Calbindin-D9k mRNA expression in the rat uterus following exposure to methoxychlor: a comparison of oral and subcutaneous exposure.

Calbindin-D(9k) (CaBP-9k) is a cytosolic calcium-binding protein that is induced by estrogenic compounds possibly through estrogen receptors. We compared CaBP-9k mRNA expression in the uterus with uterotrophic response in immature rats exposed to methoxychlor (MC), an environmental chemical with estrogenic activity. MC was orally or subcutaneously administered to 3-week-old female Sprague-Dawley rats for 3 days.

Analysis of gene expression profiles in the offspring of rats following maternal exposure to xenoestrogens.

Many environmental chemicals are known endocrine disruptors (EDs). These have the potential to alter endocrine systems via various mechanisms that include binding to hormone receptors, thereby either mimicking or blocking the hormone actions and causing abnormal gene expression. Here, to elucidate the molecular mechanism(s) underlying the detrimental effects associated with the estrogenicity of these chemicals, we determined whether gene profiles were altered in rats exposed to 4-tert-octyphenol (OP) and diethylstilbestrol (DES) in utero.

Identification of estrogen-regulated genes by microarray analysis of the uterus of immature rats exposed to endocrine disrupting chemicals.

Environmental estrogenic compounds which bind to the estrogen receptor (ER) can block or alter endogenous functions of estrogen in reproductive and developmental stages. A microarray technology is a very valuable method for the prediction of hormone-responsive activities in various gene expressions. Thus, we investigated the altered gene expression by estrogen and endocrine disruptors (EDs) using microarray technology in the uterus of immature rats.

Differential expression of uterine calcium transporter 1 and plasma membrane Ca2+ ATPase 1b during rat estrous cycle.

Calcium-related proteins include the calcium transporters 1 and 2 (CaT1 and CaT2), plasma membrane Ca2+-ATPase 1b (PMCA1b), and calbindin-D9k and -D28k. The expression of CaT1 and PMCA1b and their potential roles in the uterine tissue remain to be clarified. Thus, in the present study, the expression patterns of CaT1 and PMCA1b were examined to predict their roles in rat uterus during the estrous cycle.

Anti-progestogenic effect of flutamide on uterine expression of calbindin-D9k mRNA and protein in immature mice.

A calcium binding protein, calbindin-D9k (CaBP-9k), is a cytosolic protein and regulated by steroid hormones in the reproductive tissues. Mouse CaBP-9k gene was predominantly regulated by progesterone (P4), whereas rat CaBP-9k was mainly regulated by 17beta-estradiol (E2) in the uterus. The induction of CaBP-9k can be employed as a biomarker for steroidal substrates as endocrine disruptors (EDs).

Biodegradation of methoxychlor and its metabolites by the white rot fungus Stereum hirsutum related to the inactivation of estrogenic activity.

The white rot fungus Stereum hirsutum was used to degrade methoxychlor [2,2,2-trichloro-1,1-bis(4-methoxyphenyl)ethane] in culture and the degraded products were extensively determined. The estrogenic activity of the degraded products of methoxychlor was examined using cell proliferation and pS2 gene expression assays in MCF-7 cells. S.

Estrogenic reduction of styrene monomer degraded by Phanerochaete chrysosporium KFRI 20742.

The characteristic biodegradation of monomeric styrene by Phanerochaete chrysosporium KFRI 20742, Trametes versicolor KFRI 20251 and Daldinia concentrica KFRI 40-1 was carried out to examine the resistance, its degradation efficiency and metabolites analysis. The estrogenic reduction effect of styrene by the fungi was also evaluated. The mycelium growth of fungi differentiated depending on the concentration levels of styrene.

Repeated 28-day oral toxicity study of ketoconazole in rats based on the draft protocol for the "Enhanced OECD Test Guideline No. 407" to detect endocrine effects.

We performed a 28-day repeated-dose toxicity study of ketoconazole, a widely used an antimycotic drug, based on the draft protocol of the "Enhanced OECD Test Guideline 407" (Enhanced TG407) to investigate whether ketoconazole has endocrine-mediated properties according to this assay. Seven-week-old SD rats were administered with ketoconazole daily by oral gavage at doses of 0, 6.25, 25 or 100 mg kg(-1) day(-1) for at least 28 days.

Induction of interleukin-8 expression in porcine peripheral blood mononuclear cells by trans10-cis12 conjugated linoleic acid.

