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Article ; Online: Cumulative effects of antiandrogenic chemical mixtures and their relevance to human health risk assessment.

Howdeshell, Kembra L / Hotchkiss, Andrew K / Gray, L Earl

International journal of hygiene and environmental health

2016 Volume 220, Issue 2 Pt A, Page(s) 179–188

Abstract: Toxicological studies of defined chemical mixtures assist human health risk assessment by establishing how chemicals interact with one another to induce an effect. This paper reviews how antiandrogenic chemical mixtures can alter reproductive tract ... ...

Abstract	Toxicological studies of defined chemical mixtures assist human health risk assessment by establishing how chemicals interact with one another to induce an effect. This paper reviews how antiandrogenic chemical mixtures can alter reproductive tract development in rats with a focus on the reproductive toxicant phthalates. The reviewed studies compare observed mixture data to mathematical mixture model predictions based on dose addition or response addition to determine how the individual chemicals in a mixture interact (e.g., additive, greater, or less than additive). Phthalate mixtures were observed to act in a dose additive manner based on the relative potency of the individual phthalates to suppress fetal testosterone production. Similar dose additive effects have been reported for mixtures of phthalates with antiandrogenic pesticides of differing mechanisms of action. Overall, data from these phthalate experiments in rats can be used in conjunction with human biomonitoring data to determine individual hazard indices, and recent cumulative risk assessments in humans indicate an excess risk to antiandrogenic chemical mixtures that include phthalates only or phthalates in combination with other antiandrogenic chemicals.
MeSH term(s)	Androgen Antagonists/toxicity ; Animals ; Drug Interactions ; Humans ; Models, Biological ; Risk Assessment
Chemical Substances	Androgen Antagonists
Language	English
Publishing date	2016-11-19
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, N.I.H., Intramural
ZDB-ID	2009176-X
ISSN	1618-131X ; 1438-4639
ISSN (online)	1618-131X
ISSN	1438-4639
DOI	10.1016/j.ijheh.2016.11.007
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Zs.A 5334: Show issues

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Article ; Online: Use of the Adverse Outcome Pathway (AOP) framework to evaluate species concordance and human relevance of Dibutyl phthalate (DBP)-induced male reproductive toxicity.

Arzuaga, Xabier / Walker, Teneille / Yost, Erin E / Radke, Elizabeth G / Hotchkiss, Andrew K

Reproductive toxicology (Elmsford, N.Y.)

2019 Volume 96, Page(s) 445–458

Abstract: Dibutyl phthalate (DBP) is a phthalate ester used as a plasticizer, and solvent. Studies using rats consistently report that DBP exposure disrupts normal development of the male reproductive system in part via inhibition of androgen synthesis. However, ... ...

Abstract	Dibutyl phthalate (DBP) is a phthalate ester used as a plasticizer, and solvent. Studies using rats consistently report that DBP exposure disrupts normal development of the male reproductive system in part via inhibition of androgen synthesis. However, studies using xenograft models report that in human fetal testis DBP exposure is unlikely to impair testosterone synthesis. These results question the validity of the rat model for assessment of male reproductive effects caused by DBP. The Adverse Outcome Pathway (AOP) framework was used to evaluate the available evidence for DBP-induced toxicity to the male reproductive system. Three relevant biological elements were identified: 1) fetal rats are more sensitive than other rodents and human fetal xenografts to DBP-induced anti-androgenic effects, 2) DBP-induced androgen-independent adverse outcomes are conserved amongst different mammalian models and human fetal testis xenografts, and 3) DBP-induced anti-androgenic effects are conserved in different mammalian species when exposure occurs during postnatal life stages.
MeSH term(s)	Adverse Outcome Pathways ; Animals ; Dibutyl Phthalate/toxicity ; Endocrine Disruptors/toxicity ; Genitalia, Male/drug effects ; Humans ; Male
Chemical Substances	Endocrine Disruptors ; Dibutyl Phthalate (2286E5R2KE)
Language	English
Publishing date	2019-06-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	639342-1
ISSN	1873-1708 ; 0890-6238
ISSN (online)	1873-1708
ISSN	0890-6238
DOI	10.1016/j.reprotox.2019.06.009
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Zs.A 2316: Show issues

