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At least 19 recordsLinked to original sources
PubMed1996

Inhibition of gap junctional intercellular communication in heptachlor- and heptachlor epoxide-treated normal human breast epithelial cells.

Based on the concern of organochlorides in the environment and in human tissue, this study was designed to determine whether various noncytotoxic levels of heptachlor and heptachlor epoxide could inhibit, reversibly, gap junctional intercellular communication in human breast epithelial cells (HBEC). Cytotoxicity and gap junctional intercellular communication (GJIC) were evaluated by lactate dehydrogenase assay and fluorescence redistribution after photobleaching analysis, respectively. Both heptachlor and heptachlor epoxide were noncytotoxic up to 10 microg/ml. At this concentration, heptachlor and heptachlor epoxide inhibited GJIC of normal human breast epithelial cells after 1 h treatment. Within a 24 h treatment with heptachlor and heptachlor epoxide at 10 microg/ml, recovery of GJIC had not returned. GJIC completely recovered after a 12 h treatment of 1 microg/ml heptachlor epoxide, but it did not recover after a 24 h treatment of 1 microg/ml heptachlor. RT-PCR and Western blots were analyzed to determine whether the heptachlor or heptachlor epoxide might have altered the steady-state levels of gap junction mRNA and/or connexin protein levels or phosphorylation state. No significant difference in the level of connexin 43 (Cx43) message between control and heptachlor-treated cells was observed. Western blot analyses showed hypophosphorylation patterns in cells treated with 10 microg/ml heptachlor and heptachlor epoxide for 1 h with no recovery within 24 h. Immunostaining of Cx43 protein in normal HBEC indicated that heptachlor and heptachlor epoxide caused a loss of Cx43 from the cell membranes at noncytotoxic dose levels. Taken together, these results suggest that heptachlor and heptachlor epoxide can alter GJIC at the post-translational level, and that, under the conditions of exceeding a threshold concentration in the breast tissue containing 'initiated' cells for a long time and not being counteracted by anti-tumor-promoting chemicals, they could act as breast tumor promoters.

Base Sequence↗
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↗
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↗
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↗
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↗
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↗
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

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↗
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↗
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↗