Peroxidase as a marker enzyme in estrogen-responsive tissues

Jellinck, Peter H.; Newcombe, Anne-Marie; Keeping, Hugh S.

doi:10.1016/0065-2571(79)90020-7

Cited by 26 publications

(10 citation statements)

References 50 publications

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“…An inverse relationship between oestrogen receptor content and peroxidase activity in dif¬ ferent parts of the uterus was unexpected because oestrogen-induced increases in this enzyme have been shown previously (DeSombre & Lyttle 1979) to parallel increases in uterine weight and DNA, while experiments with progesterone and antioestrogens also support a receptor-mediated process (DeSombre & Lyttle 1979;Jellinck et al 1979;Lyttle et al 1979). However, the results may be explained by the heterogeneous distribution of cells capable of producing peroxidase in the rat uterus (Churg & Anderson 1974) or else, by the enzyme being in a different form (Olsen & Little 1979) in the endometrium and the cervix.…”

Section: Discussionmentioning

confidence: 88%

“…Treatment of rats with DMBA did not influence the activity or distribution of peroxidase in the uterus even though the animals developed mam¬ mary tumours which often contain this enzyme Jellinck et al 1979). The variation in the relative activities of peroxidase in different parts of the uterus and differences in distribution of this enzyme in rat and in man may help to explain the relative susceptibility of the cervix and endometrium to toxic and carcinogenic agents.…”

Section: Discussionmentioning

confidence: 95%

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Distribution of oestrogen-induced peroxidase in the rat uterus

Affleck¹,

Keeping²,

Newcombe³

et al. 1981

Acta Endocrinologica

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The activity of oestrogen-induced peroxidase in sections along the uterus of normal and mammary tumour-bearing adult rats was measured. Oestradiol increased the activity of this enzyme in the cervix as well as in other parts of the uterus in ovariectomized or immature rats. Peroxidase activity per mg protein was twice as high in the cervix as in the rest of the uterus where it was evenly distributed along both horns. The concentrations of oestrogen receptors in the cytosol and nucleus in each uterine horn and in the cervix was also determined and found to be lower in the cervix than in other sections of the uterus.The rapid increase in uterine peroxidase activity after treatment of ovariectomized or immature rats with oestrogen (Lyttle & Jellinck 1972; Jellinck & Lyttle 1973) has led to the proposal Lyttle & DeSombre 1977) that this enzyme may be a useful specific marker for tissues whose growth is regulated by oestrogen. In recent studies, Tsibris et al. (1978a) determined the distri¬ bution of oestrogen and progesterone receptors in the cytoplasm of five sections along the length of the human uterine endometrium obtained from non-cancerous pre-menopausal hysterectomy spe¬ cimen. They also measured the peroxidase activity of these sections (Tsibris et al. 1978b). The concen¬ tration of both types of steroid receptors was found to be highest in the fundus and lowest in the cervix while the enzyme was located either exclusively or maximally in the cervix. It was therefore con¬ sidered of interest to measure peroxidase activity along the length of the rat uterus and also to compare the concentration of nuclear oestrogen receptors in the cervix with that of the rest of the uterus. Materials and MethodsDetermination of uterine peroxidase activity Mature female Sprague Dawley rats (Canadian Breeding Laboratories, St. Constant, Quebec) weighing 290-320 g were injected sc with oestradiol-17ß (10 ug m 0.5 ml saline containing 10% ethanol) 10 h before sacrifice. Six of the animals used bore mammary tumours induced by the gastric instillation of a single dose (15 mg) of dimethylbenz(a)anthracene (DMBA). Uteri (499 ± 37 mg) were removed, cut into 1-1.5 cm sections with scissors as illustrated in Fig. 1 and each section weighed and homo¬ genized in 3 ml of Tris-HCl (0.01 m) pH 7.2 in a Potter-Elvehjem homogenizer with a Teflon pestle. The homogenate was centrifuged at 40 000 g for 30 min and peroxidase solubilized by re-homogenizing the sediment in Tris-HCl buffer containing 0.5 M CaCl2 (Lyttle & DeSombre 1977). It was centrifuged again for 30 min and the supernatant (0.05-0.2 ml) used for determining peroxidase activity by measuring the rate of oxidation of guaiacol at 470 nm (Himmelhoch et al. 1967). The concentration of protein in the uterine extracts was determined by the Bradford dye-binding method using bovine y-globulin (Cohn fraction II) as standard (Brad¬ ford 1976). In some experiments, mature rats ovariecto¬ mized under methoxyflurane (Metofane) anaesthesia 14 -21 days before sacrifice, and also immature (22-26 da...

