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PubMed1991

Endrin-induced histopathological changes and lipid peroxidation in livers and kidneys of rats, mice, guinea pigs and hamsters.

Endrin toxicity may be due to an oxidative stress associated with increased lipid peroxidation, decreased glutathione content, and inhibition of glutathione peroxidase activity. Extensive interspecies variability exists in sensitivity towards endrin. Therefore, histopathological changes and lipid peroxidation in the livers and kidneys of rats, mice, hamsters, and guinea pigs were examined 24 hr after the administration of 4 mg endrin/kg body weight orally in corn oil. Degeneration and necrotic changes with inflammatory cell infiltration were observed in livers and kidneys, and interspecies variability occurred. Fatty changes in the form of hepatic foam cells with cytoplasmic vacuolation were present. Lipofuscin pigments, associated with lipid peroxidation, were observed in hepatocytes and Kupffer cells. These histopathological conditions were prevented in rats which had been pretreated with butylated hydroxyanisole, vitamins E and C, or cysteine, antioxidants and free radical scavengers which have previously been shown to inhibit lipid peroxidation. The extent of endrin-induced lipid peroxidation correlated well with the degree of histopathological changes. Thus, histological changes consistent with the induction of an oxidative stress were observed following the administration of endrin to various animal species.

Animals↗
PubMed1987

Convulsions caused by endrin poisoning in Pakistan.

From July through September 1984, acute convulsions caused by endrin poisoning occurred in the subdistrict of Talagang, Attock District, Punjab province, Pakistan. Eighteen of the 21 affected villages were surveyed; 70% of the cases for which ages were known (106 of 152) were in children 1 to 9 years of age; 9.8% of all affected persons (19 of 194) died. The outbreak occurred in villages on the main roads of the subdistrict and peaked in early September. Endrin was detected in the blood of 12 of 18 patients with a history of convulsions but was not found in the blood of four hospitalized control patients. One composite sugar sample taken from the homes of three persons had an endrin level of 0.04 ppm. Because of the high toxicity, repeated association with large-scale outbreaks of neurologic illness, and the difficulties of monitoring distribution, endrin should not be used for agricultural purposes.

Child↗
PubMed1996

TCDD endrin and lindane induced increases in lipid metabolites in maternal sera and amniotic fluids of pregnant C57BL/6J and DBA/2J mice.

TCDD, endrin and lindane induce an oxidative stress and enhance lipid peroxidation in fetal and placental tissues of mice. The levels of the products resulting from altered lipid metabolism, including malondialdehyde (MDA), formaldehyde (FA), acetaldehyde (ACT) and acetone (ACON) have been determined in maternal sera and amniotic fluids of pregnant C57BL/6J and DBA/2J mice after oral administration of single fetotoxic doses of TCDD, endrin and lindane on day 12 of gestation, using high pressure liquid chromatography (HPLC). Under these conditions, TCDD given at a dose of 30 micrograms/kg body weight to C57BL/6J mice produced 2.5-3.9 and 1.7-4.0 fold increases in the levels of the four metabolites in maternal sera and the amniotic fluids, respectively. TCDD given to DBA/2J mice at a dose of 60 micrograms/kg produced 1.5-1.7 and 1.7-2.2 fold increases in the levels of these metabolites in maternal sera and the amniotic fluids, respectively. Endrin, when given at a dose of 4.5 mg/kg body weight to either mouse strain, produced increases of 1.9-3.1 and 1.7-3.2-fold in the levels of the four metabolites in maternal sera and the amniotic fluids, respectively, in the C57BL/6J mice and increases of 1.4-1.6 and 1.2-1.5 fold in the levels of these metabolites in maternal sera and the amniotic fluids, respectively, in the DBA/2J mice. Lindane given at a dose of 30 mg/kg body weight to C57BL/6J mice produced 1.5-2.0 and 1.3-1.7-fold increases in the four metabolites in maternal serum and amniotic fluids, respectively, while administration of this same dose to DBa/2J mice produced 1.2-1.5 and 1.1-1.5 fold increases, respectively. Increases in the levels of lipid metabolites occur in maternal serum and amniotic fluid as a result of enhanced lipid peroxidation in response to TCDD, endrin and lindane. Lipid peroxidation may participate in the fetotoxic effects of these xenobiotics and these effects are observed regardless of the Ah-responsiveness of the mice, although higher levels of the metabolites are produced by TCDD in Ah-responsive mice.

Amniotic Fluid↗
PubMedDate not supplied

Protective effects of antioxidants against endrin-induced lipid peroxidation, glutathione depletion, and lethality in rats.