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Article: Hazards of diethyl phthalate (DEP) exposure: A systematic review of animal toxicology studies

Weaver, James A / Beverly, Brandiese E.J / Keshava, Nagalakshmi / Mudipalli, Anuradha / Arzuaga, Xabier / Cai, Christine / Hotchkiss, Andrew K / Makris, Susan L / Yost, Erin E

Environment international. 2020 Dec., v. 145

2020

Abstract: Diethyl phthalate (DEP) is widely used in many commercially available products including plastics and personal care products. DEP has generally not been found to share the antiandrogenic mode of action that is common among other types of phthalates, but ... ...

Abstract	Diethyl phthalate (DEP) is widely used in many commercially available products including plastics and personal care products. DEP has generally not been found to share the antiandrogenic mode of action that is common among other types of phthalates, but there is emerging evidence that DEP may be associated with other types of health effects.To inform chemical risk assessment, we performed a systematic review to identify and characterize outcomes within six broad hazard categories (male reproductive, female reproductive, developmental, liver, kidney, and cancer) following exposure of nonhuman mammalian animals to DEP or its primary metabolite, monoethyl phthalate (MEP).A literature search was conducted in online scientific databases (PubMed, Web of Science, Toxline, Toxcenter) and Toxic Substances Control Act Submissions, augmented by review of online regulatory sources as well as forward and backward searches. Studies were selected for inclusion using PECO (Population, Exposure, Comparator, Outcome) criteria. Studies were evaluated using criteria defined a priori for reporting quality, risk of bias, and sensitivity using a domain-based approach. Evidence was synthesized by outcome and life stage of exposure, and strength of evidence was summarized into categories of robust, moderate, slight, indeterminate, or compelling evidence of no effect, using a structured framework.Thirty-four experimental studies in animals were included in this analysis. Although no effects on androgen-dependent male reproductive development were observed following gestational exposure to DEP, there was evidence including effects on sperm following peripubertal and adult exposures, and the overall evidence for male reproductive effects was considered moderate. There was moderate evidence that DEP exposure can lead to developmental effects, with the major effect being reduced postnatal growth following gestational or early postnatal exposure; this generally occurred at doses associated with maternal effects, consistent with the observation that DEP is not a potent developmental toxicant. The evidence for liver effects was considered moderate based on consistent changes in relative liver weight at higher dose levels; histopathological and biochemical changes indicative of hepatic effects were also observed, but primarily in studies that had significant concerns for risk of bias and sensitivity. The evidence for female reproductive effects was considered slight based on few reports of statistically significant effects on maternal body weight gain, organ weight changes, and pregnancy outcomes. Evidence for cancer and effects on kidney were judged to be indeterminate based on limited evidence (i.e., a single two-year cancer bioassay) and inconsistent findings, respectively.These results suggest that DEP exposure may induce androgen-independent male reproductive toxicity (i.e., sperm effects) as well as developmental toxicity and hepatic effects, with some evidence of female reproductive toxicity. More research is warranted to fully evaluate these outcomes and strengthen confidence in this database.
Keywords	adults ; bioassays ; body weight changes ; chemical risk assessment ; databases ; developmental toxicity ; diethyl phthalate ; environment ; females ; histopathology ; kidneys ; liver ; males ; mammals ; maternal exposure ; mechanism of action ; metabolites ; reproductive toxicology ; risk ; spermatozoa ; systematic review ; tissue weight
Language	English
Dates of publication	2020-12
Publishing place	Elsevier Ltd
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	554791-x
ISSN	1873-6750 ; 0160-4120
ISSN (online)	1873-6750
ISSN	0160-4120
DOI	10.1016/j.envint.2020.105848
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 3131: Show issues

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Article: An environmental androgen, 17beta-trenbolone, affects delayed-type hypersensitivity and reproductive tissues in male mice.

