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At least 19 recordsLinked to original sources
PubMed1986

Effect of endrin and endrin derivatives on hepatobiliary function and carbon tetrachloride-induced hepatotoxicity in male and female rats.

The effects of the cyclodiene pesticide, endrin, and its aldehyde and ketone metabolites on hepatobiliary function and CCl4-induced hepatotoxicity were investigated in Sprague-Dawley rats. The rats were given control diet or diets containing 5 or 10 ppm endrin, 10 ppm endrin aldehyde or 5 ppm endrin ketone for 15 days. Three to six rats from each treatment group were given a single ip dose (100 microliter/kg body weight) of CCl4 in corn oil (1 ml/kg) on day 15. Levels of serum glutamic-oxalacetic transaminase (SGOT), glutamic-pyruvic transaminase (SGPT), isocitrate dehydrogenase and ornithine-carbamyl transferase, bile flow and biliary excretion of an anionic model compound, phenolphthalein glucuronide (PG), were measured on day 16. Dietary treatment with endrin at either dose level did not significantly elevate serum enzyme levels, while endrin aldehyde produced a slight increase in SGOT and SGPT and endrin ketone produced a small elevation in SGPT levels. Treatment with endrin aldehyde or endrin ketone did not result in significant alterations of bile flow or biliary PG excretion. Treatment with 5 ppm endrin produced a significant reduction in bile flow and a corresponding reduction in PG excretion by male rats, whereas treatment with 10 ppm endrin reduced only the PG excretion by male rats. Female rats treated with 5 or 10 ppm endrin showed a dose-dependent choleretic effect with a commensurate increase in PG excretion. With the exception of a further slight reduction in PG excretion by male rats, treatment with the endrin or endrin derivative did not potentiate CCl4-induced alterations in hepatobiliary functions. Although the levels of some serum enzymes of rats given endrin or endrin derivatives plus CCl4 were elevated over those of rats given CCl4 alone, the increases were not of the magnitude of those that have been reported previously for chlordecone. Generally, female rats challenged with CCl4 or endrin/CCl4 exhibited greater increases in serum enzyme levels than did male rats given corresponding treatments.

Alanine Transaminase↗
PubMedDate not supplied

Elimination of endrin by mallard ducks.

Endrin is very toxic to birds and has been implicated in the deaths of birds in nature. However, it is not known how rapidly birds eliminate endrin, a factor important in determining how much is accumulated in tissues. In this study, the loss rate of endrin was followed for 64 days in mallard (Anas platyrhynchos) drakes that had been fed 20 ppm endrin for 13 days. The loss from carcass and blood was described by the equation Y = a e b square root of x where Y = the concentration of endrin in ppm, a = the concentration at day 0, e = the base of natural logarithms, b = the first order rate constant for the elimination process, and x = the number of days after cessation of endrin treatment. Endrin was lost rapidly at first; concentrations in carcasses on a wet-weight basis decreased by 50% in the first 3 days. Thereafter, endrin was eliminated more slowly; elimination of 50% of the remainder required 8.9 days, and it took 32.9 days to lose 90% of the original amount.

Animals↗
PubMed1992

Effect of endrin on the hepatic distribution of iron and calcium in female Sprague-Dawley rats.

The distribution of iron and calcium in hepatic subcellular fractions of female rats treated with endrin (1,2,3,4,10,10-hexachloro-6,7-epoxy-1,4,4 alpha,5,6,7,8,8 alpha- octahydroendo,endo-1,4:5,8-dimethanonaphthalene) was determined. Endrin in corn oil was administered orally to rats in single doses of 3, 4.5, or 6 mg/kg, and the animals were killed at 0, 12, 24, 48, or 72 hr post-treatment. Iron and calcium were determined by atomic absorption spectroscopy. The administration of endrin increased the iron content of mitochondria and decreased the iron content of microsomes and nuclei. Significant increases occurred in the calcium content of mitochondria, microsomes, and nuclei. Thus, the results indicate that with respect to the subcellular distribution of iron and calcium, endrin produces differential effects. Vitamin E succinate administration partially prevented the endrin-induced hepatic alterations in iron and calcium homeostasis. Endrin also produced dose- and time-dependent increases in the liver and spleen weight/body weight ratios, while decreasing the thymus weight/body weight ratios. The altered distribution of calcium and iron may contribute to the broad range of effects of endrin.