The chemotaxis of porcine peripheral blood polymorphonuclear cells (PMN) was enhanced by culture supernatant from peripheral blood mononuclear cells (PBMC) treated with trans10-cis12 (10t-12c) conjugated linoleic acid (CLA) or by porcine recombinant (pr) interleukin (IL)-8. To identify this chemotactic inducing factor, the culture supernatant from 10t-12c CLA treated PBMC was partially purified by gel filtration. Only fraction 9 contained enhanced PMN chemotactic activity.

Assessment of estrogenic and androgenic activities of tetramethrin in vitro and in vivo assays.

Tetramethrin, a synthetic pyrethroid insecticide, is used globally for agriculture, and thus potential environmental exposure to tetramethrin is a concern. Environmental chemicals that are hormonally active (particularly estrogen or androgen) may adversely affect the reproductive and endocrine systems. However, little is known about the estrogenic and androgenic activities of tetramethrin.

Biology and physiology of Calbindin-D9k in female reproductive tissues: involvement of steroids and endocrine disruptors.

Although Calbindin-D9k (CaBP-9k), a cytosolic calcium binding protein which has calcium binding sites, is expressed in various tissues, i.e., intestine, uterus, and placenta, potential roles of this gene and its protein are not clearly understood.

A calcium binding protein, calbindin-D9k, is mainly regulated by estrogen in the pituitary gland of rats during estrous cycle.

As a member of family of cytosolic calcium binding proteins, Calbindin-D9k (CaBP-9k) is expressed in female reproductive system and regulated by steroid hormones, estrogen (E2) and progesterone (P4), but its expression and role in pituitary gland have not been elucidated yet. Thus, in this study, we elucidated the expression of CaBP-9k mRNA and protein in pituitary gland of rats. During estrous cycle of rats, pituitary CaBP-9k level fluctuated, and its mRNA was highly elevated during an E2-dominant stage (proestrus and estrus), whereas its level disappeared at a P4-dominant stage (metestrus and diestrus).

Glucocorticoids differentially regulate expression of duodenal and renal calbindin-D9k through glucocorticoid receptor-mediated pathway in mouse model.

Dexamethasone (Dex) is a member of the glucocorticoids (GCs), and is broadly used as an anti-inflammatory medication. Continuous administration with GCs induces adverse effects and suffering in humans (i.e.

Maternal exposure to bisphenol a during late pregnancy resulted in an increase of Calbindin-D9k mRNA and protein in maternal and postnatal rat uteri.

It has been reported that Calbindin-D9k (CaBP-9k) is rapidly and strongly induced by environmental estrogenic compounds, possibly through estrogen receptors (ERalpha) in the uterus of mammals. CaBP-9k can be evaluated as an early gene marker for assaying estrogenic effects of putative environmental chemicals in the rat uterus. This study was undertaken to investigate CaBP-9k mRNA and protein expression in the postnatal rat uterus following maternal exposure to 17beta-estradiol (E2) and bisphenol A (BPA) during the neonatal period.

Egg white derivatives induce tumor necrosis factor-alpha expression in porcine peripheral blood mononuclear cells.

Porcine PBMC derived phagocytic activity in peripheral blood polymorphonuclear cells (PMN) induced by egg white derivatives (EWD) treatment was analyzed at the protein and mRNA level. EWD alone failed to induce phagocytic activity of PMN measured by flow cytometry. But PMN phagocytosis was enhanced by culture supernatant from PBMC treated with EWD, human (h)rTNF-alpha and porcine (p)rIL-1beta, respectively.

Conflict of estrogenic activity by various phthalates between in vitro and in vivo models related to the expression of Calbindin-D9k.

Phthalates are suspected to disrupt the endocrine system, especially through estrogenic effects. In the present study, we investigated the effects of various phthalates and compared them with those of estrogenic compounds that disrupt the female reproductive system. To assess the effects of these phthalates, alteration of the Calbindin-D9k (CaBP-9k) gene was measured as a biomarker because rat CaBP-9k gene carries an estrogen response element (ERE) which is involved in estrogen responsiveness of the gene during the estrous cycle.

Degradation of bisphenol A by white rot fungi, Stereum hirsutum and Heterobasidium insulare, and reduction of its estrogenic activity.

Two lignin-degrading basidiomycetes, Stereum hirsutum and Heterobasidium insulare, were used to degrade bisphenol A (BPA) in culture, and the estrogenic activity of the degradation products was examined using MCF-7 cell proliferation assays (E-screen) and analysis of pS2 mRNA expression in MCF 7 cells. Both S. hirsutum and H.

Estrogen receptor alpha pathway is involved in the regulation of Calbindin-D9k in the uterus of immature rats.

