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Effect of occupational exposure to aldrin on urinary D-glucaric acid, plasma dieldrin, and lymphocyte sister chromatid exchange.

The effects of exposure to the chlorinated cyclodiene termiticide aldrin was evaluated in pest control workers potentially exposed to this material. Sister chromatid exchange (SCE) frequencies were not elevated in workers handling aldrin. This is consistent with the fact that chlorinated cyclodienes are not genotoxic. Plasma dieldrin concentrations (up to 250 ng/ml) confirmed exposure in workers actively performing termiticide treatments and in maintenance and store workers, when compared with unexposed control workers (median concentration, 4.8 ng/ml). Urinary D-glucaric acid (DGA), an index of hepatic enzyme activity, was elevated in pesticide-exposed groups but urinary DGA was poorly correlated with plasma dieldrin level. This indicates that concurrent exposures of these groups to other pesticides may have influenced mixed-function oxidase metabolic activity.

Adolescent↗

Lipid peroxidation dependent aldrin epoxidation in liver microsomes, hepatocytes and granulation tissue cells.

Lipid peroxidation activity was determined in liver microsomes, hepatocytes and cultured granuloma cells by measuring ethane and pentane production with an improved capillary gas chromatographic method. Lipid peroxidation initiated by ferrous ions and NADPH produced significantly more hydrocarbons at 4% O2 than under atmospheric (21% O2), hyperoxic or hypoxic conditions. In liver microsomes ferrous ions and ascorbic acid stimulated the non-enzymatic lipid peroxidation and concomitantly the epoxidation of aldrin. The results demonstrate that epoxidation of aldrin can be triggered by the iron initiated lipid peroxidation.

Aldrin↗

Protein degradation and related enzyme profiles on a sublethal toxicity of aldrin in the tissues of Rana hexadactyla.

The effects of a sublethal toxicity of aldrin were studied in the brain, muscle, kidney, and intestine of Rana hexadactyla after 1, 2, and 4 weeks of exposures. Aldrin toxicity resulted in a depletion of protein, an increase in amino acid levels, and an enhancement of the activity of protease and amino transferases. The changes were maximum after a 4-week exposure.

Aldrin↗

In vitro disruption of ATP dependent active transport following treatment with aldrin and its epoxy analog dieldrin in a fresh water teleost, Labeo rohita.

Tissue homogenates of brain, gill, liver and kidney of Labeo rohita were subjected in vitro to the various concentrations as 5.00, 1.66, 0.55, 0.18 and 0.06 mu M of 2 organochlorine pesticides aldrin and dieldrin and the disruption of ATP dependent active transport (involving ATPase) was studied. The inhibition of total ATPase, Mg2+ and Na+, K+-dependent ATPase by both the pesticides was quite similar and there was an increased inhibition with increased concentration of the toxicant, however, at the lowest concentrations of both the pesticides stimulation was observed in all tissues except gill Mg2+ ATPase where insignificant inhibition was observed after dieldrin treatment. Inhibition of ATPase system was noted maximum in brain followed by gill, kidney and liver of the experimental fish, however in each tissue maximum inhibition of ATPase was noted after dieldrin treatment than that of th e aldrin treatment. Therefore, the observed action of these pesticides might be related to the ability of the compounds to alter the cellular membrane configuration by binding with the lipid portion of the membrane and this blocking the movement of substances by active transport.

Adenosine Triphosphatases↗

Electron microscopical investigation on aldrin-induced hepatocyte pathology in Rana catesbeiana, with special emphasis on peroxisomes.

We examined the effect of aldrin on hepatocyte ultrastructure in liver of Rana catesbeiana. The frogs were experimentally exposed to chemical substance and liver fragments processed for routine transmission electron microscopy. Hepatic peroxisomes were visualized after incubation with alkaline 3,3'-diaminobezidine (DAB) method. Ultrastructural analysis revealed progressive hepatocyte changes induced by this drug. After 2-weeks, in the hepatocytes the nuclear envelop and the cisternae of both smooth and rough endoplasmic reticulum (SER und RER, respectively) were unusually enlarged. Reduction of glycogen granules associated with an increased frequency of lysosomes was observed. Normal appearing peroxisomes were present in clusters. Lipid droplets were also visualuzed. After 4-weeks, there was a new increase of glcogen associated with a great number of mitochondria and peroxisomes. Moreover, SER und RER were still dilated. Intracellular lipid inclusions became more abundant. These results suggest that the aldrin 250 induces ultrastructural changes in the hepatocyte of Rana catesbeiana.

