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PubMedDate not supplied

Carcinogenicity of heptachlor and heptachlor epoxide.

Heptachlor and its metabolite heptachlor epoxide are unequivocally carcinogenic in rats and mice. The chemicals induced carcinomas of the liver, which were highly significant. There were neoplasms at other sites in rats. Neoplasms at all sites, as well as malignant tumors, were increased in heptachlor-treated male rats. There were similar increases in benign and malignant neoplasms of endocrine organs, particularly in female rats. Neoplasms of the thyroid and pituitary were increased in male rats and neoplasms of the reproductive system, including the ovary and uterus, in female rats given heptachlor. Mice also developed hepatic vein thrombosis and thrombosis of the atria of the heart. Nephritis, myocarditis, encephalitis, hepatitis, polyarteritis and atrophy of the testes were observed in rats.

Animals↗
PubMed2001

Effects of heptachlor epoxide on components of various signal transduction pathways important in tumor promotion in mouse hepatoma cells. Determination of the most sensitive tumor promoter related effect induced by heptachlor epoxide.

The effects of the organochlorine (OC) liver tumor promoter heptachlor epoxide (HE; 0, 0.1, 1, 10, and 50 microM) on several cellular tumor promoter-sensitive parameters were studied in mouse 1c1c7 hepatoma cells in an effort to identify the most sensitive biomarker for OC promoter exposure and the critical pathway and target of OC promoters. The levels of Ca2+ in the endoplasmic reticulum (ER) store, connexin43 (Cx43), PLCgamma(1), nPKCvarepsilon, and AP-1 DNA binding in nucleus were studied to screen for effects induced by submicromolar HE levels. While all the parameters tested elicited effects, particulate PLCgamma(1) and AP-1 DNA binding were found to be the most sensitive parameters affected by HE on both dose and temporal bases. Their levels were increased with 10- to 100-fold lower HE concentrations than were required to affect nPKCvarepsilon or Cx43. Further, with the lower HE dosages, particulate PLCgamma(1) and nuclear AP-1 were positively modulated by HE after 1 h versus 3 or 72 h for nPKCvarepsilon and Cx43. Ca2+ store depletion was probably the third most sensitive parameter, after AP-1 and PLCgamma(1). These results suggest the tyrosine kinase growth factor receptor pathway is the probable critical pathway for HE-induce tumor promotion with the critical target most likely being upstream of PLCgamma(1) and AP-1. This work also demonstates that upon exposure to a tumor promoter such as HE, many hepatocellular effects or changes result, suggesting that a cellular-program shift occurs similar to that described by the resistant hepatocyte model after exposure to a carcinogen or enzyme inducer.

Animals↗
PubMed2003

[The use amount of chlordane, heptachlor and heptachlor epoxide in Poland].

Chlordanes, heptachlor and heptachlor epoxide 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 chlordanes were from 0.35 to 0.42 microgram per person while of heptachlor and heptachlor epoxide from 0.51 to 0.58 microgram per person, on the average. Fish, meat and meat products and butter are a main source of chlordanes intake in a total diet in Poland, while in the case of heptachlor and heptachlor epoxide a main source are meat, meat products and animal fats.

Chlordan↗
PubMed2001

Down-regulation of particulate protein kinase Cepsilon and up-regulation of nuclear activator protein-1 DNA binding in liver following in vivo exposure of B6C3F1 male mice to heptachlor epoxide.

The effects of in vivo administration of the cyclodiene tumor promoter heptachlor epoxide on mouse liver protein kinase C were studied in male B6C3F1 mice by protein kinase C activity assays and Western blotting under conditions known to increase the incidence of hepatocellular carcinoma because protein kinase C is thought to be critical in phorbol ester-induced tumor promotion. Under these test conditions, 20 ppm dietary heptachlor epoxide for 1-20 days increased cytosolic and decreased particulate total protein kinase C activities, while 10 ppm had no effect. Further, total cytosolic and particulate protein kinase C activities were decreased within 1 hour by 10 mg/kg intraperitoneal (i.p.) heptachlor epoxide. Western blotting showed that conventional protein kinase Calpha and beta isoforms were unaffected by heptachlor epoxide. Particulate novel protein kinase Cepsilon, however, was selectively down-regulated by 1, 10, and 20 ppm dietary heptachlor epoxide, whereas the cytosolic isoform was decreased by 1 and 10 ppm heptachlor epoxide for 10 days. The high-dose treatment for 24 hours also decreased particulate novel protein kinase Cepsilon but increased the cytosolic titer. These results demonstrate that this isoform is unique in its sensitivity to heptachlor epoxide. Activator protein-1 DNA binding, a critical factor in tumor promotion, was substantially increased at 3 and 6 hours with 3.7 mg/kg (i.p.) heptachlor epoxide and at 3 and 10 days with 20 ppm dietary heptachlor epoxide. The effects of heptachlor epoxide on protein kinase C and activator protein-1 are similar to those caused by phorbol ester treatments and correlate well to heptachlor levels found to induce tumors in mice. However, heptachlor epoxide did not initially activate protein kinase C with in vivo treatments or with in vitro treatments of a plasma membrane fraction aimed at demonstrating direct activation, as has been shown for phorbol esters. The ability of heptachlor epoxide to down-regulate particulate novel protein kinase Cepsilon correlates to dosages used in in vivo tumor promotion studies. However, this may represent a negative feedback response rather than a causative effect.

