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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↗
PubMed1993

Comparative effects of endrin on hepatic lipid peroxidation and DNA damage, and nitric oxide production by peritoneal macrophages from C57BL/6J and DBA/2 mice.

1. Endrin is a polyhalogenated cyclic hydrocarbon which produces hepatic and neurologic toxicity. In order to further assess the mechanism of toxicity of endrin, the dose-dependent effects of endrin on hepatic lipid peroxidation and DNA damage, and nitric oxide (NO) production by peritoneal exudate cells (primarily macrophages) were investigated in C57BL/6J and DBA/2 mice which vary at the Ah receptor genetic locus. C57BL/6J mice are dioxin-responsive, while DBA/2 mice are dioxin-insensitive. 2. Mice of both strains were treated with 0, 1, 2 or 4 mg endrin kg-1 as a single oral dose in corn oil, and the animals were killed 24 hr post-treatment. At doses of 1, 2 and 4 mg endrin kg-1 in C57BL/6J mice, hepatic mitochondrial lipid peroxidation increased 1.2-, 2.2- and 3.2-fold, respectively, and 1.8-, 2.3- and 3.5-fold with microsomes, respectively. At these same doses in DBA/2 mice, hepatic mitochondrial lipid peroxidation increased 1.3-, 2.0- and 2.6-fold, respectively, and 1.5-, 1.9- and 2.5-fold with microsomes, respectively. 3. Increases of 2.3-, 2.4- and 4.9-fold were observed in hepatic DNA damage (elution constants) in C57BL/6J mice at doses of 1, 2 and 4 mg endrin kg-1, respectively, while at these same three doses, increases of 1.9-, 2.1- and 2.3-fold were observed for DBA/2 mice, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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↗
PubMed1981

Perinatal toxicity of endrin in rodents. III. Alterations of behavioral ontogeny.

The behavioral development of rats and hamsters was observed following perinatal exposure to endrin, a central nervous system teratogen in the hamster but not the rat [1,2]. In the hamster, prenatal exposure to endrin at 1.5 mg/kg/day on days 5-14 of gestation produced a persistent elevation in the locomotor activity. Offspring of treated hamsters ambulated 75% more than controls in the open field at 15 days and 45% more at 20 days of age. Long term observations of locomotor activity in the figure-8 mazes indicated that a significant elevation of this behavior was still present at 125 days of age. Non-locomotor behaviors of the Offspring (including sexual, rearing and running wheel behaviors) were unaffected. The dams repeatedly exposed daily to endrin at 0.75 or 1.5 mg/kg/day were markedly hypoactive using the same testing conditions in which the pups were hyperactive. This dosing regime was toxic to the dams in the 1.5 mg/kg/day dose group, killing more than half of them. In the second experiment, rats exposed perinatally to endrin at 0.15 or 0.30 mg/kg/day were 30% more active than control prior to weaning, but not as adults. These doses did not kill dams or affect the pup survival or growth. The similarity of the behavioral changes noted in the young of both species is suggestive of similar alteration of central nervous system function even though endrin produces gross morphological defects only in the hamster.

Aging↗
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↗
PubMed1996

Comparative teratological studies on TCDD, endrin and lindane in C57BL/6J and DBA/2J mice.

The teratogenic effects of endrin and lindane have been determined and compared to those induced by TCDD in the fetuses of C57BL/6J and DBA/2J mice after the administration of single oral doses to pregnant mice on day 12 of gestation. TCDD produced dose-dependent decreases in fetal weight, fetal thymic weight and placental weight, and dose-dependent increases in fetolethality, cleft palate formation and hydronephrosis at doses of 10-30 and 30-60 micrograms/kg body weight in C57BL/6J and DBA/2J mice, respectively. No maternal death was observed at the given doses in both strains of mice. Endrin (4.5 and 6 mg/kg body weight) and lindane (30 and 45 mg/kg body weight) produced significant decreases in fetal weight and placental weight in C57BL/6J and DBA/2J mice, and dose-dependent decreases in fetal thymic weight in C57BL/6J mice but not DBA/2J mice. Endrin and lindane caused 0-25 and 14-25% maternal deaths, respectively, at the above mentioned doses. Neither cleft plate nor hydronephrosis were induced by endrin or lindane in the two strains of mice. The results support the hypothesis that TCDD-induced cleft plate and hydronephrosis involve mechanisms that are Ah (aryl hydrocarbon) receptor mediated. However, other fetotoxic effects induced by TCDD, and the fetotoxic effects induced by endrin and lindane may involve additional unknown mechanisms that are not related to the Ah-receptor.