Aldrin↗

Removal of aldrin, dieldrin, heptachlor, and heptachlor epoxide using activated carbon and/or Pseudomonas fluorescens free cell cultures.

Degradation of aldrin (1,2,3,4,10,10-Hexachloro-1,4,4a,5,8,8a-hexahydro-1,4:5-8-dimethanonaphthalene), heptachlor (1H-1,4,5,6,7,8,8-heptachloro-3a,4,7,7a-tetrahydro-4,7-methano indene), dieldrin (1aalpha,2beta,2aalpha,3beta,6beta,6aalpha,7beta,7aalpha)-3,4,5,6,9,9-Hexachloro-1a,2,2a,3,6,6a,7,7a-octahydro-2,7:3,6-d-methanonaphtha[2,3-b]oxirene, and heptachlor epoxide (1aalpha, 1bbeta,2alpha,5alpha,5alphabeta,6beta,6aalpha-2,3,4,5,6,7,7-Heptachloro-1a,1b,5,5a,6,6a-hexahydro-2,5-methano-2H-inden[1,2-b]-oxirene) was tested using free cultures of Pseudomonas fluorescens under controlled conditions. Pesticide concentrations were monitored by gas chromatography during 120 h. Percentages of degradation and biodegradation rates (BDR) were calculated. Data showed a trend suggesting a relation between chemical structure and degradability. Degradation kinetics for each pesticide tested showed that the highest degradation rates were found in the first 24 h. Kinetics data were adjusted to an empirical equation in order to predict their behavior, and the correlation coefficients obtained were satisfactory. Gas chromatography/mass spectrometry (GC/MS) analysis of the final extracts allowed the identification of chlordene and monodechlorodieldrin, which have been reported as final metabolite produced in the biodegradation of this kind of compounds. Regarding adsorption of pesticides on activated vegetal carbon, we concluded that removal efficiencies between 95.45 and 97.18% can be reached, depending on the pesticide and the carbon dose applied. The values for K from the Freundlich equation were quite similar for the four pesticides (between 1.0001 and 1.04), whereas the n values were quite different for each pesticide in the following order of affinity: dieldrin > aldrin > heptachlor epoxide > heptachlor. Equilibrium times, very important for scaling up the process, were between 43 min and 1 h, for the heptachlor epoxide and the heptachlor, respectively.

Adsorption↗

Effect of aldrin on carbohydrate metabolism in Indian catfish.

Exposure of the Indian catfish (Heteropneustes fossilis) to a sublethal concentration of 0.14 p.p.m. aldrin for 3, 6, 12, 48, and 96 hrs affected carbohydrate metabolism. Muscle glycogenolysis and glycogenesis were obtained at 3 and 12 hrs, respectively. Hepatic glycogenolysis occurred at 3, 48, and 96 hrs. The treatment caused hyperglycaemia at 3, 6, 48, and 96 hrs, and hypoglycaemia at 12 hrs. Blood pyruvate values increased significantly at 3, 6, and 96 hrs. Hyperlacticaemia was observed at 3 and 12 hrs but hypolacticaemia developed at 96 hrs. The results are discussed in relation to acute stress syndrome. Also, impairment of carbohydrate metabolism by aldrin may be involved in the biochemical mechanism for its toxic action. It is concluded that evaluation of carbohydrate metabolites in fish could prove useful as a rapid method for assessing acute toxicity of pesticides.

Aldrin↗

Studies on photochemical reactions of air pollutants. XII. Photochemical epoxidation of aldrin with suspended particulates in air.

Suspended particulates collected in Yokohama, Japan over various 24-h periods were found to cause the photochemical epoxidation of aldrin to dieldrin in good yield. trans-Stilbene did not undergo the epoxidation. Upon irradiation of aldrin together with the suspended particulates in quasi-air consisting of 18O2. 100% incorporation of 18O into dieldrin was obtained. Thus, the oxygen atom in dieldrin originated not from the particulates, but from oxygen in air.