Animals↗
PubMed1981

Heptachlor epoxide in marine mammals.

The presence of heptachlor epoxide in harbour seals (Phoca vitulina) and white-beaked dolphins (Lagenorhynchus albirostris) has been confirmed by chemical derivatization and mass spectrometric analyses. An unknown compound at a retention time close to half of heptachlor epoxide interfered in the determination by electron capture detector-gas chromatography. On a WCOT CP-Sil 7 column programmed from 85 to 175 degree C two poorly separated peaks could be detected. Heptachlor epoxide contents up to 1.7 mg/kg (on a fat basis) were obtained, which were about 200 times lower than the PCB levels. The same ratio was also observed in fish from the same area.

Animals↗
PubMed2006

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↗
PubMedDate not supplied

Heptachlor, heptachlor epoxide, and other chlordane compounds in Finnish plywood workers.

Residue levels of heptachlor, heptachlor epoxide, and other chlordane compounds were determined in sera from 74 Finnish plywood workers and 52 controls. Concentrations of heptachlor epoxide in plywood workers varied from below the detection limit of 0.1 ng/g to 19.2 ng/g serum (conversion factor for SI units = 975 [1 ng/g = 0.98 microgram/l]); the mean and standard deviation were 3.2 and 3.9 ng/g, respectively. Heptachlor expoxide values in controls varied from below the detection limit to 1.2 ng/g serum. The exposure time, i.e., number of years spent working with sizings that contained heptachlor, correlated with the residue levels of heptachlor epoxide that were measured in serum samples taken from employees at two companies (p = .03). The most common chlordane compound (contaminant of heptachlor) found in the sera of plywood workers was trans-nonachlor; also found were high concentrations of heptachlor epoxide. Headache, dizziness, and eye irritation were not related to serum levels of heptachlor or chlordane compounds.

Adolescent↗
PubMed1991

Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii.

The commercial milk supply on Oahu was contaminated by heptachlor epoxide for as long as 15 months during 1981-82 at levels possibly as high as 1.2 ug/g, fat basis. Following the contamination, several investigators attempted to evaluate potential adverse health outcomes, especially among infants and young children. However, results of the initial investigations are inconclusive due to lack of reliable measures of heptachlor exposure, use of non-random sampling techniques, and lack of definitive health outcomes attributable to heptachlor epoxide. The design of a current study to assess the body concentrations of heptachlor epoxide and related pesticides in Hawaii is presented. The study is designed (1) to relate these concentrations to prior exposure via the milk contamination, and (2) to assess the reliability of breast milk and serum pesticide concentrations as objective biological markers of body burden. No attempt is made to relate these data to health outcomes; instead, the findings may provide the foundation for future health studies or surveillance of environmental exposure to pesticides in Hawaii.

Animals↗
PubMed1981

National study of chlorinated hydrocarbon insecticide residues in human milk, USA. I. Geographic distribution of dieldrin, heptachlor, heptachlor epoxide, chlordane, oxychlordane, and mirex.

Human milk samples obtained from 1436 women residing in the United States were analyzed by gas-liquid chromatography for the chlorinated hydrocarbon insecticides--dieldrin, chlordane, heptachlor, heptachlor epoxide, oxychlordane and Mirex. Dieldrin was found above the detection limit (1.0 ppb) in over 80% of all the samples collected. Chlordane was not found in any of the 1436 milk samples but its metabolite, oxychlordane, was found above the detection limit in 74% of the samples. Although heptachlor was recovered in less than 2% of the samples, its metabolite, heptachlor epoxide, was found above the detection limit in 63% of the samples. It was of considerable interest that Mirex was not positively identified in any of the samples. The proportion of samples with values above the detection limit for dieldrin, heptachlor epoxide and oxychlordane varied significantly among the five geographic regions with the southeastern United States having the highest mean residue level for each of these three contaminants. For the United States the mean fat adjusted residue levels of those samples above the detection limit were 164.2 ppb for dieldrin, 91.4 ppb for heptachlor epoxide, and 95.8 ppb for oxychlordane.

Adult↗
PubMed2006

Heptachlor epoxide induces a non-capacitative type of Ca2+ entry and immediate early gene expression in mouse hepatoma cells.

