Peroxidase: A Marker for Estrogen Expression

DeSombre, Eugene R.

doi:10.1016/b978-0-12-452811-6.50016-5

Cited by 5 publications

(5 citation statements)

References 80 publications

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“…Histochemical studies showed that the uterine cervix is also a region with a pronounced stromal density of peroxidase-containing cells. In adult animals, estrogen treatment results in uterine eosinophilia [8,9]; and most, if not all, of the induced peroxidase activity was ascribed to this eosinophilia which has been associated with nongenomic (edema, vascular permeability, histamine release) response to estrogen [8,9,35,36]. The results in this study from experiments involving enzyme inhibitors indicate that the cervical stromal cells contain at least two types of peroxidases which has also been demonstrated for uterine eosinophils in adult rats [37].…”

Section: -mentioning

confidence: 61%

“…Generally speaking, the uterine response to estrogen in immature and adult animals seems to involve two different phases: an early one involving uterine eosinophilia with release of enzymes, edema, and vascular permeability, and a later one represented by receptor-mediated genomic response [7,8]. By far, the greater part of the total biochemically assayed peroxidase activity can be ascribed to invading eosinophils [9]. In rats, a uterine eosinophilia or peroxidase response to estrogen was not seen before day 11 after birth [9-111.…”

Section: Introductionmentioning

confidence: 99%

“…The organotropic localization of estrogen-induced epithelial abnormalities in NMRI mice and women is an enigma. As mentioned, a marker for estrogen response is increased peroxidase activity [9,16]. DES is metabolized by uterine peroxidase along a pathway involving reactive intermediates [ 17,181; but other enzyme systems, e. g., prostaglandin endoperoxide synthetase and cytochrome P-450 mixed function oxidases, are also involved in DES oxidation [ 19,201. We now report results from studies aimed to analyse the effect of neonatal estrogen treatment on appearance of epithelial estrogen receptor protein, using a monoclonal antibody, and on peroxidase activity in different regions of the uterovaginal tract.…”

Section: Introductionmentioning

confidence: 99%

“…To look for a possible association between peroxidase activity and genital epithelial abnormalities, postpubertal females were killed and the uterine cervix prepared for histology. Because of the blocking effect of corticosteroids on estrogeninduced uterine eosinophilia and related peroxidase activity [8,9], in some of these experiments females were treated with a combination of DES and corticosterone.…”

Section: Introductionmentioning

confidence: 99%

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Induction of estrogen receptor, peroxidase activity, and epithelial abnormalities in the mouse uterovaginal epithelium after neonatal treatment with diethylstilbestrol

Andersson¹,

Forsberg²

1988

Teratog Carcinog Mutagen

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Neonatal female NMRI mice were treated with daily doses of 10(-2) or 5 micrograms diethylstilbestrol (DES) on one or more of days 1-5 after birth. Using immunohistochemical techniques and a monoclonal antibody to the estrogen receptor, we demonstrated an estrogen-induced precocious appearance of receptor protein in the nuclei of the uterovaginal epithelium. High levels of peroxidase activity and a pronounced stromal infiltration with peroxidase positive cells occurred in the uterine cervix and upper vagina after estrogen treatment. This regional restriction in peroxidase activity was similar to the regional restriction for estrogen-induced epithelial abnormalities (heterotopic columnar epithelium, adenosis). A combined treatment with DES and corticosterone depressed peroxidase activity but not to the control level. The distribution of abnormal epithelium was similar in DES- and DES-corticosterone-treated females. The conclusion is that neonatal estrogen treatment induces an epithelial receptor for estrogen and a high level of cervical peroxidase activity, but the relationship between these parameters and the appearance of abnormal cervicovaginal epithelial changes could not be settled in the present study.

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Section: -mentioning

confidence: 61%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Induction of estrogen receptor, peroxidase activity, and epithelial abnormalities in the mouse uterovaginal epithelium after neonatal treatment with diethylstilbestrol

Andersson¹,

Forsberg²

1988

Teratog Carcinog Mutagen

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“…Oestrogen administration has previously been shown to increase activity of peroxidase in the uterus considerably with maximal activity appearing 20-24 h after a single injection (DeSombre, 1984). This study showed for the first time that oestrogen also increases uterine peroxidase activity before this, within 1-3 h after injection.…”

Section: Discussionmentioning

confidence: 64%

Increase in uterine peroxidase activity in the rat uterus during oestrogen hyperaemia

Farley¹,

Ford²,

Rosazza³

1992

Reproduction

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The administration of oestrogen results in increased arterial blood flow in all mammalian species studied to date, but its mechanism of action has not been elucidated. Because an interval of 30-60 min is observed between oestrogen injection and uterine hyperaemia, it has been suggested that a vasoactive intermediate is involved and recent evidence suggests that catechol oestrogens are the vasoactive oestrogen intermediates. Uterine peroxidase catalyses the conversion of oestrogens to their catechol forms and thus may play an important role in oestrogen-induced uterine hyperaemia. The present studies evaluated the time course and dose-response effects of oestrogen on uterine peroxidase activity and related these to changes in uterine blood volume, an index of uterine hyperaemia in immature rats. These data demonstrated that the minimal effective hyperaemic dose of oestradiol also increased (P less than 0.05) uterine peroxidase activity. The oestradiol-induced increase in uterine peroxidase activity preceded significant increases in uterine blood volume (1 h versus 2 h, respectively). These data are consistent with a role for peroxidase-mediated conversion of oestradiol to catechol oestradiol in facilitating uterine hyperaemia in rats.

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Acute and permanent growth effects in the mouse uterus after neonatal treatment with estrogens

Halling

Forsberg

1993

Reproductive Toxicology

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Peroxidase: A Marker for Estrogen Expression

Cited by 5 publications

References 80 publications

Induction of estrogen receptor, peroxidase activity, and epithelial abnormalities in the mouse uterovaginal epithelium after neonatal treatment with diethylstilbestrol

Induction of estrogen receptor, peroxidase activity, and epithelial abnormalities in the mouse uterovaginal epithelium after neonatal treatment with diethylstilbestrol

Increase in uterine peroxidase activity in the rat uterus during oestrogen hyperaemia

Acute and permanent growth effects in the mouse uterus after neonatal treatment with estrogens

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