Abnormalities, Drug-Induced↗
PubMed2002

Comparative effects of TCDD, endrin, naphthalene and chromium (VI) on oxidative stress and tissue damage in the liver and brain tissues of mice.

The mechanism of toxicity of structurally diverse environmental toxicants including heavy metals and polyhalogenated and polycyclic hydrocarbons may involve a common cascade of events which entails an oxidative stress and production of reactive oxygen species. We have determined the comparative effects of single 0.01, 0.10 and 0.50 LD(50) doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), endrin, naphthalene and sodium dichromate (chromium VI) on lipid peroxidation, DNA fragmentation and enhanced production of superoxide anion (cytochrome c reduction) in liver and brain tissues of C57BL/6NTac mice. The effects of a single acute oral 0.50 LD(50) dose of these xenobiotics on hepatic and brain lipid peroxidation were investigated at 0, 12, 24, 48, and 96 h after treatment, while the effects of 0.10 LD(50) and 0.01 LD(50) doses of these xenobiotics were at 0, 24, 48, 72, and 96 h after treatment. Dose- and time-dependent effects were observed with all four xenobiotics. At a 0.50 LD(50) dose of TCDD, endrin, naphthalene and chromium VI, maximum increases in cytochrome c reduction (superoxide anion production) of approximately 5.7-, 5.4-, 5.3- and 4.1-fold, respectively, were observed in hepatic tissues. TCDD showed an increasing effect through 96 h. Endrin and naphthalene demonstrated a maximum effect at 12-24 h, while chromium VI exhibited a maximum effect at 48 h. With respect to lipid peroxidation, at a 0.50 LD(50) dose both endrin and chromium VI induced the maximum effect at 48 h of treatment, while naphthalene demonstrated the maximum effect after 24 h of treatment. TCDD demonstrated a continued effect through 96 h of treatment. At a 0.50 LD(50) dose TCDD, endrin, naphthalene and chromium VI produced maximum increases in hepatic lipid peroxidation of approximately 3.5-, 3.1-, 3.7- and 3.3-fold in hepatic tissues, respectively. Similar results were obtained in hepatic and brain DNA fragmentation at 0.50 LD(50) doses. Lesser effects were observed with 0.10 and 0.01 LD(50) doses of these xenobiotics as compared to the 0.50 LD(50) dose. The results clearly demonstrate that these diverse xenobiotics induce dose- and time-dependent oxidative stress and tissue damage in the liver and brain tissues of mice.

Air Pollutants↗
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↗
PubMed1966

Endrin: use of concentration in blood to diagnose acute toxicity to fish.

Channel catfish, Ictalurus punctatus (Rafinesque), were exposed to continuously renewed solutions of endrin in water. Analyses of the fish blood by gas chromatography revealed a well-defined threshold concentration of endrin in the blood, approximately 0.30 microgram per gram, that, if exceeded, results in death. Fish exposed to lethal concentrations of endrin in water for periods of time insufficient to cause death had blood-endrin concentrations markedly lower than those that died from exposture to the same water. There was little overlap in range of endrin concentration in blood between dead and living exposed fish.

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↗
PubMedDate not supplied

A surprising case of endrin poisoning in dogs.

A case of possible malicious poisoning of dogs by endrin was investigated. A variety of tissues were analysed. The stomach contents of one dog contained 5 g/kg endrin. The results are compared with recorded data from feeding studies pursued elsewhere to aid the diagnosis of dieldrin and endrin intoxication. A number of organochlorine compounds closely related chemically to endrin were tentatively identified.

Animals↗
PubMed1996

TCDD, endrin and lindane induced oxidative stress in fetal and placental tissues of C57BL/6J and DBA/2J mice.