Hotchkiss, Andrew K / Nelson, Randy J

Journal of toxicology and environmental health. Part A

2007 Volume 70, Issue 2, Page(s) 138–140

Abstract: Recently, a growth promoter for farm animals, trenbolone acetate, was identified as an environmental androgen that potentially affects reproduction. Because androgens also suppress immunity, it was hypothesized that an active metabolite of trenbolone ... ...

Abstract	Recently, a growth promoter for farm animals, trenbolone acetate, was identified as an environmental androgen that potentially affects reproduction. Because androgens also suppress immunity, it was hypothesized that an active metabolite of trenbolone acetate, 17beta-trenbolone (TB), might impair immune responses. Castrated adult CD-1 mice were injected daily with either one of two different doses of 17beta-trenbolone (TB), testosterone propionate (TP), or corn oil (vehicle). The antigen-specific immune response was assessed by measuring delayed-type hypersensitivity (DTH) responses. Reproductive response was assessed by measuring reproductive tissue mass and determining testosterone concentrations. Mice treated with TB or TP displayed larger reproductive tissue mass than males treated with corn oil. Furthermore, males exposed to the highest dose of TB displayed a reduced DTH response compared to vehicle-treated animals. In comparison, TP, at a similar dose, only minimally reduced the DTH response. These data support the reproductive and potentially immunosuppressive effects of this environmental androgen, and raise the possibility of health concerns for individuals or populations in contact with high concentrations of TB.
MeSH term(s)	Anabolic Agents/toxicity ; Androgens/toxicity ; Animals ; Castration ; Dinitrofluorobenzene ; Genitalia, Male/drug effects ; Genitalia, Male/growth & development ; Hypersensitivity, Delayed/chemically induced ; Immunosuppressive Agents/toxicity ; Male ; Mice ; Mice, Inbred Strains ; Organ Size/drug effects ; Trenbolone Acetate/analogs & derivatives ; Trenbolone Acetate/toxicity
Chemical Substances	Anabolic Agents ; Androgens ; Immunosuppressive Agents ; Dinitrofluorobenzene (D241E059U6) ; Trenbolone Acetate (RUD5Y4SV0S)
Language	English
Publishing date	2007-01-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1413345-3
ISSN	1528-7394 ; 0098-4108 ; 1087-2620
ISSN	1528-7394 ; 0098-4108 ; 1087-2620
DOI	10.1080/15287390600755091
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Zs.A 1268: Show issues

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Article ; Online: Hazards of diethyl phthalate (DEP) exposure: A systematic review of animal toxicology studies.

Weaver, James A / Beverly, Brandiese E J / Keshava, Nagalakshmi / Mudipalli, Anuradha / Arzuaga, Xabier / Cai, Christine / Hotchkiss, Andrew K / Makris, Susan L / Yost, Erin E

Environment international

2020 Volume 145, Page(s) 105848

Abstract: Background: Diethyl phthalate (DEP) is widely used in many commercially available products including plastics and personal care products. DEP has generally not been found to share the antiandrogenic mode of action that is common among other types of ... ...