Endrin depletes glutathione levels and induces lipid peroxidation in various species of animals. We have, therefore, examined the effect of antioxidants on these parameters in endrin-treated rats. Butylated hydroxyanisole (BHA), vitamin E, vitamin C, and the glutathione precursor cysteine significantly inhibited hepatic glutathione depletion and lipid peroxidation induced by 4 mg endrin/kg body weight. Furthermore, these antioxidants provided partial protection against lethality produced by 8 mg endrin/kg body weight. These results suggest but do not prove that free radical-mediated lipid peroxidation and glutathione depletion may be involved in the toxic manifestations of endrin.

Animals↗
PubMed1976

The accumulation and loss of dieldrin and endrin in the eastern oyster.

Oysters demonstrated an ability to significantly concentrate dieldrin and endrin. Concentration ratios obtained after 168-hr exposures to endrin were 1670 at 0.1 mug/L and 2780 at 50 mug/L. Dieldrin was concentrated to higher levels. Exposure to 14C-labelled dieldrin at 0.5 mug/L produced whole body concentrations 2880 times the ambient level at 168 hr, while exposure to nine mug/L of dieldrin resulted in a concentration ratio of 2070 following the same period of exposure. Both endrin and dieldrin showed distinct linear regions in semi-logarithmic plots of uptake against time. Initial uptake was rapid and was followed by somewhat slower but still rapid uptake over the next 6 to 48 hr. Uptake within each of the stages followed an exponential form.

Animals↗
PubMed1988

Toxicity of chlorpyrifos, endrin, or fenvalerate to fathead minnows following episodic or continuous exposure.

Fathead minnow larvae (Pimephales promelas) were exposed to three individual pesticides during brief or continuous exposure in 96-hr and 28- to 30-day toxicity tests. Continuous exposure 96-hr LC50 values for chlorpyrifos, endrin, and fenvalerate were 122.2, 0.7, and 0.85 micrograms/liter, respectively. Continuous exposure chronic effect concentrations were chlorpyrifos, 2.1 micrograms/liter (increased deformities); endrin, 0.38 micrograms/liter (reduction in growth); and fenvalerate, 0.36 micrograms/liter (reduction in survival and growth). Brief exposure chronic test results indicated that fathead minnow exposure to chlorpyrifos for as few as 5 hr at a concentration similar to a continuous exposure 96-hr LC50 value resulted in increased deformities and a reduction in growth, whereas a 48-hr exposure at a concentration similar to a continuous exposure 96-hr LC50 value was required to cause a reduction in growth for endrin and a reduction in survival and growth for fenvalerate. It is suggested that although constant exposure laboratory tests are essential for hazard assessment, the relationships of exposure duration and toxicant intensity to ecotoxic effects are necessary for reliable risk assessments and implementation of water quality standards.

Animals↗
PubMed1983

In vivo induction of sister-chromatid exchange in Umbra limi by the insecticides endrin, chlordane, diazinon and guthion.

Central mudminnows, Umbra limi, were exposed to the insecticides endrin, chlordane, diazinon and guthion at concentrations of 5.4 X 10(-12) M to 5.4 X 10(-9) M in the aquaria water. Endrin, chlordane and diazinon caused significant increase in the frequencies of SCE. The results of these tests in part are in contrast to previous work which did not find endrin to be mutagenic. Our results suggest that the in vivo SCE test is an efficacious method of detecting mutagenic pesticides in water.

Animals↗
PubMed1992

Endrin-induced urinary excretion of formaldehyde, acetaldehyde, malondialdehyde and acetone in rats.

Previous studies have shown that endrin induces an oxidative stress in rats as demonstrated by an increase in hepatic lipid peroxidation, a decrease in glutathione content and a decrease in the activity in selenium-dependent glutathione peroxidase. We have therefore examined the effects of orally administering 1.5, 3.0, 4.5 and 6.0 mg endrin/kg on the urinary excretion of the lipid metabolites formaldehyde, malondialdehyde, acetaldehyde and acetone. The simultaneous determination of these four lipid metabolites may be a useful biomarker for assessing exposure to xenobiotics which induce an oxidative stress and enhanced lipid peroxidation. Urine samples were collected up to 72 h post-treatment. The identities of the lipid metabolites were confirmed by gas chromatography-mass spectroscopy, while the 2,4-dinitrophenylhydrazine derivatives of these metabolic products were quantitated by high pressure liquid chromatography. Maximum increases in the excretion of the four lipid metabolites occurred at approx. 24 h post-treatment at all doses with no significant increases in excretion occurring thereafter. The maximum increases in excretion of malondialdehyde, formaldehyde, acetaldehyde and acetone were approx. 160%, 93%, 121% and 162%, respectively, relative to control values. Seventy-two hours after endrin administration, the liver weight/body weight and spleen weight/body weight ratios significantly increased while the thymus weight/body weight ratio markedly decreased. The results demonstrate that endrin induces dose- and time-dependent alterations in lipid metabolism with the enhanced excretion of specific metabolic products in the urine.