Air Pollutants↗

Conversion of dieldrin to aldrin by intestinal bacteria in rats.

The present study provides the evidence that dieldrin is reductively metabolized to aldrin by intestinal bacteria in rats. When dieldrin was incubated with the cecal contents of rats, aldrin, a reduced metabolite of the epoxide, was isolated from the incubation mixture. The metabolite was identified unequivocally by UV and mass spectral comparison with an authentic sample, and on the basis of its TLC and HPLC behavior. The cecal contents of rats exhibited epoxide reductase activity toward dieldrin under anaerobic conditions. However, only marginal activity was observed under aerobic conditions. Four pure strains of intestinal bacteria exhibited epoxide reductase activities to varying degrees under anaerobic conditions. The highest activity was observed in Clostridium sporogenes. Cell-free extracts of the intestinal bacteria in rat cecal contents showed reductase activity when supplemented with both NAD(P)H and FMN under anaerobic conditions.

Aldrin↗

Aldrin and dieldrin: a review of research on their production, environmental deposition and fate, bioaccumulation, toxicology, and epidemiology in the United States.

In the last decade four international agreements have focused on a group of chemical substances known as persistent organic pollutants (POPs). Global agreement on the reduction and eventual elimination of these substances by banning their production and trade is a long-term goal. Negotiations for these agreements have focused on the need to correlate data from scientists working on soil and water sampling and air pollution monitoring. Toxicologists and epidemiologists have focused on wildlife and human health effects and understanding patterns of disease requires better access to these data. In the last 20 years, substantial databases have been created and now are becoming available on the Internet. This review is a detailed examination of 2 of the 12 POPs, aldrin and dieldrin, and how scientific groups identify and measure their effects. It draws on research findings from a variety of environmental monitoring networks in the United States. An overview of the ecologic and health effects of aldrin and dieldrin provides examples of how to streamline some of the programs and improve access to mutually useful scientific data. The research groups are located in many government departments, universities, and private organizations. Identifying databases can provide an "information accelerator" useful to a larger audience and can help build better plant and animal research models across scientific fields.

Aldrin↗

Significance of acute and chronic renal disease in Osborne-Mendel rats ingesting dieldrin or aldrin.

Renal lesions developed in Osborne-Mendel male and female rats ingesting dieldrin or aldrin in the diet. Chronic interstitial nephritis was seen in rats surviving for 52 wk or longer. The incidence of nephritis was highest and the lesion was most severe in male rats given the higher dose levels of dieldrin, 50 ppm or higher. Over one-half of the rats fed dieldrin or aldrin at 150 ppm, and many fed 100 ppm, died from renal necrosis and sometimes hepatic necrosis during the first year. More female rats died from renal necrosis than did male rats. Rats dying from renal necrosis did not develop tumors; those from severe chronic nephritis either did not have tumors or had preneoplastic lesions that would have become tumors if the animal had lived longer. Thus acute and chronic effects should both be examined carefully when evaluating the safety of a chemical. In addition to causing the death of the animal, acute and chronic toxic effects can prevent the development of malignant tumors by shortening the animal's life span or by causing illness and inhibiting the development of a tumor that otherwise might occur in a healthy animal.

Aldrin↗

[Dietary intake of dieldrin and aldrin in Poland].

Dieldrin and aldrin exposure from a particular food items in Poland in 1970-1996 was calculated by multiplying its annualized mean consumption rates by residue concentration in the food. Estimated daily dietary intakes of dieldrin and aldrin were from 1.0 do 1.3 micrograms per person in 1970-1985 and from 0.50 do 0.58 microgram per person in 1990-1996, on the average. Fish and dairy products are a main source of dieldrin in a total diet in Poland.

Aldrin↗

Radioimmunoassay for dieldrin and aldrin.

A radioimmunoassay for dieldrin and aldrin has been developed which can detect picomole levels of either compound. The specificity of the antibodies, determined with respect to several other organochlorine insecticides, indicates that most of the binding energy is directed to the polychlorinated bicyclic ring system. DDT, 2,4,5-T, dechachlorobiphenyl (a PCB standard), and several other insecticides which may be found in samples containing dieldrin and aldrin should not interfere with the radioimmunoassay.

