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PubMed1986

Anti-estrogenic action of chlordecone in rat pituitary gonadotrophs in vitro.

Estradiol-17 beta (E2) enhances the response of rat pituitary gonadotrophs to gonadotrophin-releasing hormone (GnRH) in vitro. This effect of E2 on rat gonadotrophs in vitro was applied as a model to study the estrogenic or anti-estrogenic activity of chlordecone in gonadotrophs. Rat pituitary cell cultures were treated with E2 (10(-10) M), chlordecone (10(-7) to 10(-5) M), or both before a 6-hr challenge of D-Lys6-GnRH (GnRH-A). Secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) during the 6-hr of GnRH-A treatment was measured. Pretreatment of cells with E2 for 2 days increased the GnRH-A-stimulated LH and FSH secretion approximately twofold. This effect of E2 was antagonized by the coexistence of chlordecone in a dose-dependent manner. The effect of E2 (10(-10) M) could be totally abolished by 10(-6) M chlordecone. Further, chlordecone alone had little or no effect on basal secretion of LH and FSH, but it significantly suppressed the response of gonadotrophs to GnRH-A. [Mirex, a compound with a similar chemical structure to chlordecone, did not suppress GnRH-A-stimulated secretion of LH or FSH under any condition tested.] The present study demonstrated that chlordecone had two specific effects on rat pituitary gonadotrophs: (1) to antagonize the effects of estrogen, and (2) to reduce the response of gonadotrophs to GnRH-A. Thus, chlordecone is not estrogenic in rat pituitary cells in vitro.

Animals↗
PubMed1980

Inhibition of mouse brain synaptosomal ATPases and ouabain binding by chlordecone.

The effect of chlordecone on the mouse brain synaptosomal Na+-K+ ATPase, Mg2+ ATPase and p-nitrophenyl phosphatase (PNPPase) activities was determined. In addition, the effect of chlordecone on [3H] ouabain binding to synaptosomes was also investigated. The in vitro data show that chlordecone inhibits PNPPase, Na+-K+ ATPase, and Mg2+ ATPase activities with ID50 values of 4, 5 and 7 micrograms respectively. Treatment of mice with symptomatogenic doses of chlordecone resulted in a decreased synaptosomal Na+-K+ and oligomycin-sensitive (mitochondrial) Mg2+ ATPases. The decrease was dose-dependent. The oligomycin-insensitive Mg2+ ATPase activity was unaffected either in vitro or in vivo. The binding of [3H] ouabain to synaptosomal membranes was inhibited by chlordecone in a dose-dependent manner in both in vitro and in vivo experiments. The binding of [14C] chlordecone to synaptosomes occurs even at nanomolar concentrations. The marked inhibition of brain synaptosomal ATPases and ouabain binding by chlordecone suggests that chlordecone may impair active transport mechanisms in synaptosomal membranes.

4-Nitrophenylphosphatase↗
PubMedDate not supplied

Postovulatory reduction of fertility in chlordecone treated female rats.

The chlorinated pesticide, chlordecone, is widely recognized for its production of reproductive deficits. This reproductive sterility has been attributed to chlordecone's apparent "estrogenicity" and its ability to inhibit the release of luteinizing hormone (LH) from the anterior pituitary. However, it was recently noted that the pesticide could also reduce fertility when exposure was delayed until the day following ovulation. This led to the suggestion that chlordecone's actions on reproductive function continued into the postovulatory period. Results of the following studies substantiate this suggestion. Follicular development and ovulation were induced in immature female rats with a combined treatment of pregnant mare serum (PMS) and human chorionic gonadotropin (HCG). Chlordecone (25-75 mg/kg) administration at the time of PMS exposure did not inhibit the ovulatory response to HCG. Furthermore, when adult proestrous female rats were treated with chlordecone, normal numbers of ova were observed the following day. However, implantation sites were never observed in females that had been exposed to chlordecone. Moreover, offspring production was eliminated when mated females were exposed to doses of 50 or 75 mg/kg chlordecone on days 1, 2, or 3 following mating. In contrast, offspring production was normal when the exposure was delayed until the fourth day after mating. Since the vulnerable gestational period overlaps or precedes the time of implantation, these results suggest that ova viability and/or implantation is reduced by the chlordecone exposure.

