Prenatal Chlordane exposure: Effects on plasma corticosterone concentrations over the lifespan of mice

Cranmer, Joan M.; Cranmer, Morris F.; Goad, Phillip T.

doi:10.1016/0013-9351(84)90128-2

Cited by 20 publications

(6 citation statements)

References 14 publications

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“…The phyto-estrogen genistein, nonylphenol, and the pesticide o,p'DDT were the most potent of the pseudo-estrogens tested. The environmental estrogens demonstrating induced luciferase activity in the ER-CALUX assays have also been previously shown to be estrogenic in both in vivo and in vitro assays: 4-nonylphenol (Jobling and Sumpter, 1993;Soto et al, 1991;White et al, 1994), o.p'DDT (Bitman, 1969, Fry and Toone, 1981, Klotz et al, 1996, methoxychlor (Gray et al, 1989, Schlenk et al, 1997, endosulfan (Arnold et al, 1996), dieldrin (Haake et al, 1987) and chlordane (Cranmer et al, 1984). Comparison of the potency values relative to estradiol shows that in general, lower potency values for environmental estrogens are calculated in the ER-CALUX than demonstrated with other ER-mediated reporter gene assays, such as transient transfections of ERE-reporter genes in HeLa and MCF-7 cells (Table 2).…”

Section: Figmentioning

confidence: 91%

Development of a stably transfected estrogen receptor-mediated luciferase reporter gene assay in the human T47D breast cancer cell line

Legler

Brink²,

Brouwer³

et al. 1999

Toxicological Sciences

392

239

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Development of an estrogen receptor-mediated, chemical-activated luciferase reporter gene-expression (ER-CALUX) assay was attempted by stable transfection of luciferase reporter genes in a number of cell lines. Stable transfection of the chimeric Gal4 estrogen receptor and luciferase gene constructs in MCF-7 breast cancer and Hepa.1c1c7 mouse hepatoma cell lines, as well as transfection of a newly constructed luciferase reporter gene pEREtata-Luc in the ECC-1 human endometrial cell line, resulted in constitutive, nonestradiol-inducible clones. Stable transfection of pEREtata-Luc in the T47D breast cancer cell line, however, resulted in an extremely sensitive, highly responsive cell line. Following a 24-h exposure to estradiol (E2), stably transfected T47D.Luc cells demonstrated a detection limit of 0.5 pM, an EC50 of 6 pM, and a maximum induction of 100-fold relative to solvent controls. No clear reduction in responsiveness has been found over extended culture periods (50 passages). Anti-estrogens ICI 182,780, TCDD, and tamoxifen inhibited the estradiol-mediated luciferase induction. Genistein, nonylphenol, and o,p'DDT were the most potent (pseudo-)estrogens tested in this system (EC50 100, 260, and 660 nM, respectively). Determination of interactive effects of the (pseudo-)estrogens nonylphenol, o,p'DDT, chlordane, endosulfan, dieldrin, and methoxychlor revealed that, in combination with 3 pM E2, (pseudo-)estrogens were additive. Slightly more than additive effects (less than 2-fold) were found for combinations of dieldrin and endosulfan tested in the range of 3 to 6 M. At these concentrations, the combination of endosulfan and chlordane demonstrated additive interaction. The ER-CALUX assay with T47D cells can provide a sensitive, responsive, and rapid in vitro system to detect and measure substances with potential (anti-)estrogenic activity.

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Section: Figmentioning

confidence: 91%

Development of a stably transfected estrogen receptor-mediated luciferase reporter gene assay in the human T47D breast cancer cell line

Legler

Brink²,

Brouwer³

et al. 1999

Toxicological Sciences

392

239

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“…Increased plasma levels of corticosterone were observed in the offspring of mice treated during gestation, which suggested an effect on neuroendocrinological feedback, possibly resulting from the liver's reduced ability to metabolize corticosterone (Cranmer et al, 1984 ).…”

Section: _20 Yearsmentioning

confidence: 99%

Agency for Toxic Substances and Disease Registry's 1997 priority list of hazardous substances. Latent effects—carcinogenesis, neurotoxicology, and developmental deficits in humans and animals

et al. 1999

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In support of Superfund re-authorization legislation, the Division of Toxicology of the Agency for Toxic Substances and Disease Registry (ATSDR) prepared a chemical-specific consultation document for Congress that identified those chemicals with carcinogenic, neurological, or developmental adverse effects having a latency period longer than 6 years. The review was limited to the top 50 substances listed on ATSDR's 1997 Priority List of Hazardous Substances (Priority List). Among the top 50 chemicals, a review of the technical literature indicated that 38 (76%) were classified as "reasonably anticipated," "possibly," or "probably" capable of causing cancer in humans, based either on human and animal data. Eight chemicals (16%) had well-established cancer latency periods in humans of 6 years or more following exposure. Three substances (6%)--arsenic, creosote, and benzidine--had data indicating latency periods longer than 6 years. The technical literature review likewise confirmed the potential for neurological and developmental effects with a latency of 6 years. Twenty-seven (54%) of the top 50 substances caused acute and/or chronic neurotoxic effects; a number of these also caused neurological effects that persisted beyond 6 years (or the equivalent in animal studies) such as: behavioral problems, neurological deficiencies, reduced psychomotor development, cognitive deficiencies, and reduced IQ. Twenty-eight substances (56%) caused adverse developmental effects in offspring of exposed individuals or animals including increased fetal and infant mortality, decreased birth weights and litter sizes, and growth delays. Latency periods for related chemicals are expected to be similar due to structural and toxicological similarities.

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“…A later experiment by Cranmer et al [1984] maintained mice exposed prenatally to chlordane (0.16 or 8.0 mg/kg daily) until they reached 800 days of age. Plasma corticosterone levels of male mice born to mothers exposed to 0.16 mg/kg were significantly elevated at 101 days of age; at 400 days, elevations were present in both dose groups.…”

Section: Laboratory Studiesmentioning

confidence: 99%

Pesticides as a source of developmental disabilities

Weiss

1997

Ment. Retard. Dev. Disabil. Res. Rev.

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Prenatal Chlordane exposure: Effects on plasma corticosterone concentrations over the lifespan of mice

Cited by 20 publications

References 14 publications

Development of a stably transfected estrogen receptor-mediated luciferase reporter gene assay in the human T47D breast cancer cell line

Development of a stably transfected estrogen receptor-mediated luciferase reporter gene assay in the human T47D breast cancer cell line

Agency for Toxic Substances and Disease Registry's 1997 priority list of hazardous substances. Latent effects—carcinogenesis, neurotoxicology, and developmental deficits in humans and animals

Pesticides as a source of developmental disabilities

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