The abilities of TCDD, endrin and lindane to induce oxidative stress in fetal and placental tissues have been studied after the oral administration of these xenobiotics to pregnant C57BL/6J and DBA/2J mice. Production of superoxide anion, lipid peroxidation and DNA-single strand breaks (SSB) was determined in live fetal and placental tissues 48 hr after administration of single teratogenic doses of the compounds on day 12 of gestation. Oxidative stress and its biomarkers were also determined in livers of day 18 fetuses after administration on day 12 of gestation. TCDD given at doses of 30 and 60 micrograms/kg body weight to the C57BL/6J and DBA/2J mice, respectively, produced increases of 1.3-2.7-fold in superoxide anion production, 1.6-1.9-fold in lipid peroxidation and 2.1-4.4-fold in DNA-SSB. Endrin, given at a dose of 4.5 mg/kg body weight to C57BL/6J and DBA/2J mice, produced increases of 1.3-2.8-fold in superoxide production, 1.4-1.8-fold in lipid peroxidation and 1.4-4.7-fold in DNA-SSB. Lindane when given at a dose of 30 mg/kg body weight to C57BL/6J and DBA/2J mice produced increases of 1.6-3.0-fold in superoxide production, 1.3-2.1-fold in lipid peroxidation and 1.4-5.0-fold in DNA-SSB. The results suggest that superoxide production, lipid peroxidation and DNA-SSB in fetal and placental tissues may participate in the fetotoxic effects of TCDD and other polyhalogenated cyclic hydrocarbons, and that TCDD-induced oxidative damage in fetal and placental tissues is mediated at least in part by the Ah-receptor. The results also indicate that TCDD as an inducer of oxidative tissue damage in the embryos and placentas is approximately 150 and 1000 times more potent than endrin and lindane, respectively, in C57BL/6J mice, and 75 and 500 times more potent than endrin and lindane, respectively, in the DBA/2J mouse strain.

Administration, Oral↗
PubMed2000

Role of p53 tumor suppressor gene in the toxicity of TCDD, endrin, naphthalene, and chromium (VI) in liver and brain tissues of mice.

It has been postulated that tumor suppressor genes are involved in the cascade of events leading to the toxicity of diverse xenobiotics. Therefore, we have assessed the comparative effects of 0.01, 0.10, and 0.50 median lethal doses (LD(50)) of 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), endrin, naphthalene, and sodium dichromate (VI) [Cr(VI)] on lipid peroxidation, DNA fragmentation, and enhanced production of superoxide anion (cytochrome c reduction) in liver and brain tissues of p53-deficient and standard C57BL/6NTac mice to determine the role of p53 gene in the toxic manifestations produced by these diverse xenobiotics. In general, p53-deficient mice are more susceptible to all four xenobiotics than C57BL/6NTac mice, with dose-dependent effects being observed. Specifically, at a 0.50 LD(50) dose, naphthalene and Cr(VI) induced the greatest toxicity in the liver tissue of mice, and naphthalene and endrin exhibited the greatest effect in the brain tissue. At this dose, TCDD, endrin, naphthalene, and Cr(VI) induced 2.3- to 3.7-fold higher increases in hepatic lipid peroxidation and 1.8- to 3.0-fold higher increases in brain lipid peroxidation in p53-deficient mice than in C57BL/6NTac mice. At a 0. 10 LD(50) dose, TCDD, endrin, naphthalene, and Cr(VI) induced 1.3- to 1.8-fold higher increases in hepatic lipid peroxidation and 1.4- to 1.9-fold higher increases in brain lipid peroxidation in p53-deficient mice than in C57BL/6NTac mice. Similar results were observed with respect to DNA fragmentation and cytochrome c reduction (superoxide anion production). For example, at the 0.10 LD(50) dose, the four xenobiotics induced increases of 1.6- to 3. 0-fold and 1.5- to 2.1-fold in brain and liver DNA fragmentation, respectively, and increases of 1.5- to 2.3-fold and 1.4- to 2.5-fold in brain and liver cytochrome c reduction (superoxide anion production), respectively, in p53-deficient mice compared with control C57BL/6NTac mice. These results suggest that the p53 tumor suppressor gene may play a role in the toxicity of structurally diverse xenobiotics.

Animals↗