Analysis of Variance↗
PubMedDate not supplied

Neurochemical correlates of chlordecone neurotoxicity.

The neurotoxic organochlorine insecticide chlordecone (Kepone) was examined in several in vitro and in vivo neurochemical systems in an attempt to identify neurochemical alterations that might be relevant to the central nervous system manifestations of chlordecone toxicity in humans. In vitro, chlordecone was a remarkably potent inhibitor of brain mitochondrial oxidative phosphorylation and associated Ca2+ transport (Ki congruent to 10(-7) M). At a high concentration of chlordecone (10(-5) M), destabilization of biological membranes was observed. Both of these effects appeared to contribute to inhibition of synaptosomal Ca2+ uptake, which was accompanied by a pronounced, although paradoxical, stimulation of neurotransmitter release. Studies of the disposition of [14C]chlordecone revealed that the concentrations that elicited neurochemical changes in vitro were comparable to the brain tissue chlordecone concentrations achieved with a 40 mg/kg tremorigenic dose in intact animals. However, no neurochemical correlates of chlordecone toxicity were observed in studies of dopamine and norepinephrine turnover in chlordecone-intoxicated animals. These findings are discussed in relation to the development of neurochemical assays appropriate for investigating neurotoxic agents.

Animals↗
PubMedDate not supplied

Chlordecone-induced hepatic dysfunction.

Chlordecone (Kepone) is a decachloroketone analog of the dodecachlorohydrocarbon mirex and is used as a stomach poison insecticide. Despite the structural similarity to mirex, chlordecone is unlike mirex in general organ-specific toxic properties. Chlordecone is primarily accumulated in the liver, where it causes a variety of morphological and biochemical alterations. Although less effective than mirex as a hepatotoxin, it causes liver enlargement, focal necrosis, mitochondrial changes, fatty infiltration of hepatocytes, and proliferation of endoplasmic reticulum. Chlordecone accumulation and morphological alterations in the liver were also observed in occupationally exposed human patients. Induction of hepatic microsomal mixed-function oxidases (MFOs) and impaired production and utilization of hepatocellular energy are the principal biochemical aberrations produced by chlordecone. Chronic exposure causes carcinogenesis in mice and rats. Hyperplastic nodules, which progress to hepatocellular carcinomas, are the principal pathological lesions. Acute and chronic exposures to chlordecone result in hepatobiliary dysfunction manifested as impaired excretion of anionic compounds accompanied by choleresis. Exposure to chlordecone results of greatly potentiated haloalkane hepatotoxicity, representing a most potent toxic interaction at otherwise individually nontoxic levels. In view of the demonstrated carcinogenic effect of chlordecone, such interactions at very low levels assume extraordinary significance in terms of chronic toxicological and pathological manifestations induced by combinations of toxic chemicals.

Adenosine Triphosphatases↗
PubMed1982

Chlordecone-induced alterations in content and subcellular distribution of calcium in mouse brain.

The neurotoxic insecticide chlordecone was administered orally to "young" (4-6 wk old) and "old" (6 mo old) mice in a dose of 25 mg/kg X d in 10 ml/kg corn oil. Age-matched control mice received 10 ml/kg X d corn oil. The acute (24 h after a single dose) and subchronic (24 h after 8 daily doses) effects of chlordecone on content and subcellular distribution of Ca in the brain were studied. Significant differences in Ca content and subcellular distribution were found between the young and old control mice. Whole brains of old mice had significantly greater amounts of total brain Ca, protein-bound Ca, and mitochondrial Ca than did those of young mice, but significantly less nuclear and cytosol Ca. Acute exposure to chlordecone (no signs of neurotoxicity) increased significantly total brain, protein-bound, nuclear, mitochondrial, and myelin Ca in brains from young mice. However, under the same chlordecone exposure conditions, old mice had significantly decreased total brain, protein-bound, and mitochondrial Ca with significantly increased nuclear Ca content. It is suggested that aging caused altered biochemical responses to the neurotoxic agent, at least at subtoxic doses or exposure times. When young mice received chlordecone for 8 d and were suffering severe chlordecone-induced tremors, at the times of sacrifice, their brains were found to have significantly decreased total, protein-bound, myelin, and synaptosomal Ca. Nuclear Ca was increased. The increased excitation of the central nervous system evidenced as severe tremors induced by chlordecone might be due, at least in part, to chlordecone-induced Ca deficiency in brain synaptosomes. Such Ca deficiency may decrease the Ca-dependent release of the CNS inhibitory transmitters gamma-aminobutyric acid (GABA) and dopamine.

