Male-mediated developmental toxicity

Anderson, Diana

doi:10.1016/j.taap.2005.01.022

Cited by 35 publications

(23 citation statements)

References 84 publications

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“…Anderson also summarized several low-dose studies [Anderson, 2005]. Chronic low-dose exposure to 1,3-butadiene increased the frequency of adverse pregnancy outcomes, which is consistent with recent epidemiological data that support the possibility that occupational exposure to 1,3-butadiene induces adverse reproductive effects in humans.…”

Section: Transgenerational Effects Of Low-dose Mutagenesissupporting

confidence: 71%

“…The evidence for such effects in humans is very limited, e.g., based on observations of increased cancer prevalence in the vicinity of nuclear power plants and increased cancer incidence among children of male smokers [Anderson, 2005]. The majority of studies of exposed humans have failed to provide convincing evidence of exposure-related adverse heritable effects, including a study of the rate of birth defects among the offspring of ~18,000 cancer survivors, who presumably received high doses of mutagenic agents [Anderson, 2005].…”

Section: Transgenerational Effects Of Low-dose Mutagenesismentioning

confidence: 99%

“…Anderson reviewed studies of adverse effects in animals and humans exposed to environmental chemicals, including cyclophosphamide, 1,3-butadiene, and urethane. Using an animal model of male-mediated teratogenicity, offspring of male rodents acutely exposed to cyclophosphamide had numerous birth defects as well as chromosome abnormalities and increased tumor incidences [Anderson, 2005].…”

Section: Transgenerational Effects Of Low-dose Mutagenesismentioning

confidence: 99%

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Assessing human germ‐cell mutagenesis in the Postgenome Era: A celebration of the legacy of William Lawson (Bill) Russell

Wyrobek

Mulvihill

Wassom

et al. 2007

Environ and Mol Mutagen

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Birth defects, de novo genetic diseases, and chromosomal abnormality syndromes occur in ~5% of all live births, and affected children suffer from a broad range of lifelong health consequences. Despite the social and medical impact of these defects, and the 8 decades of research in animal systems that have identified numerous germ-cell mutagens, no human germ-cell mutagen has been confirmed to date. There is now a growing consensus that the inability to detect human germ-cell mutagens is due to technological limitations in the detection of random mutations rather than biological differences between animal and human susceptibility. A multidisciplinary workshop responding to this challenge convened at The Jackson Laboratory in Bar Harbor, Maine. The purpose of the workshop was to assess the applicability of an emerging repertoire of genomic technologies to studies of human germ-cell mutagenesis. Workshop participants recommended large-scale human germ-cell mutation studies be conducted using samples from donors with high-dose exposures, such as cancer survivors. Within this high-risk cohort, parents and children could be evaluated for heritable changes in (a) DNA sequence and chromosomal structure, (b) repeat sequences and minisatellites, and (c) global gene expression profiles and pathways. Participants also advocated the establishment of a bio-bank of human tissue samples from donors with well-characterized exposure, including medical and reproductive histories. This mutational resource could support large-scale, multipleendpoint studies. Additional studies could involve the examination of transgenerational effects NIH Public AccessAuthor Manuscript Environ Mol Mutagen. Author manuscript; available in PMC 2007 November 8. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript associated with changes in imprinting and methylation patterns, nucleotide repeats, and mitochondrial DNA mutations. The further development of animal models and the integration of these with human studies are necessary to provide molecular insights into the mechanisms of germcell mutations and to identify prevention strategies. Furthermore, scientific specialty groups should be convened to review and prioritize the evidence for germ-cell mutagenicity from common environmental, occupational, medical, and lifestyle exposures. Workshop attendees agreed on the need for a full-scale assault to address key fundamental questions in human germ-cell environmental mutagenesis. These include, but are not limited to, the following: Do human germ-cell mutagens exist? What are the risks to future generations? Are some parents at higher risk than others for acquiring and transmitting germ-cell mutations? Obtaining answers to these, and other critical questions, will require strong support from relevant funding agencies, in addition to the engagement of scientists outside the fields of genomics and germ-cell mutagenesis.

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Section: Transgenerational Effects Of Low-dose Mutagenesissupporting

confidence: 71%

Section: Transgenerational Effects Of Low-dose Mutagenesismentioning

confidence: 99%

Section: Transgenerational Effects Of Low-dose Mutagenesismentioning

confidence: 99%

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Assessing human germ‐cell mutagenesis in the Postgenome Era: A celebration of the legacy of William Lawson (Bill) Russell

Wyrobek

Mulvihill

Wassom

et al. 2007

Environ and Mol Mutagen

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“…And, considering that the male partner contributes for a half of genetic information for the developing offspring, he should be examined as the responsible for teratogenesis and adverse alterations in the offspring development (Anderson, 2005).…”

Section: Introductionmentioning

confidence: 99%

Toxic effects of different doses of cyclophosphamide on the reproductive parameters of male mice

Kanno

Sensiate

Paula

et al. 2009

Braz. J. Pharm. Sci.