Abstract	Background: Diethyl phthalate (DEP) is widely used in many commercially available products including plastics and personal care products. DEP has generally not been found to share the antiandrogenic mode of action that is common among other types of phthalates, but there is emerging evidence that DEP may be associated with other types of health effects. Objective: To inform chemical risk assessment, we performed a systematic review to identify and characterize outcomes within six broad hazard categories (male reproductive, female reproductive, developmental, liver, kidney, and cancer) following exposure of nonhuman mammalian animals to DEP or its primary metabolite, monoethyl phthalate (MEP). Methods: A literature search was conducted in online scientific databases (PubMed, Web of Science, Toxline, Toxcenter) and Toxic Substances Control Act Submissions, augmented by review of online regulatory sources as well as forward and backward searches. Studies were selected for inclusion using PECO (Population, Exposure, Comparator, Outcome) criteria. Studies were evaluated using criteria defined a priori for reporting quality, risk of bias, and sensitivity using a domain-based approach. Evidence was synthesized by outcome and life stage of exposure, and strength of evidence was summarized into categories of robust, moderate, slight, indeterminate, or compelling evidence of no effect, using a structured framework. Results: Thirty-four experimental studies in animals were included in this analysis. Although no effects on androgen-dependent male reproductive development were observed following gestational exposure to DEP, there was evidence including effects on sperm following peripubertal and adult exposures, and the overall evidence for male reproductive effects was considered moderate. There was moderate evidence that DEP exposure can lead to developmental effects, with the major effect being reduced postnatal growth following gestational or early postnatal exposure; this generally occurred at doses associated with maternal effects, consistent with the observation that DEP is not a potent developmental toxicant. The evidence for liver effects was considered moderate based on consistent changes in relative liver weight at higher dose levels; histopathological and biochemical changes indicative of hepatic effects were also observed, but primarily in studies that had significant concerns for risk of bias and sensitivity. The evidence for female reproductive effects was considered slight based on few reports of statistically significant effects on maternal body weight gain, organ weight changes, and pregnancy outcomes. Evidence for cancer and effects on kidney were judged to be indeterminate based on limited evidence (i.e., a single two-year cancer bioassay) and inconsistent findings, respectively. Conclusions: These results suggest that DEP exposure may induce androgen-independent male reproductive toxicity (i.e., sperm effects) as well as developmental toxicity and hepatic effects, with some evidence of female reproductive toxicity. More research is warranted to fully evaluate these outcomes and strengthen confidence in this database.
MeSH term(s)	Animals ; Female ; Liver ; Male ; Neoplasms ; Phthalic Acids/toxicity ; Pregnancy ; Reproduction ; Risk Assessment
Chemical Substances	Phthalic Acids ; diethyl phthalate (UF064M00AF)
Language	English
Publishing date	2020-09-19
Publishing country	Netherlands
Document type	Journal Article ; Review ; Systematic Review
ZDB-ID	554791-x
ISSN	1873-6750 ; 0160-4120
ISSN (online)	1873-6750
ISSN	0160-4120
DOI	10.1016/j.envint.2020.105848
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Article: The anogenital distance index of mice (Mus musculus domesticus): an analysis.

Hotchkiss, Andrew K / Vandenbergh, John G

Contemporary topics in laboratory animal science

2005 Volume 44, Issue 4, Page(s) 46–48

Abstract: The anogenital distance (AGD) is sexually dimorphic in Mus musculus domesticus, with the male AGD approximately twice as long as that in female mice. Among female mice, the AGD varies as a function of prenatal androgen exposure. The anogenital distance ... ...

Abstract	The anogenital distance (AGD) is sexually dimorphic in Mus musculus domesticus, with the male AGD approximately twice as long as that in female mice. Among female mice, the AGD varies as a function of prenatal androgen exposure. The anogenital distance index (AGDI) has been developed to serve as an indicator of prior androgen exposure due to intrauterine position (IUP). Concerns have been raised that the AGDI may not be an appropriate indicator of female IUP in mice. To further refine the AGDI, we have applied some commonly used and suggested transformations to the original data set of female CD-1 mice of known IUP, weaning body mass, and AGD. Our analysis suggests that the residual log transformation and untransformed body mass AGDIs are the most accurate means to predict the IUP of the pup. However, the IUP is only one mechanism by which a fetus may be exposed to hormonal variations in utero. Additional analyses revealed that the AGDI is influenced not only by the IUP of the female fetus but also by the identity of the dam (indicative of maternal influences) and the number of male fetuses found in the particular uterine horn. Therefore, the AGDI is not strictly a predictor of female IUP but of the intrauterine androgen environment in mice.
MeSH term(s)	Anal Canal/anatomy & histology ; Androgens/metabolism ; Animals ; Body Weights and Measures/statistics & numerical data ; Female ; Genitalia/anatomy & histology ; Male ; Mice/anatomy & histology ; Pregnancy ; Prenatal Exposure Delayed Effects ; Sex Characteristics
Chemical Substances	Androgens
Language	English
Publishing date	2005-07
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1060-0558
ISSN	1060-0558
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Article ; Online: Quantification of the Uncertainties in Extrapolating From In Vitro Androgen Receptor Antagonism to In Vivo Hershberger Assay Endpoints and Adverse Reproductive Development in Male Rats.