It has been demonstrated in our previous studies that Calbindin-D9k (CaBP-9k) is a potent biomarker for screening estrogen-like chemicals in the rat model. Although treatments with 17beta-estradiol (E2) and endocrine disrupting compounds resulted in the up-regulation of uterine CaBP-9k, the mechanism of CaBP-9k induction by these compounds through two subtypes of estrogen receptors (ERalpha and ERbeta) is unclear. Thus, in the present study, immature rats were treated with propyl pyrazole triol (PPT, an ERalpha-selective ligand), diarylpropionitrile (DPN, an ERbeta-selective ligand), E2, or dimethyl sulfoxide (DMSO, a vehicle control) for three days in order to clarify which subtype of ER is involved in the uterine CaBP-9k induction.

Potential estrogenic and antiandrogenic effects of permethrin in rats.

Many environmental chemicals including pesticides have been reported to possess hormonal activities, and thus are classified as endocrine disruptors. Permethrin, a synthetic pyrethroid insecticide, is used worldwide, which provides potential environmental exposure. However, relatively few studies have reported on hormonal activities, particularly estrogenic and androgenic activities of permethrin, and the results of these studies are in some respects contradictory.

Novel progestogenic activity of environmental endocrine disruptors in the upregulation of calbindin-D9k in an immature mouse model.

Endocrine disruption is a major global health concern in the industrialized world. The induction of uterine calbindin-D9k (CaBP-9k), which belongs to a large family of intracellular calcium binding proteins, was used to assess the exposure of endocrine disruptors (EDs) in an immature mouse model. Sex steroid hormones have been demonstrated to regulate uterine CaBP-9k expression in the uterus of rats and mice.

Effect of genistein as a selective estrogen receptor beta agonist on the expression of Calbindin-D9k in the uterus of immature rats.

Genistein, a phytoestrogen possessing a high affinity for estrogen receptor beta (ERbeta), is of increasing interest because of its possible influence on the physiology of mammalian reproductive tracts. Although estrogen has been demonstrated to regulate Calbindin-D9k (CaBP-9k) in the rat uterus as with other calcium binding proteins, the role of ERbeta on the modulation of CaBP-9k remains to be elucidated. To elucidate the effect of genistein as a selective ERbeta agonist on uterine expression of CaBP-9k mRNA and protein, immature female rats were injected with genistein daily for three consecutive days in a dose-dependent (0.

Differential transcriptional and translational regulations of calbindin-D9k by steroid hormones and their receptors in the uterus of immature mice.

Calbindin-D(9k) (CaBP-9k) is a cytosolic calcium binding protein mainly expressed in the duodenum, placenta and uterus, and intestinal CaBP-9k is regulated by 1, 25-dyhydroxyvitamin D3. However, despite the presence of vitamin D receptors, uterine CaBP-9k is not under the control of vitamin D, but seems to be regulated by sex steroids. This steroids-dependent regulation of CaBP-9k is not only limited to a tissue-specific manner but also extends to a species-specific manner.

Transfer of maternally injected endocrine disruptors through breast milk during lactation induces neonatal Calbindin-D9k in the rat model.

The uterus is a highly estrogen-responsive tissue, which can be measured through changes in CaBP-9k expression. In this study, we investigated the potential for estrogenic compounds 4-tert-octylphenol (OP), nonylphenol (NP), bisphenol A (BPA), diethylstilbestrol (DES) and 17beta-estradiol (E2) to be transferred through breast milk from dam to neonate during lactation using the induction of CaBP-9k in uterine tissue as a biomarker. Dams were treated with OP, NP and BPA, dissolved in corn oil, at doses of 200, 400 and 600 mg/kg body weight per day l for 5 days after delivery.

Antibacterial and antifungal effects of essential oils from coniferous trees.

Essential oils have potential biological effects, i.e., antibiotic, anticarcinogenic, and sedative effects during stress.

Induction of calbindin-D9k messenger RNA and protein by maternal exposure to alkylphenols during late pregnancy in maternal and neonatal uteri of rats.

Environmental chemicals are proposed to possess hormone-like properties, such as mimicking natural hormones, inhibiting the action of hormones, and inducing abnormal gene expression. Among environmental chemicals, the alkylphenol products (APs), octylphenol (OP) and nonylphenol (NP), are derived from alkylphenol ethoxylates and have been reported to be environmentally persistent. Thus, in the present study, we examined the effect of two APs, OP and NP, on the expression of Calbindin-D(9k) (CaBP-9k) following maternal exposure during late pregnancy in maternal and fetal uteri.