Analysis of Variance↗
PubMedDate not supplied

Perinatal toxicity of endrin in rodents. I. Fetotoxic effects of prenatal exposure in hamsters.

The potential of the insecticide endrin to induce fetal toxicity was determined in hamsters exposed to the compound on either day 8 or days 5--14 of gestation. Endrin was administered by oral gavage as a solution in corn oil. Doses used included 0.5--10.0 mg/kg on day 8 and 0.75 to 3.5 mg/kg/day on days 5--14. Exposure to a single dose of endrin resulted in significant incidences of fused ribs and meningoencephaloceles at levels of 5 mg/kg or greater. No significant effects were noted in either maternal mortality and weight gain or in fetal mortality or weight gain. The administration of multiple doses of endrin resulted in few fetal defects, although a significant dose-related increase in fetal mortality and decrease in fetal weight was seen. Significant maternal lethality and weight reductions were noted at doses of 1.5 mg/kg/day or greater. At sacrifice, maternal liver and fetal tissues were collected and subsequently analyzed for endrin and a major metabolite, 12-ketoendrin. Endrin was found to cross the placenta and 20 ppb were found in fetuses from litters exposed to 2.5 mg/kg/day. Maternal livers from this dose group contained an average of 2500 pbb of endrin.

Abnormalities, Drug-Induced↗
PubMed1992

Endrin-induced increases in hepatic lipid peroxidation, membrane microviscosity, and DNA damage in rats.

Endrin is a polyhalogenated cyclic hydrocarbon pesticide which produces hepatic and neurologic toxicity. Previous studies have indicated that endrin induces hepatic lipid peroxidation. In order to further assess the possible role of lipid peroxidation in the toxicity of endrin, the dose- and time-dependent effects of endrin on hepatic lipid peroxidation, membrane microviscosity and DNA damage in rats were examined. Rats were treated with 0, 3.0, 4.5, or 6.0 mg endrin/kg as a single oral dose in corn oil, and the animals were killed 0, 12, 24, 48, or 72 h post-treatment. Dose-dependent increases in hepatic mitochondrial and microsomal lipid peroxidation and microviscosity as well as nuclear DNA single strand breaks were observed as early as 12 h post-treatment. Maximum increases in these three parameters occurred 24 h after endrin administration at all three doses. While the incidence in DNA damage decreased with time after 24 h, the incidence of lipid peroxidation and microviscosity of microsomal and mitochondrial membranes remained relatively constant. Dose- and time-dependent increases in liver and spleen weight/body weight ratios with decreases in thymus weight/body weight ratios were observed. The data indicate that endrin administration induces hepatic lipid peroxidation which may be responsible for the increased membrane microviscosity as a result of membrane damage as well as enhanced DNA damage.

Analysis of Variance↗
PubMed1989

Role of the brain t-butylbicyclophosphorothionate receptor in vertebrate resistance to endrin, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane and cypermethrin.

Certain populations of mosquitofish (Gambusia affinis) are highly resistant to endrin (42-fold), but are not cross-resistant to cypermethrin. These populations show relatively low levels of resistance (2-fold) to 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) and t-butylbicyclophosphorothionate (TBPS). Studies comparing specific [35S]TBPS binding to brain membrane preparations from resistant and susceptible fish indicate a reduced binding capacity for TBPS in membranes from resistant fish. Endrin was about twice as potent in competitively inhibiting [35S] TBPS binding in vitro to membranes from susceptible fish as compared to membranes from resistant fish, suggesting that TBPS binding sites in resistant fish brain are less sensitive to endrin. Endrin was 37 times as potent in competitively inhibiting [35S]TBPS binding in vivo to membranes from susceptible fish compared to membranes from resistant fish, indicating that a contributory factor is involved in endrin resistance. Data for TBPS inhibition of [35S]TBPS binding revealed an approximate 2-fold difference between resistant and susceptible for both in vitro and in vivo IC50, indicating that an altered TBPS binding site is the only factor involved in TBPS resistance. DDT did not inhibit [35S] TBPS binding, suggesting that DDT resistance is not due to changes at the TBPS receptor. These data support the hypothesis that two factors operate in vertebrate resistance to endrin, whereas only one of these factors confers TBPS resistance. These resistance mechanisms are not functional against cypermethrin.