Gray, Leon E / Furr, Johnathan R / Lambright, Christy S / Evans, Nicola / Hartig, Phillip C / Cardon, Mary C / Wilson, Vickie S / Hotchkiss, Andrew K / Conley, Justin M

Toxicological sciences : an official journal of the Society of Toxicology

2019 Volume 176, Issue 2, Page(s) 297–311

Abstract: Multiple molecular initiating events exist that disrupt male sexual differentiation in utero including androgen receptor (AR) antagonism and inhibition of synthesis, and metabolism of fetal testosterone. Disruption of androgen signaling by AR antagonists ...

Abstract	Multiple molecular initiating events exist that disrupt male sexual differentiation in utero including androgen receptor (AR) antagonism and inhibition of synthesis, and metabolism of fetal testosterone. Disruption of androgen signaling by AR antagonists in utero reduces anogenital distance (AGD) and induces malformations in F1 male rat offspring. We are developing a quantitative network of adverse outcome pathways that includes multiple molecular initiating events and key events linking anti-AR activities to permanent reproductive abnormalities. Here, our objective was to determine how accurately the EC50s for AR antagonism in vitro or ED50s for reduced tissue growth in the Hershberger assay (HA) (key events in the adverse outcome pathway) predict the ED50s for reduced AGD in male rats exposed in utero to AR antagonists. This effort included in-house data and published studies from the last 60 years on AR antagonism in vitro and in vivo effects in the HA and on AGD after in utero exposure. In total, more than 250 studies were selected and included in the analysis with data from about 60 potentially antiandrogenic chemicals. The ability to predict ED50s for key events and adverse developmental effects from the in vitro EC50s displays considerable uncertainty with R2 values for HA and AGD of < 6%. In contrast, there is considerably less uncertainty in extrapolating from the ED50s in the HA to the ED50s for AGD (R2 value of about 85%). In summary, the current results suggest that the key events measured in the HA can be extrapolated with reasonable certainty to predict the ED50s for the adverse in utero effects of antiandrogenic chemicals on male rat offspring.
MeSH term(s)	Androgen Receptor Antagonists ; Animals ; Genitalia, Male/pathology ; Male ; Rats ; Receptors, Androgen ; Reproduction ; Uncertainty
Chemical Substances	Androgen Receptor Antagonists ; Receptors, Androgen
Language	English
Publishing date	2019-08-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfaa067
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Zs.A 1709: Show issues

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Article ; Online: Proposed Key Characteristics of Male Reproductive Toxicants as an Approach for Organizing and Evaluating Mechanistic Evidence in Human Health Hazard Assessments.

Arzuaga, Xabier / Smith, Martyn T / Gibbons, Catherine F / Skakkebæk, Niels E / Yost, Erin E / Beverly, Brandiese E J / Hotchkiss, Andrew K / Hauser, Russ / Pagani, Rodrigo L / Schrader, Steven M / Zeise, Lauren / Prins, Gail S

Environmental health perspectives

2019 Volume 127, Issue 6, Page(s) 65001

Abstract: Background: Assessing chemicals for their potential to cause male reproductive toxicity involves the evaluation of evidence obtained from experimental, epidemiological, and mechanistic studies. Although mechanistic evidence plays an important role in ... ...