Acetaldehyde↗
PubMed1992

A high endrin concentration in a fatal case.

Gas chromatography coupled to mass spectrometry was employed to quantify endrin in biological fluids in a death attributed to endrin overdose. The blood concentration of endrin was 544.9 mg/l. Results are discussed in the light of the existing literature.

Adult↗
PubMed1983

Physiological mechanism of toxic action of DDT and endrin in two euryhaline freshwater fishes, Anguilla vulgaris and Mugil cephalus.

RBC counts, Ht value and Hb content in both species exposed to DDT and endrin concentrations were not significantly different from those of controls. WBC counts in both species exposed to the two pesticides for 96 hr decreased significantly at different concentrations. The variance ratios of cations and anions were consistently more concentrated in the serum of DDT- and endrin-exposed fishes. Serum cholesterol was sharply elevated in all the lots exposed to pesticides. Exposure to sublethal concentrations of DDT and endrin impaired liver function, as evidenced by the transfer of major cations from hepatic tissue to the serum and by elevated serum cholesterol.

Animals↗
PubMed1993

Comparative studies on lipid peroxidation and DNA-single strand breaks induced by lindane, DDT, chlordane and endrin in rats.

1. A variety of structurally dissimilar polyhalogenated cyclic hydrocarbons produce similar toxic effects. The molecular mechanisms involved in the production of these toxic manifestations is not known. 2. We have proposed that reactive oxygen species may be involved, and have therefore examined the time-dependent effects of lindane (30 mg/kg), DDT (40 mg/kg), chlordane (120 mg/kg), and endrin (4.5 mg/kg) on the production of hepatic mitochondrial and microsomal lipid peroxidation and DNA single strand breaks, two indices of oxidative stress. 3. All four xenobiotics resulted in significant increases in hepatic lipid peroxidation and DNA damage. Earliest (6 hr) increases in both lipid peroxidation and DNA damage were observed following lindane administration. Time-dependent increases in both parameters were observed following endrin administration. 4. Maximum increases in DNA single strand breaks of 2.8- and 2.5-fold were observed 12 hr after DDT and chlordane administration, respectively, while a 4.4-fold increase was observed 24 hr after endrin administration. 5. The results demonstrate that the four structurally dissimilar polyhalogenated hydrocarbons produce oxidative tissue damage which may contribute to the toxic manifestations of these xenobiotics, and exhibit different toxicokinetic properties.

Animals↗
PubMed1993

In vitro induction of reactive oxygen species by 2,3,7,8-tetrachlorodibenzo-p-dioxin, endrin, and lindane in rat peritoneal macrophages, and hepatic mitochondria and microsomes.

Hepatic mitochondria and microsomes as well as peritoneal macrophages from female Sprague-Dawley rats were incubated for up to 30 min at 37 degrees C in the presence of 0-200 ng/ml 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 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), and lindane (hexachlorocyclohexane). Production of reactive oxygen species was determined by chemiluminescence and cytochrome c reduction, while potential tissue damage was assessed by alterations in membrane fluidity. Chemiluminescence, a sensitive but nonspecific measure of free radical generation, increased 40-70% when macrophages (3 x 10(6) cells/ml), mitochondria and microsomes (1 mg/ml) were incubated with the three polyhalogenated cyclic hydrocarbons (PCH). Maximum increases in chemiluminescence occurred within 5-10 min of incubation and persisted for over 30 min. The cytochrome c reduction assay is most specific for superoxide anion production. When hepatic mitochondria were incubated with endrin and lindane for 15 min at 100 ng/ml, increases in cytochrome c reduction of 6.5- and 7.5-fold occurred, respectively, while when microsomes were incubated with these same two PCH, increases in cytochrome c reduction of 8.6- and 11.6-fold occurred, respectively. When mitochondria, microsomes, and macrophages were incubated with TCDD under identical conditions, small increases in superoxide anion production were detected. Changes in microsomal membrane fluidity were determined spectrofluorometrically following incubation with the three PCH using diphenyl-1,3,5-hexatriene as the fluorescent probe. TCDD, endrin, and lindane enhanced microsomal membrane apparent microviscosity by 2.3-, 2.1-, and 2.5-fold, respectively, indicating a significant decrease in membrane fluidity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Endrin: effects on the entire life cycle of a saltwater fish, Cyprinodon variegatus.

