The Metabolism of Diethylstilbestro

Metzler, Manfred

doi:10.3109/10409238109113599

Cited by 93 publications

(9 citation statements)

References 122 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…DES implants in poultry were outlawed in 1959 when DES residues were found in chicken liver, however this did not affect the use of DES in cattle, which remained ubiquitous until it was ultimately phased out in 1979. By the 1980s, more than 80% of US cattle were estimated to have been exposed, and considerable release of DES into the environment through feed lots and cattle waste has been well documented (Metzler, 1981; Zervos and Rodricks, 1982). …”

Section: Evidence Of the Potential For Estrogenic Endocrine Disruptormentioning

confidence: 99%

Long-term effects of environmental endocrine disruptors on reproductive physiology and behavior

Patisaul

Adewale

2009

Front. Behav. Neurosci.

205

139

View full text Add to dashboard Cite

It is well established that, over the course of development, hormones shape the vertebrate brain such that sex specific physiology and behaviors emerge. Much of this occurs in discrete developmental windows that span gestation through the prenatal period, although it is now becoming clear that at least some of this process continues through puberty. Perturbation of this developmental progression can permanently alter the capacity for reproductive success. Wildlife studies have revealed that exposure to endocrine disrupting compounds (EDCs), either naturally occurring or man made, can profoundly alter reproductive physiology and ultimately impact entire populations. Laboratory studies in rodents and other species have elucidated some of the mechanisms by which this occurs and strongly indicate that humans are also vulnerable to disruption. Use of hormonally active compounds in human medicine has also unfortunately revealed that the developing fetus can be exposed to and affected by endocrine disruptors, and that it might take decades for adverse effects to manifest. Research within the field of environmental endocrine disruption has also contributed to the general understanding of how early life experiences can alter reproductive physiology and behavior through non-genomic, epigenetic mechanisms such as DNA methylation and histone acetylation. These types of effects have the potential to impact future generations if the germ line is affected. This review provides an overview of how exposure to EDCs, particularly those that interfere with estrogen action, impacts reproductive physiology and behaviors in vertebrates.

show abstract

Section: Evidence Of the Potential For Estrogenic Endocrine Disruptormentioning

confidence: 99%

Long-term effects of environmental endocrine disruptors on reproductive physiology and behavior

Patisaul

Adewale

2009

Front. Behav. Neurosci.

205

139

View full text Add to dashboard Cite

show abstract

“…Biomimetic SOD also inhibits both the initiating [Solanki et al, 19841 and complete carcinogenic action [Egner PA and Kensler TW, unpublished observations) of 7,12-dimethylbenz[a]anthracene in mouse skm. Other carcinogens with diverse target specificities, such as benzene, anthracyclines, diethylstilbestrol, bleomycin, and aromatic amines, can also produce oxy radicals that may be important to their respective "promoter" activities [Greenlee et al, 198 1;Doroshow, 1983;Metzler, 1981;Borek and Troll, 1983;Nakayama et al, 1983;Stier et al, 1980; Kensler and Trush, 19841. …”

mentioning

confidence: 99%

Role of oxygen radicals in tumor promotion

1984

View full text Add to dashboard Cite

Tumor promoters provoke the elaboration of oxygen radicals by direct chemical generation and through the indirect activation or alteration of cellular sources including membrane oxidases, peroxisomes, and electron transport chains in mitochondria and endoplasmic reticulum. Although direct measurement of amplified oxygen radical production in response to tumor promoters in target tissues remains problematic, studies with scavengers of reactive oxygen species demonstrate inhibition of biochemical and biological sequelae of tumor promoter exposure and provide strong presumptive evidence for oxygen radical involvement in this late stage of carcinogenesis. The critical macromolecular targets for these oxygen radicals remain undefined; however, they may include lipids, DNA, DNA repair systems, and other enzymes.

show abstract

“…Therefore, the presence of DES seems to pull E2 out of the other metabolism pathways and push it into 17-Oglucuronidation. Since DES can also undergo glucuronidation, sulfation, and other metabolism pathways in humans (Metzler, 1981), its level may decrease gradually in serum. The overall in vivo activation of DES on E2-17-O-glucuronidation still awaits identification in pharmacokinetic studies in human beings.…”

Section: Discussionmentioning

confidence: 99%