrin plus CH(3)HgCl. Histologic and ultrastructural changes were confined to the proximal tubules. Alterations in these tubules were consistent and reproducible for each regimen and did not become more severe with duration of exposure. The straight segment of the proximal tubule (pars recta) was more severely affected by dieldrin and CH(3)HgCl than the convoluted portion. Female rats were more markedly affected than males. Pars recta tubule cells of male and female rats exposed to dieldrin showed an increase of smooth endoplasmic reticulum (SER). Male rats displayed a greater increase in SER than females. Pars recta tubule cells of animals given CH(3)HgCl also exhibited increased amounts of SER, degenerating mitochondria and cell death. Pars recta tubules of females were dilated and contained within the lumens many spherical, hematoxylin-positive staining, cytoplasmic masses, which were visible by light microscopy. These masses were characterized ultrastructurally by the presence of an SER aggregate in an area of material similar to cell matrix. In addition, cells of the pars recta of female animals contained electron-dense membranous cytosomes not present in control animals. Pars recta cells of males showed an increase in SER, but the dense membranous cytosomes observed in the pars recta cells of female rats were not seen. Rats exposed to dieldrin plus CH(3)CgCl showed less morphologic alteration of the pars recta tubules than animals given methyl mercuric chloride; however, increased amounts of SER and more degeneration in tubule cells were observed in these animals when compared to control animals. The findings are discussed in relation to the conversion of CH(3)HgCl to inorganic mercury in vivo and the known toxicity of inorganic mercury to the pars recta. Decreased tubular alteration in males and dieldrin-treated animals may be explained by sexual differences in renal enzyme levels or activities and the induction of microsomal enzyme systems by dieldrin.

Animals↗
PubMed2000

The turnover of phospholipid fatty acyl chains is activated by the insecticide Dieldrin in Bufo arenarum oocytes.

Dieldrin is a widespread environmental contaminant hazardous to many wildlife species. Some evidence obtained with Bufo arenarum oocytes indicates that Dieldrin decreases the fertilization rate in amphibian oocytes, but little is known about mechanisms by which the pesticide affects fertilization. Therefore, we investigated the effect of Dieldrin on oocyte phospholipid metabolism. Freshly obtained oocytes, prelabeled with 2 3H-glycerol or 9-10 3H palmitate, were exposed to 4 mg/L Dieldrin for 2 hours. Dieldrin reduced the amount of 2 3H-glycerol incorporation in all phosphoglycerides classes: PI, PA, PS, and SPH were affected in 80% of the cases and PC and PE were only reduced in 39% of the cases. The incorporation in neutral lipids was not affected. On the contrary, 9,10 3H-palmitate incorporation increased in PC, PI, and PA, but TAG and FFA decreased. The more efficient incorporation of 3H-palmitate compared with 3H-glycerol in Dieldrin-treated oocytes suggests the operation of an alternative route other than de novo synthesis for phospholipids. The retailoring of phosphoglycerides via a deacylation-acylation pathway was demonstrated. These changes in phospholipid metabolism could be associated with the activation of certain enzymes produced by the pesticide.

Acylation↗