Abstract	Background: Assessing chemicals for their potential to cause male reproductive toxicity involves the evaluation of evidence obtained from experimental, epidemiological, and mechanistic studies. Although mechanistic evidence plays an important role in hazard identification and evidence integration, the process of identifying, screening and analyzing mechanistic studies and outcomes is a challenging exercise due to the diversity of research models and methods and the variety of known and proposed pathways for chemical-induced toxicity. Ten key characteristics of carcinogens provide a valuable tool for organizing and assessing chemical-specific data by potential mechanisms for cancer-causing agents. However, such an approach has not yet been developed for noncancer adverse outcomes. Objectives: The objective in this study was to identify a set of key characteristics that are frequently exhibited by exogenous agents that cause male reproductive toxicity and that could be applied for identifying, organizing, and summarizing mechanistic evidence related to this outcome. Discussion: The identification of eight key characteristics of male reproductive toxicants was based on a survey of known male reproductive toxicants and established mechanisms and pathways of toxicity. The eight key characteristics can provide a basis for the systematic, transparent, and objective organization of mechanistic evidence relevant to chemical-induced effects on the male reproductive system. https://doi.org/10.1289/EHP5045.
MeSH term(s)	Animals ; Genitalia, Male/drug effects ; Hazardous Substances ; Humans ; Male ; Risk Assessment/methods ; Risk Assessment/standards ; Toxicity Tests/methods ; Toxicity Tests/standards
Chemical Substances	Hazardous Substances
Language	English
Publishing date	2019-06-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	195189-0
ISSN	1552-9924 ; 0091-6765 ; 1078-0475
ISSN (online)	1552-9924
ISSN	0091-6765 ; 1078-0475
DOI	10.1289/EHP5045
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Zs.B 1360: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 379: Show issues

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Article: Synchronized expression of retinoid X receptor mRNA with reproductive tract recrudescence in an imposex-susceptible mollusc.

Sternberg, Robin M / Hotchkiss, Andrew K / Leblanc, Gerald A

Environmental science & technology

2008 Volume 42, Issue 4, Page(s) 1345–1351

Abstract: The biocide tributyltin (TBT) causes the development of male sex characteristics in females of some molluscan species, a phenomenon known as imposex. Recent evidence suggests that the retinoid X receptor (RXR) participates in TBT-induced imposex. ... ...

Abstract	The biocide tributyltin (TBT) causes the development of male sex characteristics in females of some molluscan species, a phenomenon known as imposex. Recent evidence suggests that the retinoid X receptor (RXR) participates in TBT-induced imposex. Accordingly, we hypothesized that RXR may contribute to the seasonal development of the male reproductive tract in molluscs and would be expressed in concert with this phenomenon. RXR was cloned and sequenced from an imposex-susceptble species, the eastern mud snail Ilyanassa obsoleta. The DNA-binding domain of the receptor protein was 100 and 97% identical to those of the rock shell Thais clavigera and the freshwater snail Biomphalaria glabrata. The ligand-binding domain was 93 and 92% identicalto the LBD of these two molluscan species, respectively. Phylogenetic analyses revealed that RXR is an ancient nuclear receptor whose origin predates the emergence of the Bilateria. Interestingly, though inexplicably, the molluscan RXRs were more similar to sequences of vertebrate RXRs than to the RXRs of other lophotrochozoan invertebrates. Next, the expression of RXR mRNA levels in the reproductive tract was determined through the reproductive cycle. RXR mRNA levels increased commensurate with reproductive tract recrudescence in both sexes. However, the timing of coordinate recrudescence-RXR expression differed between sexes. Results demonstrate that RXR expression is associated with reproductive tract recrudescence in both sexes; although, the timing of recrudescence may dictate sex-specific development. Retinoid signaling initiated by TBT during an inappropriate time in females may result in imposex.
MeSH term(s)	Amino Acid Sequence ; Animals ; Female ; Male ; Molecular Sequence Data ; Mollusca/anatomy & histology ; Phylogeny ; RNA, Messenger/genetics ; Reproduction ; Retinoid X Receptors/chemistry ; Retinoid X Receptors/genetics ; Sequence Homology, Amino Acid ; Species Specificity
Chemical Substances	RNA, Messenger ; Retinoid X Receptors
Language	English
Publishing date	2008-03-05
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	0013-936X
ISSN	0013-936X
DOI	10.1021/es702381g
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Article: The contribution of steroidal androgens and estrogens to reproductive maturation of the eastern mud snail Ilyanassa obsoleta.