Animals↗
PubMed1987

An electron microscopic study of endrin induced alterations in unmyelinated fibers of mouse sciatic nerve.

This study examined the ultrastructural alterations in peripheral nerve of adult mouse following repeated sublethal exposures to endrin, a toxic chlorinated hydrocarbon which produces symptoms indicative of neuromuscular dysfunction. Male mice were given 20 daily ip injections of endrin in sesame oil (0.2 ml) in doses that increased from 1.5 mg/kg on days 0-3, to 2.0 mg/kg on days 4-11, and to 4.0 mg/kg on days 12-19. Controls were given the same intraperitoneal volume of sesame oil without endrin. Animals were sacrificed by glutaraldehyde perfusion after 4, 7, 14, and 20 days of exposure and 14 and 92 days postinjection and sciatic nerve tissue was prepared for electron microscopy. Myelinated nerve fibers, myelin and associated Schwann cells from endrin exposed animals appeared similar to those of controls and normal animals. Various morphological alterations were observed in many unmyelinated axons from endrin exposed animals. Such alterations included swelling, dissolution of microtubules and neurofilaments, the presence of unusual numbers of axoplasmic vesicles, both scattered and in packets, and less often, extreme vacuolation. In those Schwann cells associated with damaged axons the cytoplasm and the adaxonal space frequently contained vesicles, often in packets invaginating the axolemma. The results of this study indicate that repeated subacute doses of endrin can produce morphological alterations in unmyelinated peripheral nerve fibers and their associated Schwann cells without apparent damage to myelinated nerve fibers. The results are discussed relative to other studies producing similar nerve damage and to the potential mechanisms responsible for such damage.

Animals↗
PubMed1979

Carcinogenicity of endrin.

Endrin is carcinogenic for rats, and most likely also for mice and dogs. Endrin caused significant incidences of malignant neoplasms at all sites. In one study, female rats were susceptible to the development of neoplasms of the endocrine organs, particularly carcinomas of the adrenal and pituitary glands as well as neoplasms of the reproductive system. In other studies, female rats tended to have carcinomas of the endocrine system, the mammary gland and reproductive system, and male and female rats lymphomas. Rats developed unusual malignant neoplasms, such as Kupffer cell sarcomas of the liver and sarcomas of the mammary gland, uterus, and stomach. There also were toxic changes, particularly in male rats, ingesting endrin. These lesions included interstitial fibrosis of the kidney; polyarteritis of the mesenteric, pancreatic and other arteries; and atrophy of the testes. Such lesions generally interfere with the health of the rats and with the development of neoplasms. Dog receiving endrin for two years had bone marrow hyperplasia, lesions of the thyroid gland and lesions of the skeletal muscle, and hyperplasias or neoplasms of other organs. One female dog had an early carcinoma of the thyroid gland. Mice ingesting endrin developed increased incidences of carcinomas of the liver and sarcomas of the uterus.

Adenoma↗
PubMed1990

Endrin-induced depletion of glutathione and inhibition of glutathione peroxidase activity in rats.

1. Recent studies have shown that endrin induces lipid peroxidation and may produce toxicity through an oxidative stress. We have therefore examined the effect of endrin administration to rats on glutathione content and the activities of glutathione metabolizing enzymes. 2. The oral administration of endrin resulted in dose- and time-dependent decreases in hepatic and renal glutathione content with maximum depletion (90%) occurring in liver at approximately 24 hr post-treatment. 3. Decreases in glutathione content were also observed in lung, brain, spleen and heart. 4. Endrin (4 mg/kg) decreased selenium dependent glutathione peroxidase activity in liver and kidney by 64 and 50%, respectively, while small increases were observed in the activities of glutathione reductase and glutathione S-transferase. 5. The toxicity of endrin may be at least in part related to oxidative tissue damage associated with depletion of glutathione and inhibition of glutathione peroxidase activity.

