Comparative metabolism of methoxychlor, methiochlor, and DDT in mouse, insects, and in a model ecosystem.
01 Nov 1970-Journal of Agricultural and Food Chemistry (American Chemical Society)-Vol. 18, Iss: 6, pp 1145-1152
About: This article is published in Journal of Agricultural and Food Chemistry.The article was published on 1970-11-01. It has received 214 citations till now. The article focuses on the topics: Methoxychlor.
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01 Sep 2002
TL;DR: Each toxicological profile succinctly characterizes the toxicologic and adverse health effects information for the hazardous substance described therein and begins with a public health statement that describes, in nontechnical language, a substance's reevant toxicological properties.
Abstract: DDT, DDE, and DDD ii DISCLAIMER The use of company or product name(s) is for identification only and does not imply endorsement by the Agency for Toxic Substances and Disease Registry. Toxicological profiles are revised and republished as necessary, but no less than once every three years. For information regarding the update status of previously released profiles, contact ATSDR at: V FOmWORD This toxicological profile is prepared in accordance with guidelines* developed by the Agency for Toxic Substances and Disease Registry (ATSDR) and the Environmental Protection Agency (EPA). The original guidelines were published in the Federal Register on April 17, 1987. Each profile will be revised and republished as necessary. The ATSDR toxicological profile succinctly characterizes the toxicologic and adverse health effects information for the hazardous substance described therein. Each peer-reviewed profile identifies and reviews the key literature that describes a hazardous substance's toxicologic properties. Other pertinent literature is also presented, but is described in less detail than the key studies. The profile is not intended to be an exhaustive document; however, more comprehensive sources of specialty information are referenced. The focus of the profiles is on health and toxicologic information; therefore, each toxicological profile begins with a public health statement that describes, in nontechnical language, a substance's reIevant toxicological properties. Following the public health statement is information concerning levels of si,gnificant human exposure and, where known, significant health effects. The adequacy of information to determine a substance's health effects is described in a health effects summary. Data needs that are of significance to protection of public health are identified by ATSDR and EPA. Each profile includes the following: The examination, summary, and interpretation of available toxicologic information and epidemiologic evaluations on a hazardous substance to ascertain the levels of significant human exposure for the substance and the associated acute, subacute, and chronic health effects; A determination of whether adequate information on the health effects of each substance is available or in the process of development to determine levels of exposure that present a significant risk to human health of acute, subacute, and chronic health effects; and Where appropriate, identification of toxicologic testing needed to identify the types or levels of exposure that may present significant risk of adverse health effects in humans. principal audiences for the toxicological profiles are health professionals at the federal, state, and local levels; interested private sector organizations and groups; and members of the public. …
330 citations
TL;DR: The data collectively show that the primary adult effects of early exposure to MXC are reproductive, show that 5 mg/kg/day is not a NO(A)EL in rats with this exposure paradigm, and imply that the sites of action are both central and peripheral.
268 citations
TL;DR: Some of the structural requirements for ERα and ERβ activity are identified and the complexity involved in determining the mechanism of action of endocrine-active chemicals that simultaneously act as agonists or antagonists through one or more hormone receptors is demonstrated.
Abstract: We previously demonstrated differential interactions of the methoxychlor metabolite 2,2-bis( p -hydroxyphenyl)-1,1,1-trichloroethane (HPTE) with estrogen receptor α (ERα), ERβ, and the androgen receptor (AR). In this study, we characterize the ERα, ERβ, and AR activity of structurally related methoxychlor metabolites. Human hepatoma cells (HepG2) were transiently transfected with human ERα, ERβ, and AR plus an appropriate steroid-responsive luciferase reporter vector. After transfection, cells were treated with various concentrations of HPTE or structurally related compounds in the presence (for detecting antagonism) and absence (for detecting agonism) of 17β-estradiol and dihydrotestosterone. The monohydroxy analog of methoxychlor, as well as monohydroxy and dihydroxy analogs of 2,2-bis( p -hydroxyphenyl)-1,1-dichloroethylene, had ERα agonist activity and ERβ and AR antagonist activity similar to HPTE. The trihydroxy metabolite of methoxychlor displayed only weak ERα agonist activity and did not alter ERβ or AR activities. Replacement of the trichloroethane or dichloroethylene group with a methyl group resulted in a compound with ERα and ERβ agonist activity that retained antiandrogenic activities. This study identifies some of the structural requirements for ERα and ERβ activity and demonstrates the complexity involved in determining the mechanism of action of endocrine-active chemicals that simultaneously act as agonists or antagonists through one or more hormone receptors.
232 citations
Cites background from "Comparative metabolism of methoxych..."
..., 1985), and dihydroxy-DDE is formed during the metabolism of methoxychlor in mice (Kapoor et al., 1970)....
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TL;DR: The possible involvement of mono-oxygenase in biotransformation in methoxychlor into estrogenic metabolites in vivo is discussed and the demethylated products were resolved by thin-layer chromatography into three chromatographically distinct components more polar than methoxy chlor.
223 citations
TL;DR: This review summarizes the effects of EDCs on ovarian function by describing how they interfere with hormone signaling via two mechanisms: altering the availability of ovarian hormones, and altering binding and activity of the hormone at the receptor level.
Abstract: Endocrine-disrupting chemicals (EDCs) are exogenous agents with the ability to interfere with processes regulated by endogenous hormones One such process is female reproductive function The major reproductive organ in the female is the ovary Disruptions in ovarian processes by EDCs can lead to adverse outcomes such as anovulation, infertility, estrogen deficiency, and premature ovarian failure among others This review summarizes the effects of EDCs on ovarian function by describing how they interfere with hormone signaling via two mechanisms: altering the availability of ovarian hormones, and altering binding and activity of the hormone at the receptor level Among the chemicals covered are pesticides (eg dichlorodiphenyltrichloroethane and methoxychlor), plasticizers (eg bisphenol A and phthalates), dioxins, polychlorinated biphenyls, and polycyclic aromatic hydrocarbons (eg benzo[a]pyrene)
220 citations
Cites background from "Comparative metabolism of methoxych..."
...Studies in rodents have determined that upon entering the body, MXC is absorbed and sequentially demethylated by hepatic CYP450 enzymes to form a mono-hydroxylated metabolite commonly known as mono-OH and a bishydroxylated metabolite known as HPTE (Imai & Coulston 1968, Kapoor et al. 1970)....
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