The effects of the organochlorine (OC) liver tumor promoter heptachlor epoxide (HE) and a related non-tumor promoting OC, delta-hexachlorocyclohexane (delta-HCH), on the dynamics of intracellular calcium (Ca2+) were investigated in mouse 1c1c7 hepatoma cells. HE induced a non-capacitative, Ca2+ entry-like phenomenon, which was transient and concentration-dependent with 10 and 50 microM HE. The plasma membrane Ca2+ channel blocker SKF-96365 antagonized this HE-induced Ca2+ entry. delta-HCH failed to induce Ca2+ entry, rather it antagonized the HE-induced Ca2+ entry. Both HE and delta-HCH induced Ca2+ release from endoplasmic reticulum (ER) at treatment concentrations as low as 10 microM; at 50 microM, the former induced 5x as much Ca2+ release as the latter. The HE-induced Ca2+ release from the ER was antagonized using the IP3 receptor/channel blocker xestospongin C, suggesting that HE induces ER Ca2+ release through the IP3 receptor/channel pore. These results show that the effect of HE on cellular Ca2+ mimics that of mitogens such as epidermal and hepatocyte growth factors. They also provide insight into the similarities and differences between tumorigenic and non-tumorigenic OCs, in terms of the mechanisms and the extent of the [Ca2+]i increased by these agents.

Animals↗
PubMed1987

[Contamination of game in Schleswig-Holstein. 2. Residues of dieldrin, heptachlor epoxide and other cyclodiene insecticides in the liver fat of hares (Lepus europaeus L.)].

Increased levels of Dieldrin (0.01-2.94 mg/kg fat, median mean = 0.38 mg/kg fat) and cis-Heptachlor Epoxide (less than 0.01-1.38 mg/kg fat, mean = 0.20 mg/kg fat) were determined by GC/ECD in liver fat of 199 hares (Lepus europaeus L.) from Schleswig-Holstein, North Germany. This investigation was carried out within the scope of a game investigation program. The dependence of these residues on endogenous and exogenous factors are discussed. Oxychlordane and trans-Nonachlor, residues of Chlordane, were also analysed in liver fat by GC/MS. The application of the cyclodiene insecticides Aldrin/Dieldrin, Heptachlor and Chlordane has been prohibited in West Germany for several years; the residues indicate the high soil persistence of these substances.

Animals↗
PubMed1977

Dominant lethal studies with technical chlordane, HCS-3260, and heptachlor: heptachlor epoxide.

Male albino mice in groups of eight were each given single doses, either by gavage or by intraperitoneal injection, of either technical chlordane (50 or 100 mg/kg), HCS-3260 (50 or 100 mg/kg), or heptachlor:heptachlor epoxide (25:75) (7.5 or 15 mg/kg). The males were subsequently mated with three untreated females for six consecutive weeks. No dominant lethal changes among females that had mated with the treated males were produced.

Animals↗
PubMed2004

Liquid chromatographic separation of the enantiomers of trans-chlordane, cis-chlordane, heptachlor, heptachlor epoxide and alpha-hexachlorocyclohexane with application to small-scale preparative separation.

Analytical high-performance liquid chromatographic separations of the individual enantiomers of five polychlorinated compounds were obtained on polysaccharide stereoselective HPLC columns. The enantiomers of the pesticides trans-chlordane, cis-chlordane and heptachlor were separated on CHIRALCEL OD using a hexane mobile phase. The enantiomers of the heptachlor metabolite, heptachlor epoxide, were separated on CHIRALPAK AD using a methanol mobile phase. The enantiomers of alpha-hexachlorocyclohexane (alpha-HCH), were separated on CHIRALCEL OJ using a hexane/2-propanol mobile phase. Similar chromatographic conditions using preparative columns were used to isolate approximately 250 mg of each of the individual enantiomers. The purified individual enantiomers have been submitted for testing of their endocrine disruptor (ED) activity.

Chlordan↗
PubMed1977

Confirming heptachlor and heptachlor epoxide in food samples by gas-liquid chromatography of their photoderivates.

The food sample extract is cleaned up on a Florisil column and the 6% ethyl ether in petroleum ether cluate is subjected to repeated concentrations, using a micro-Snyder column, to expel volatile materials that absorb ultraviolet (UV) light. The sample and standard solutions of heptachlor and heptachlor epoxide are placed in quartz cells and exposed to UV radiation in the dark. Characteristic photoderivatives of the respective pesticides which form in the sample extract are identified and measured by comparison with those formed in the irradiated standard solutions, using electron capture gas-liquid chromatography. Recoveries of the 2 pesticides from 13 products, fortified at levels from 0.01 to 0.3 ppm and determined after derivatization, ranged from 67 to 110%.

Chromatography, Gas↗