Animals↗
PubMed1992

Endrin-induced production of nitric oxide by rat peritoneal macrophages.

The effect of oral endrin administration to rats on the production of nitric oxide (NO) by peritoneal macrophages was investigated. Nitric oxide formation was measured as nitrite. Endrin (4.5 mg/kg) enhanced the secretion of NO by approx. 300%. The effect of endrin on NO formation was both dose- and time-dependent. Ellagic acid, which has been shown to be a potent antioxidant, inhibited the elevation of NO production induced by endrin. These results suggest that the toxicity of endrin may at least in part be due to the production of an oxidative stress.

Administration, Oral↗
PubMed1985

A case of fatal endrin poisoning.

Ingestion of 12 g of endrin by a 49-year-old man caused convulsions persisting for 4 days, hypersalivation, hyperthermia, renal insufficiency, thrombocytopenia and recurrent hypotension. Death followed after 11 days, due to pulmonary complications (infection and haemorrhage) and hypoxaemia causing bradycardia and cardiac arrest. Endrin and dieldrin concentrations in blood 4 hours, 6 and 11 days after ingestion were respectively 450, 86 and 71 micrograms/l for endrin and 60, 19 and 19 micrograms/l for dieldrin. Dieldrin was also present, possibly because the endrin preparation contained traces of dieldrin. Endrin concentrations 11 days after ingestion were 0.071 mg/l in blood, in adipose tissue 89.5 mg/kg, in the heart 0.87 mg/kg, in the brain 0.89 mg/kg, in the kidneys 0.55 mg/kg and in the liver 1.32 mg/kg.

Endrin↗
PubMed1992

Seizures after eating a snack food contaminated with the pesticide endrin. The tale of the toxic taquitos.

In September 1988 we investigated reports of seizures in persons who had eaten taquitos, a commercially prepared snack food. We identified and interviewed 5 persons with new-onset seizures within 12 hours of eating taquitos, all purchased during a 1-week period from a single store. Leftover taquitos were found to contain endrin, a highly toxic chlorinated hydrocarbon pesticide. Although tissue confirmation of exposure to endrin was not possible and the level of contamination in the tested taquitos was below that previously thought to be capable of inducing seizures, the pattern of symptoms and the common time and place of purchase strongly suggested that the seizures were due to endrin-contaminated taquitos. The source of endrin contamination could not be determined. This episode is the first report of illness associated with endrin-contaminated food products in the United States.

Adolescent↗
PubMed1971

Histopathologic lesions in cutthroat trout (Salmo clarki) exposed chronically to the insecticide endrin.

Pathologic conditions associated with exposure to endrin were found in the gill, liver, pancreas, brain and gonad of cutthroat trout. Edema, hemorrhage and possibly intracapillary congestion characterized gill damage after exposure to the highest level of endrin in bath. Hepatic lesions in young trout were of a type frequently described as preceding the development of hepatomas in nutritionally deficient fish. The increased incidence and severity of hepatic degenerative changes observed in fish exposed to high levels of endrin suggested nutritional deficiency enhanced by exposure to endrin. Marked hyperplasia of pancreatic islets and irregular, atypical oocytes were observed after exposure to high endrin levels.

Animals↗
PubMed1978

Endrin and malathion toxicity to flagfish (Jordanella floridae).

Endrin and malathion effects on survival, growth, and reproduction of flagfish were determined in a flow-through system. Endrin chronic effects on first-generation growth and reproduction occurred only at 0.3 microgram/L, the highest concentration tested. The mean endrin residues in the first-generation fish at 65 days were about 15,000 times the water concentration in all concentrations tested. Malathion concentrations of 31.5 microgram/L and 24.7 microgram/L, the highest concentrations tested, had detrimental effects on first-generation survival. During the same period malathion concentrations as low as 10.9 microgram/L significantly affected growth. Neither insecticide, at the concentrations tested, had any detectable effects on the second generation during a 30-day exposure period. Acute toxicities to juvenile fish were also determined in the same flo-through system. The 96-hr LC50's were 0.85 microgram/L for endrin and 349 microgram/L for malathion.

Animals↗