The sheepshead minnow (Cyprinodon variegatus) was continuously exposed for 23 wk to the organochlorine insecticide endrin, from the embryonic state through hatching until adulthood and spawing. The resultant progeny were monitored to determine the effects of the toxicant on their survival, growth, and reproduction. Average measured exposure concentrations were O (control), 0.027, 0.077, 0.12, 0.31, and 0.72 microgram/liter. Embryos exposed to 0.31 and 0.72 microgram/liter hatched early; all fry exposed to 0.72 microgram/liter died by day 9 of exposure. At 0.31 microgram/liter, fry were initially stunted and some died. Survivors seemed unaffected until maturity, when some females died during spawning; fewer eggs were fertile and survival of exposed progeny decreased. No significant effects were observed th roughout this fish's life cycle at an exposure concentration of 0.12 microgram/liter. Four-week-old juvenile fish accumulated 2,500 times the concentration of endrin in the exposure water; adults, 6,400 times; and their eggs, 5,700 times. The specific application factor (calculated by dividing the limits on the maximum acceptable toxicant concentration, greater than 0.12 and less than 0.31 microgram/liter, by the concentration lethal to 50% of the juvenile fish in 96 hr, 0.34 microgram/liter) ranged from 0.35 to 0.91. To our knowledge this is the first toxicity test carried out through the entire life cycle of an oviporous esturarine fish. Data from this experiment and from experiments with another estuarine fish and four freshwater fish all demonstrate that there is little difference between endrin concentrations that produce acute effects and concentrations that do not affect the fish in chronic exposures lasting four or more weeks.

Age Factors↗
PubMed1979

The successful use of "high level" PEEP in near fatal Endrin poisoning.

The insecticide Endrin is a highly toxic chlorinated hydrocarbon which can cause severe CNS and respiratory derangement. Death usually follows intoxication within 24 hours. A 19-year-old male developed convulsions and gross pulmonary edema after the ingestion of Endrin. His trachea was intubated and constant positive pressure ventilation with PEEP of up to 28 cm H2O was instituted. The patient survived and recovery appeared to be complete. Severe pulmonary edema is not a common finding in patients who have Endrin poisoning. The use of PEEP above 15 cm H2O is a controversial issue; however, we believe that it contributed significantly to the survival of our patient.

Adult↗
PubMed1975

The metabolic fate of endrin in the rabbit.

1. [14C]Endrin, administered orally to rabbits, is excreted in the faeces as unchanged endrin (50% of that administered) and in the urine as a mixture of polar metabolites. 2. The major biotransformation is hydroxylation at the methylene bridge (C-12) to yield anti-12-hydroxyendrin. syn-Hydroxylation at C-12 also occurs. 3. The hydroxylated metabolites are excreted mainly as their sulphate conjugates. 4. Glucuronide conjugates are also excreted. anti-12-Hydroxyendrin is rapidly conjugated in vitro on incubation with rabbit liver microsomal glucuronyl transferase and UDPGA. 5. Comparative aspects of the metabolism of endrin in rats and rabbits are discussed.

Administration, Oral↗
PubMed1985

A suspected case of endrin toxicosis in a cat.

Endrin toxicosis was diagnosed in a cat after it ingested birds poisoned with endrin. The animal lived next to a feed mill where an avicide was used. Analysis by gas chromatography of vomitus from the cat revealed the presence of endrin.

Animals↗
PubMed1967

Endrin resistance in the pine mouse.

Wild pine mice with a history of treatment with endrin exhibited a 12-fold greater tolerance to the pesticide than did mice having no history of endrin treatment. A genetic basis for the resistance would be expected, in view of the fact that the resistant mice had been exposed to endrin for 11 years. However, sublethal dosages conferred a degree of resistance on both mouse populations; this indicates the possibility of an inducible resistance.

Animals↗
PubMed1985

Mortality study of industrial workers exposed to aldrin, dieldrin and endrin.

Vital status and cause of death were assessed for 232 of a group of 233 workers engaged in the manufacturing and formulation of aldrin, dieldrin, endrin and (for a limited period) Telodrin. This group is part of the total exposed population of more than 1000 workers and was selected for follow up on account of the high exposures in the initial years of manufacturing and formulation and of the long exposure (mean 11 years) and observation (mean 24 years) periods. Total observed mortality was 25 versus 38 expected on the basis of the death statistics of the male Dutch population. Of the 9 cancer deaths, 3 were caused by lung cancer, while the remaining 6 were each of a different nature. Although in this group exposures have been high and exposure, as well as observation periods, were long enough for meaningful evaluation, this study revealed no indication of a specific carcinogenic activity of aldrin, dieldrin or endrin in manufacturing plant workers exposed to these products.

Aged↗