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The cyclophosphamide is used in cancer treatment. The aim of this study was evaluating the effect of different doses of this drug on male mice reproductive parameters. The cyclophosphamide was administered in the doses 100, 150, 200 e 250 mg.kg -1 , intraperitoneal route, for six weeks. As a result, it was observed a decrease in body mass and a decrease in testicles and kidney's weight, in all animals treated with cyclophosphamide. Only the groups that received the doses 100, 150 mg.kg -1 of cyclophosphamide were able to fertilize their females. There was higher incidence of post-implantation losses, reabsorptions and decrease in fetal viability in the group that received the dose of 150 mg.kg . Based on the methodology used and results obtained, it was concluded that the cyclophosphamide was toxic, considering the decrease in animal's body mass and testicle's weight; promoted hepatotoxicity and nephrotoxic effect; influenced in the animals spermatogenesis taking them to infertility and/or subfertility; decreased fetal viability, despite it didn't cause significant malformations in the offspring.Uniterms: Cyclophosphamide/effects. Cyclophosphamide/toxicity. Spermatogenesis/experimental study. Chemotherapeutics/adverse effects. Fertility/experimental study.A ciclofosfamida é utilizada no tratamento de câncer. Este estudo visa avaliar os efeitos das diferentes doses do fármaco nos parâmetros reprodutivos de camundongos machos. A ciclofosfamida foi administrada nas doses de 100, 150, 200 e 250 mg kg -1 , via intraperitoneal por seis semanas. Como resultado observou-se diminuição de massa corporal, redução no peso de testículos e rins em todos os animais tratados com a ciclofosfamida. Apenas os grupos que receberam as doses de 100 e 150 mg kg -1 do quimioterápico foram capazes de fertilizar as fêmeas. Houve maior incidência de perdas pós-implantação, reabsorção e diminuição da viabilidade fetal no grupo que recebeu a dose de 150 mg kg -1 . Observou-se redução nos pesos dos epidídimos e fígado dos animais tratados com as doses de 150, 200 e 250 mg kg -1 . Espermatozóides anômalos foram encontrados nas doses de 200 e 250mg kg -1 . Com base na metodologia empregada e nos resultados obtidos, conclui-se que a ciclofosfamida foi tóxica considerando-se a redução de massa corporal e o peso dos testículos dos animais; promoveu hepatotoxicidade e efeito nefrotóxico; influenciou na espermatogênese dos animais de forma a levá-los a um estado de infertilidade e/ou subfertilidade; diminuiu viabilidade fetal, entretanto não causou malformações significativas na prole.Unitermos: Ciclofosfamida/efeitos. Ciclofosfamida/toxicidade. Espermatogênese/estudo experimental. Quimioterápicos/efeitos adversos. Fertilidade/ estudo experimental.

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“…In addition, the rs2013162 rare allele exhibited a genome-wide significant relationship with CL(P) in a study by Beaty et al [17]. Stratification of the sample population using Asian ancestry as a factor yielded stronger evidence of association with IRF6 rs62013162 [17].…”

Section: Discussionmentioning

confidence: 96%

Interferon Regulatory Factor 6 (IRF6) and Gene – Environment Interactions in Non-Syndromic Orofacial Cleft Cases in Saudi Arabia-A Case Control Study

Alamoudi¹,

Sabbagh²,

Innes³

et al. 2018

J Oral Hyg Health

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The association between interferon regulatory factor 6 (IRF6) and nonsyndromic orofacial cleft (NSOFC) is affected by ethnicity. Also, gene-environment interactions (GEI) may play an important role in its etiology.Objectives: This case-control study investigated whether IRF6 gene variants were associated with NSOFC in Saudi Arabian population and whether the gene was affected by maternal environmental exposures. Methods:We extracted DNA from saliva samples obtained from 171 infant-parent triad cases and 189 matched controls (age, gender, and location) from January 2010-December 2011; this study included a total of 11 referral hospitals in Saudi Arabia. IRF6 (rs2013162, rs2235375, and rs2235371) polymorphisms were genotyped using restriction-digestion polymerase chain reaction. Data on environmental exposures, for GEI analyses, were collected through questionnaire-led interviews with parents. Results:We found statistically significant over transmission of the common IRF6 rs2013162 allele among cleft lip with or without palate CL(P) cases. No associations were found for either of the other two IRF6 SNPs. Maternal exposure to antipyretics, folic acid, fever, antibiotics, illnesses, common cold/flu, paternal water pipe smoking, stress, x-rays, and/or chemicals could significantly interact with the maternal IRF6 (rs2013162 and rs2235375) gene variants, affecting the likelihood of having an offspring with NSOFC. Conclusion:The common allele at IRF6 rs2013162 was significantly over transmitted among CL(P) cases. This study provides hypotheses for future investigations into genetic and environmental factors and their interaction in the etiology of NSOFC.

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Male-mediated developmental toxicity

Cited by 35 publications

References 84 publications

Assessing human germ‐cell mutagenesis in the Postgenome Era: A celebration of the legacy of William Lawson (Bill) Russell

Assessing human germ‐cell mutagenesis in the Postgenome Era: A celebration of the legacy of William Lawson (Bill) Russell

Toxic effects of different doses of cyclophosphamide on the reproductive parameters of male mice

Interferon Regulatory Factor 6 (IRF6) and Gene – Environment Interactions in Non-Syndromic Orofacial Cleft Cases in Saudi Arabia-A Case Control Study

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