Animals↗
PubMed1989

Age-related changes in rat brain ATPases during treatment with chlordecone.

Chlordecone was reported to produce neurotoxicity by modulating the Na+ pump in adult rat brain. The present in vitro and in vivo studies were initiated to investigate its effect on maturing rat brain ATPases. Neonates were exposed to chlordecone for 20 d indirectly through lactation by treating the mothers po and from 21 to 50 d as adults. Brain P2 fractions were prepared from treated and control rats. Na+,K+, oligomycin-sensitive (O.S.) and oligomycin-insensitive (O.I.) Mg2+-ATPase activities were increased with age up to d 20. Na+,K+- and O.S. Mg2+-ATPases were inhibited in both in vitro and in vivo treatment with chlordecone. Both these enzymes were more sensitive to chlordecone in the neonatal brains as compared to adult rats (20-50 d). The activity of Mg2+-ATPase but not of Na+,K+-ATPase was restored to normal activity after 20 d of withdrawal of chlordecone treatment. O.I. Mg2+-ATPase was insensitive to chlordecone treatment in all age groups. Ca2+-ATPase activity was not increased with age; however, it was more sensitive to chlordecone in neonates as compared to adults. These results suggest that the Na+ pump, Ca2+-ATPase, and ATP synthesizing enzymes are highly sensitive to chlordecone during early postnatal development.

Adenosine Triphosphatases↗
PubMed1992

Effects of chlordecone on food intake and body weight in the male rat.

The effects of the chlorinated pesticide chlordecone on food intake, body weight, and water intake were examined in adult male rats. Chlordecone treatment produced a dose dependent suppression of food intake. Loss of body weight accompanied the reduced food intake. However, chlordecone did not suppress water intake. Chlordecone treated animals maintained on a liquid diet also demonstrated reduced food intake, suggesting that chlordecone has a specific effect on feeding behavior and not a general effect on ingestive behaviors. The potential contribution of chlordecone-induced tremor to the suppressed food intake and the loss of body weight was considered. When treatment occurred immediately before a 24 hr fast, controls and animals given 75 mg/kg showed no differences in the body weight decline, even though tremor occurred in the pesticide-treated rats. Thus, it is unlikely that tremor alone produced the body weight loss observed in the present experiment. Similarly, animals were capable of initiating eating behavior even though tremor was present. In addition, chlordecone treatment inhibited food intake within 2 hr. Consequently, these results suggest that chlordecone suppresses food intake which in turn produces the decline in body weight.

Animals↗
PubMedDate not supplied

Single injection with chlordecone reduces behavioral receptivity and fertility of adult rats.

The effects of chlordecone on fertility were examined in adult, intact female rats. Rats were treated with 25, 50 or 75 mg/kg chlordecone and initial exposure occurred either on the morning before mating or on the morning after mating. When exposure occurred on the morning of proestrus, mating behavior 8 to 9 hours was significantly reduced by 50 or 75 mg/kg chlordecone. Yet, when housed overnight with sexually experienced males, most females showed sperm in the vaginal smear. However, only 23% of the 50 mg/kg group and none of the 75 mg/kg group delivered offspring. Females given 25 mg/kg chlordecone showed behavior and fertility identical to oil injected controls. When females were treated with chlordecone after mating, 41% of the females given 50 mg/kg chlordecone produced litters while 33% of the 75 mg/kg females delivered offspring. Under both conditions, fertility was substantially reduced. In previous studies, chlordecone's reduction of the preovulatory luteinizing hormone (LH) surge has been offered as an explanation for the pesticide's reproductive deficits. The present studies indicate that the failure of chlordecone-treated females to ovulate cannot totally account for the decreased fertility.

Animals↗
PubMed1980

Comparative effects of chlordecone and mirex on rat cardiac ATPases and binding of 3H-catecholamines.