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 95%

Distribution of oestrogen-induced peroxidase in the rat uterus

Affleck¹,

Keeping²,

Newcombe³

et al. 1981

Acta Endocrinologica

View full text Add to dashboard Cite

show abstract

“…Therefore, in this study, immature female mice were used. Peroxidase activity is readily induced in rodent uteri by E2 and has been characterized extensively as an estrogenic response (Lyttle and DeSombre et al 1977a;Jellinck et al 1979). …”

Section: Discussionmentioning

confidence: 99%

Role of the aryl hydrocarbon receptor and Cyp1b1 in the antiestrogenic activity of 2,3,7,8-tetrachlorodibenzo- p -dioxin

Takemoto

Nakajima

Fujiki

et al. 2004

Archives of Toxicology

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The role of aryl hydrocarbon receptor (AhR) and cytochrome P450 (Cyp) 1 family in the antiestrogenic activity of 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) was investigated in vivo. Immature (21 days old) AhR, Cyp1a2, or Cyp1b1 knockout (-/-) mice were treated intraperitoneally with estradiol (E2, 20 ng/mouse per day, for 14 consecutive days) and/or TCDD (200 ng/mouse per day, on days 7, 9, 11, and 13). Uterine wet weight and uterine peroxidase activity (UPA) were measured as markers of estrogen responsiveness. UPA was a better marker of estrogen responsiveness than the uterine wet weight. In AhR wild-type (+/+) mice, UPA (208.1+/-81.6 units/g tissue) was increased by the administration of E2 (to 297.2+/-178.7 units/g). The administration of TCDD significantly ( p<0.01) decreased the UPA (10.5+/-3.4 units/g) compared with that in the control mice. Co-administration of TCDD with E2 also significantly ( p<0.05) decreased the UPA (18.8+/-19.9 units/g) compared with that in E2-treated mice. In AhR(-/-) mice, UPA (162.9+/-146.7 units/g) was significantly ( p<0.01) increased by the administration of E2 (486.8+/-108.2 units/g). In contrast to the results in AhR(+/+) mice, UPA was not affected by the administration of TCDD (51.8+/-70.6 units/g) compared with control, and co-administration of TCDD with E2 (545.8+/-189.4 units/g) compared with that in E2-treated mice. In Cyp1a2/1b1(+/+) mice, UPA was significantly ( p<0.05) increased by the administration of E2 (70.0+/-36.4 units/g). Co-administration of TCDD with E2 significantly ( p<0.05) decreased the UPA (29.6+/-22.2 units/g) compared with that in E2-treated mice. In Cyp1a2(-/-) mice, co-administration of TCDD with E2 significantly ( p<0.01) decreased the UPA (6.8+/-5.1 units/g) compared with that in E2-treated mice. In Cyp1b1(-/-) mice, UPA (5.5+/-8.1 units/g) was significantly ( p<0.05) increased by the administration of E2 (56.6+/-34.1 units/g). In contrast to the results in Cyp1a2/1b1(+/+) mice or Cyp1a2(-/-) mice, UPA was not affected by the co-administration of TCDD and E2 (52.6+/-30.1 units/g) compared with that in E2-treated mice. This is the first demonstration that Cyp1b1 as well as AhR is involved in the antiestrogenic effects of TCDD.

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“…In previous work, we have shown that the induction of peroxidase in immature rat uteri by estrogens could be influenced by treating the animals with thyroid hormones (20), progesterone (10). or the catechol estrogen, 2-hydroxyestradiol (2 1).…”

Section: Discussionmentioning

confidence: 99%

Estrogen–androgeri interaction: selective inhibition of estrogen-induced uterine peroxidase by testosterone and 5α-dihydrotestosterone

Jellinck¹,

Affleck²,

Newcombe³

1983

Can. J. Biochem. Cell Biol.

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The effect of testosterone (T) and dihydrotestosterone (DHT) on the induction of peroxidase and glucose-6-phosphate dehydrogenase (G6PDH) in the immature rat uterus by estradiol (E2) was investigated. T (0.5-12.5 mg/rat) given on 3 successive days produced a large increase in uterine weight but, in contrast to E2, did not induce peroxidase or significantly augment uterine G6PDH. However, this androgen, even at a very low dose (50 micrograms/rat three times), inhibited the induction of peroxidase without a corresponding effect on G6PDH when given concurrently with E2 and was more effective than DHT. Inhibition by androgen was also observed when diethylstilbestrol was used to stimulate uterine growth. Combined treatment with E2 (3 micrograms/rat) and T (3 mg/rat) produced a cytosolic and nuclear estrogen receptor pattern in the uterus similar to that observed with E2 alone after various time intervals. The results speak against a direct inhibitory action or T on E2-induced uterine peroxidase via the estrogen receptor and confirm the lack of aromatization of T to E2 in the immature rat. Possible mechanisms for modifying the action of estrogens by androgens are discussed, particularly in the light of E2-induced eosinophilia. It is proposed that steroid hormones can interact in several ways and that uterine peroxidase provides a useful indicator to study steroid hormone action.

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Peroxidase as a marker enzyme in estrogen-responsive tissues

Cited by 26 publications

References 50 publications

Distribution of oestrogen-induced peroxidase in the rat uterus

Distribution of oestrogen-induced peroxidase in the rat uterus

Role of the aryl hydrocarbon receptor and Cyp1b1 in the antiestrogenic activity of 2,3,7,8-tetrachlorodibenzo- p -dioxin

Estrogen–androgeri interaction: selective inhibition of estrogen-induced uterine peroxidase by testosterone and 5α-dihydrotestosterone

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