Sternberg, Robin M / Hotchkiss, Andrew K / Leblanc, Gerald A

General and comparative endocrinology

2008 Volume 156, Issue 1, Page(s) 15–26

Abstract: Molluscs exposed to endocrine-disrupting chemicals (EDCs) have exhibited changes in reproductive tract development that are typically associated with androgen or estrogen signaling in vertebrates. However, a role for androgens and estrogens in molluscan ... ...

Abstract	Molluscs exposed to endocrine-disrupting chemicals (EDCs) have exhibited changes in reproductive tract development that are typically associated with androgen or estrogen signaling in vertebrates. However, a role for androgens and estrogens in molluscan reproductive endocrinology has yet to be established. In this study, we investigated putative roles for steroidal androgens and estrogens in recrudescence of the eastern mud snail Ilyanassa obsoleta. Our objectives were to: (1) identify associations among concentrations of testosterone and 17beta-estradiol, sex, and reproductive status in mud snails that suggest these hormones are involved in recrudescence; and (2) determine whether mud snails express NR3C4-like (androgen receptor) and NR3A-like (estrogen receptor) mRNAs in a manner indicative of a role in recrudescence. Temporal changes in testosterone levels in males were consistent with a positive role in recrudescence. Such a trend was not evident in females or for 17beta-estradiol in either sex. Efforts to identify an androgen receptor from the mud snail using targeted, degenerate RT-PCR were unsuccessful. However, an estrogen receptor (ER) cDNA was identified that is highly similar to known ERs of other molluscs. Studies with the ER of other molluscs have shown that this protein does not actually bind estrogens. We therefore considered the possibility that the mud snail ER may regulate reproductive maturation as a ligand-independent transcription factor based upon its tissue abundance. Males expressed greater levels of ER mRNA than did females over the entire reproductive cycle, and this difference was most evident during recrudescence. ER mRNA levels were significantly elevated during recrudescence in males but not females. In conclusion, testosterone may have a role in male reproductive tract recrudescence; however, this putative activity is independent of a NR3C4-type androgen receptor. The ER also may function in male recrudescence, though apparently independent of 17beta-estradiol. The retinoid signaling pathway is discussed as a possible alternative hormone/receptor-mediated signaling pathway that regulates male recrudescence.
MeSH term(s)	Amino Acid Sequence ; Androgens/physiology ; Animals ; Estradiol/metabolism ; Estrogens/physiology ; Female ; Male ; Molecular Sequence Data ; Phylogeny ; RNA, Messenger/metabolism ; Receptors, Androgen/metabolism ; Receptors, Estrogen/analysis ; Receptors, Estrogen/metabolism ; Reproduction/physiology ; Sexual Maturation/physiology ; Snails/physiology ; Testosterone/metabolism
Chemical Substances	Androgens ; Estrogens ; RNA, Messenger ; Receptors, Androgen ; Receptors, Estrogen ; Testosterone (3XMK78S47O) ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2008-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1851-x
ISSN	1095-6840 ; 0016-6480
ISSN (online)	1095-6840
ISSN	0016-6480
DOI	10.1016/j.ygcen.2007.12.002
Database	MEDical Literature Analysis and Retrieval System OnLINE

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