The effects of chlordecone and mirex on the rat myocardial ATPases and binding of 3H-dopamine and 3H-norepinephrine to the NAK-fraction were determined both by in vitro and in vivo treatment. The in vitro data showed that chlordecone significantly inhibited mitochondrial Mg2+ ATPase and Na+--K+ ATPase in a concentration dependent manner with ID50 values of 5 x 10(-8) and 2 x 10(-6) M, respectively. Mitrex, a close structural analog of chlordecone did not inhibit mitochondrial Mg2+ ATPase but inhibited about 15% of N+--K+ ATPase activity. Rats treated with symptomatogenic doses of chlordecone showed a marked and significant decrease of myocardial Na+--K+ ATPase and the residual Mg2+ ATPase activities. The decrease in the enzyme activities was dose dependent and significant. However, mirex treated rats showed a slight decrease in the myocardial Na+--K+ ATPase. The potency of chlordecone to inhibit the ATPase system was parallel to its ability to decrease the dopamine and norepinephrine binding of the myocardial NAK-fraction. Preincubation of the NAK-fraction with various concentrations of chlordecone resulted in a decreased binding of dopamine and norepinephrine. The decrease was significant and concentration dependent. Similar findings were observed in rats pretreated with chlordecone. Mirex did not show any effect, either in vitro or in vivo treatment, on the binding of dopamine or norepinephrine to the myocardial NAK-fraction. These results suggest that chlordecone may be altering the sodium pump activity by inhibiting both ATP hydrolysis and ATP synthesis and thus reducing other cellular events such as catecholamine uptake.

Adenosine Triphosphatases↗
PubMed1987

Potentiation of carbon tetrachloride hepatotoxicity by chlordecone: dose-response relationships and increased covalent binding in vivo.

Chlordecone greatly potentiates carbon tetrachloride (CCl4) hepatotoxicity. In order to quantitate the degree of this potentiation, the effects of a range of doses of CCl4 on two microsomal enzymatic functions and liver enzyme release were examined in chlordecone-treated and control rats. Male Sprague-Dawley rats were pretreated with 15 mg chlordecone per kilogram body weight (BW) intragastrically or with vehicle. After 48 hours, 0 to 250 microliters CCl4 per 100 g body weight were given intraperitoneally (IP), and the rats were killed 24 hours later. Chlordecone treatment produced approximately a 17-fold potentiation of the CCl4-dependent loss of cytochrome P-450 and glucose-6-phosphatase activity, so that a dose of 6 microliters CCl4 per 100 g body weight in the chlordecone-treated animals resulted in a similar amount of damage as observed with 100 microliters CCl4 per 100 g body weight in controls. A similar potentiation by chlordecone was seen with CCl4 induced increases in serum glutamic-oxaloacetic transaminase (SGOT) levels. Chlordecone treatment also increased hepatic cytochrome P-450 levels by 67% and resulted in an increase in the covalent binding of [14-C]-CCl4-derived metabolites to microsomal protein and lipid in vivo.

Animals↗
PubMed1982

Effects of chlordecone and its structural analogs on p-nitrophenyl phosphatase.

The effects of chlordecone, mirex, and four photoderivatives of mirex on K+-stimulated p-nitrophenyl phosphatase (KPNPPase) in rat brain synaptosomes were determined. Additionally, the effect of chlordecone on the substrate and K+ activation kinetics and the inhibition of KPNPPase at 17, 27, and 37 degrees C were determined. The sensitivity of KPNPPase to various chemicals was highly variable. Chlordecone was the most effective inhibitor with an IC50 of 6.2 X 10(-6)M. All other chemicals showed a maximum inhibition of 20% at 20 muM concentration. The order of inhibition at 20 muM concentration was chlordecone (100%) greater than 8-monohydro mirex (20%) greater than 2,8-dihydromirex (10%) greater than mirex (10%) greater than 10-monohydro mirex (9%) greater than 5,10-dihydro mirex (2%). Double reciprocal plots of the data obtained on the effect of chlordecone on the substrate and K+ activation kinetics showed that the Vmax and Km were decreased with respect to paranitrophenyl phosphate, while it was competitive inhibition with respect to K+ activation. Chlordecone inhibited KPNPPase more at 37 degrees C than at 27 degrees C and 17 degrees C suggesting a positive temperature effect. These results suggest that chlordecone is the most effective inhibitor among its structural analogs tested on KPNPPase in rat brain synaptosomes.