Aldrin↗

Tissue glycolytic potentials of penaeid prawn, Metapenaeus monoceros during methylparathion, carbaryl and aldrin exposure.

Changes in midgut gland and muscle tissue glycolytic potentials of penaeid prawn, Metapenaeus monoceros following exposure to methylparathion, carbaryl and aldrin were studied. A decrease in total carbohydrates, glycogen and pyruvate and an increase in lactate levels were observed. An increase in phosphorylase 'a' and aldolase activity levels suggested increased formation of trioses during selected insecticide toxicity. The decrease in the lactate dehydrogenase activity levels and an increase in the lactate content indicative of reduced mobilization of pyruvate into the citric acid cycle. During selected insecticide exposure, the prawn tissues adopting some sort of regulatory pathways such as enhanced glycolysis and a shift of metabolic emphasis from aerobiosis to anaerobiosis. All the above mentioned changes were more pronounced in the midgut gland compared to muscle tissue. The per cent decrease or increase are more under aldrin exposure followed by carbaryl and methylparathion exposure. The selected insecticides in the present investigation, though belongs to different representative groups, but appears to be neurotoxic leading to disturbances in the carbohydrate catabolism.

Adenosine Triphosphatases↗

Aldrin toxicity on amphibian neuronal, hepatic and muscular tissue oxidative enzymes.

Aldrin toxicity was studied in the brain, liver and muscle of Rana hexadactyla. It was observed that sublethal concentration of aldrin inhibited the activities of SDH, MDH and ICDH while it elevated the activities of LDH and G-6-PDH. The increase and the decrease was progressive with the exposure period. The changes were attributed to the induced toxic effects such as oxygen distress, energy crisis and microstructural changes.

Aldrin↗

Benzo[a]pyrene- and aldrin-metabolizing activities in cultured human and rat hepatoma cell lines.

Five established hepatoma cell lines, 1 of rat origin and 4 derived from human liver carcinoma, were compared for their capacity to perform metabolic activation of one polycyclic hydrocarbon, benzo[a]pyrene (BP), and one cyclodiene chlorinated insecticide, aldrin. The results of these investigations indicated both species and individual differences among these cell lines. Aldrin was found to be converted into dieldrin much more efficiently by the rat hepatoma cell line than by any human cell lines, whereas 2 human lines displayed the highest BP-metabolizing activity whether measured as the amounts of water-soluble products or estimated by cytotoxic cell-mediated assays. Results also showed that one particular human cell line can replace, advantageously, V79 hamster cells as target in a cell-mediated assay owing to its incapability to metabolize BP and its high sensitivity to BP metabolites.

Aldrin↗

[Accumulation and depuration of aldrin in the oyster Crassostrea rhizophorae, of the Ciénaga Grande de Santa Marta (Colombian Caribbean)].

Laboratory experiments were conducted at different salinities (35, 26 and 17/1000) to determine accumulation and depuration rates of the organochlorine compound aldrin by the oyster Crassostrea rhizophorae, Ciénaga Grande de Santa Marta (Colombian Caribbean). Residual levels were detected in tissues after 24 hours of exposure, showing increases directly related to the exposure concentration. For all the exposure concentrations the highest retention values were measured at 26/1000 salinities, followed by 17/1000, and the lowest values at the highest salinity. The highest bioconcentration values were 96115.5 (at 26/1000), 37938.9 (at 17/1000), and 22605.1, (35/1000) times the environmental concentration. The depuration process varied across salinity levels. At 26/1000 there was a clear decrease in the residual levels during the first five days, eliminating in this period the same amount as oysters kept at 17/1000 for 20 days and surpassing the amount eliminated by those kept at 35/1000 for 20 days. A rapid decrease in the amount of residues is followed by a slow elimination of the aldrin remaining in tissues.

Aldrin↗

[Effects of DDT and aldrin on swine cell line IB-RS-2].

Swine cells IB-RS-2 were exposed to 0,1-100 microgram/ml medium of DDT and aldrin for 48 hours. The data obtained showed that both compounds decreased cell growth. This effect depends on the concentration and on the time of cell exposition to the insecticides. These compounds also decreased the levels of cellular protein, RNA and DNA. The degrees of changes with aldrin were less than with DDT.

Aldrin↗