4-Nitrophenylphosphatase↗
PubMed2005

Comparison of chlordecone effects on autoimmunity in (NZBxNZW) F(1) and BALB/c mice.

It has been shown previously that chronic treatment with relatively low doses of chlordecone accelerates the development of systemic lupus erythematosus (SLE) in ovariectomized female (NZBxNZW) F(1) mice. In this study, the effect of chronic chlordecone treatment on SLE was evaluated in ovary-intact female (NZBxNZW) F(1) mice, as well as in female mice from a strain that is not lupus-prone, BALB/c. Chlordecone was administered chronically via implanted sustained-release pellets, and mice were monitored over time for the appearance of elevated autoantibodies (anti-dsDNA and anti-chromatin) and for the development of renal impairment, both indicators of SLE. Chlordecone treatment in (NZBxNZW) F(1) mice shortened significantly the time to onset of elevated autoantibody titers and renal disease in a dose-related manner. The doses required to produce this effect were similar to those observed previously to accelerate SLE development in ovariectomized females. Treatment of female BALB/c mice with chlordecone for up to one year did not produce elevated autoantibody titers or renal disease, suggesting an inability of chlordecone to cause a break in tolerance in this strain. These observations confirm the ability of chronic chlordecone to influence SLE, but demonstrate the importance of genetic background for this effect.

Animals↗
PubMed1996

Estradiol-chlordecone (Kepone) interactions: additive effect of combinations for uterotropic and embryo implantation functions.

Chlordecone (Kepone) is a polychlorinated hydrocarbon that has a low affinity for the estrogen receptor. Although the compound has been shown to be an estrogen antagonist for some responses within the central nervous system, and in hypophyseal gonadotrophic cells, such an action for other responses has not been reported. In the present study ovariectomized immature rats were used to determine the uterotropic effects of chlordecone in the presence or absence of estradiol. Administration of 30 mg/kg chlordecone per day for 3 days increased the response to 0.01, 0.1 and 1 microgram/kg per day of estradiol benzoate (EB). No additive or inhibitory effect was found with chlordecone plus 10 micrograms/kg EB. Likewise, the uterine response to 15 or 30, but not 45, mg/kg chlordecone was enhanced by the co-administration of 0.1 microgram/kg EB. A second response, initiation of embryo implantation in hypophysectomized, progesterone-primed, delayed implanting pregnant rats was tested. Subliminal doses of estradiol or chlordecone were additive for initiating normal implantation in more than 80% of the animals. The results indicate that chlordecone is not an estrogen antagonist for functions that require the action of the estrogen receptor in the uterus. The mechanism(s) involved in the additive action have not been determined but emphasize the need to consider xenoestrogen-natural estrogen interactions when assessing risks for reproductive toxins.

Animals↗
PubMed1978

Treatment of chlordecone (Kepone) toxicity with cholestyramine. Results of a controlled clinical trial.

Industrial workers exposed to the organochlorine pesticide, chlordecone (Kepone), had signs of toxicity in several organs. The extent of toxicity was proportional to the levels of this chemical in the tissues. In 22 patients, chlordecone was eliminated slowly from blood (half time of 165 +/- 27 days--mean +/- S.E.M.) and fat (half time of 125 days, with a range of 97 to 177), chiefly in the stool. Output of chlordecone in bile was 10 to 20 times greater than in stool, suggesting that chlordecone is reabsorbed in the "ntestine. Cholestyramine, an anion-exchange resin that binds chlordecone, increased its fecal excretion by seven times. In a five-month trial, cholestyramine significantly accelerated elimination of chlordecone from blood, with a half life of 80 +/- 4 days (S.E.M.) (P less than 0.005) and fat (half life of 64 days, with a range of 52 to 85) (P less than 0.05). Cholestyramine offers a practical means for detoxification of persons exposed to chlordecone and possibly to other lipophilic toxins.

Adolescent↗
PubMed1982

Surface changes in oviduct, uterus and vaginal cells of neonatal mice after estradiol-17 beta and the insecticide chlordecone (Kepone) treatment: a scanning electron microscopic study.

Surface changes in cells lining the oviduct, uterus and vagina of a neonatal mouse were studied after treatment with estradiol-17 beta (E2) or the insecticide chlordecone. One-day-old mice received daily intraperitoneal injections of 1 of 6 injection mixtures (0.05 ml) for 10 days. The daily dosages per animal were as follows: sesame oil only, 10 microgram E2, 15, 30, 60 and 125 microgram chlordecone suspended in sesame oil. Estradiol-treated mice were terminated after 5 and 10 injections, whereas all other mice were terminated at the end of 10 injections. After 5 and 10 estradiol injections, accelerated ciliation was recorded in the oviduct and increased secretory activity in the uterus or uterine glands. In the vagina, epithelial mucification proceeded to complete cornification with the cornified cell surfaces showing a prominent and complex pattern of microridges. Chlordecone treatments produced dose-dependent cell surface changes in the reproductive tract that were either characteristic of estrogenic stimulation or atypical responses. Chlordecone stimulatory action mimicked estrogen in the form of accelerated ciliation, secretory activity in oviductal and uterine cells as well as mucification leading to complete cornification of vaginal epithelium. Chlordecone doses of 60 microgram or higher produced atypical cellular expansions or swelling in the nonciliated cells of the oviduct and uterus in the mucified vaginal epithelial cells. Also, cornified vaginal cells of chlordecone-treated mice exhibited smoother cell surfaces with decreased microridge patterns when compared to estradiol-treated mice. The stimulatory mechanism of chlordecone action and the probable cause of cellular abnormality are discussed in the text.

Animals↗
PubMed1987

Influence of chlordecone and mirex exposure on benzo[a]pyrene metabolism of rat-liver microsomes.

The metabolism of benzo[a]pyrene (BP) in hepatic microsomes isolated from rats exposed to chlordecone or mirex was compared to that of untreated rats and rats treated with 3-methylcholanthrene (3-MC) or phenobarbital (PB). Treatment with chlordecone resulted in a two- to three-fold increase in cytochrome P-450 content but the BP-hydroxylase activity per mg microsomal protein was unaffected. Addition of alpha-naphthoflavone (alpha-NF) or chlordecone caused changes in BP-hydroxylase activity indicating that chlordecone-induced cytochromes P-450 were similar to control. H.p.l.c. analyses of BP metabolites confirmed this similarity. Treatment with mirex caused a two-fold induction of cytochrome P-450, and BP-hydroxylase activity expressed per mg microsomal protein was increased 1.3-fold. Addition of chlordecone or alpha-NF caused changes in BP-hydroxylase activity, indicating differences between control and mirex-induced cytochromes P-450. H.p.l.c. analyses of BP metabolites confirmed this difference. Treatment with chlordecone or mirex increased microsomal epoxide hydrolase activity three-fold. Chlordecone accumulated in hepatic nuclei.

Animals↗
PubMed1985

Chlordecone toxicity: effect of withdrawal of treatment on ATPase inhibition.

Adult male Sprague-Dawley rats were treated P.O with 10 mg/kg/day chlordecone for 10 days. Five rats from control group receiving corn oil and five rats from chlordecone group were sacrificed for tissue preparations. The remaining rats in chlordecone group were withdrawn from treatment and left in cages for 45 days. At 15, 30 and 45 days after withdrawal, 5 rats from each group with equal number of controls were sacrificed. Brain, liver and kidney were removed and subcellular fractions were prepared. Na+-K+, oligomycin-sensitive and oligomycin-insensitive Mg2+ ATPases were determined. Rats treated with chlordecone for 10 days showed a significant reduction of Na+-K+ ATPase activity in brain and kidney. The decreased enzyme activity in kidney but not in brain returned to normal within 15 days of treatment withdrawal. In brain the enzyme activity stayed at reduced level throughout the experimental period. Oligomycin-sensitive Mg2+ ATPase activity in all the tissues was decreased significantly in chlordecone treated rats. The enzyme activity returned to normal levels in all tissues gradually by 30 days of treatment withdrawal. Oligomycin-insensitive Mg2+ ATPase activity was not decreased in any tissue by chlordecone treatment. These results suggest that chlordecone effects on ATPase system are reversible except for Na+-K+ ATPase in brain.

Adenosine Triphosphatases↗