Effects of Estrogens on Microtubule Assembly: Significance for Aneuploidy

Metzler, Manfred; Pfeiffer, Erika; Schuler, Maik; Rosenberg, Brigitte

doi:10.1007/978-1-4612-2332-0_22

Cited by 6 publications

(4 citation statements)

References 11 publications

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“…The syndromes that involve sex chromosomes include Klinefelter’s syndrome (47, XXY or in some cases 48, XXXY; 49, XXXXY) and Turner Syndrome (a defected or missing X chromosome in women). Estrogen pathways predominantly control chromosomal segregation and microtubule assembly during meiosis—a major target to EDCs [ 100 ]. Exposure to EDCs leading to aneuploidy in germ cells not only causes developmental defects and infertility in offspring, but also leads to miscarriages and infertility of sperm cells [ 101 , 102 ].…”

Section: Resultsmentioning

confidence: 99%

Endocrine Disruptors Acting on Estrogen and Androgen Pathways Cause Reproductive Disorders through Multiple Mechanisms: A Review

Amir

Shah

Mamoulakis

et al. 2021

IJERPH

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Increasing contamination of the environment by toxic compounds such as endocrine disrupting chemicals (EDCs) is one of the major causes of reproductive defects in both sexes. Estrogen/androgen pathways are of utmost importance in gonadal development, determination of secondary sex characteristics and gametogenesis. Most of the EDCs mediate their action through respective receptors and/or downstream signaling. The purpose of this review is to highlight the mechanism by which EDCs can trigger antagonistic or agonistic response, acting through estrogen/androgen receptors causing reproductive defects that lead to infertility. In vitro, in vivo and in silico studies focusing on the impact of EDCs on estrogen/androgen pathways and related proteins published in the last decade were considered for the review. PUBMED and PUBCHEM were used for literature search. EDCs can bind to estrogen receptors (ERα and ERβ) and androgen receptors or activate alternative receptors such as G protein-coupled receptors (GPCR), GPR30, estrogen-related receptor (ERRγ) to activate estrogen signaling via downstream kinases. Bisphenol A, dichlorodiphenyltrichloroethane, dichlorodiphenyldichloroethylene, polychlorinated biphenyls and phthalates are major toxicants that interfere with the normal estrogen/androgen pathways leading to infertility in both sexes through many ways, including DNA damage in spermatozoids, altered methylation pattern, histone modifications and miRNA expression.

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Section: Resultsmentioning

confidence: 99%

Endocrine Disruptors Acting on Estrogen and Androgen Pathways Cause Reproductive Disorders through Multiple Mechanisms: A Review

Amir

Shah

Mamoulakis

et al. 2021

IJERPH

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“…Formation of oxygen-free radicals by redox cycling of estrogens or DNA modification by reactive estrogen metabolites may explain some of the structural and numeric chromosomal changes observed in response to estrogen exposure (131,132). Damage to DNA by ROS generated by estrogen treatment, i.e., 8-OHdG, lipid-DNA adducts, and DNA strand breaks, may induce structural and numeric alterations in chromosomes and may be important lesions capable of producing mutagenic changes in the genome.…”

Section: Indirect Evidence Of Mutations Induced By Estrogensmentioning

confidence: 98%

“…More recent experiments have shown that some estrogens are capable of producing such instability (126,129,130). For instance, estrogens induce numeric changes in chromosomes (genome mutation or aneuploidy) with and without apparent DNA damage (131). Both DES and E 2 are potent inhibitors of mitosis in vitro and are capable of inducing genomic mutations in cultured cells (132).…”

Section: Indirect Evidence Of Mutations Induced By Estrogensmentioning

confidence: 98%

Chapter 4: Estrogens as Endogenous Genotoxic Agents--DNA Adducts and Mutations

Cavalieri¹,

Frenkel²,

Liehr³

et al. 2000

JNCI Monographs

522

412

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“…Recent study has shown that some estrogen metabolites are capable of producing genome instability [41]. DNA modification by these reactive estrogen metabolites might explain some of the structural and numeric chromosomal changes observed in response to estrogen exposure [42]. In conclusion, estrogen metabolites can produce multiple types of genetic insults contributing to the induction of genomic instability.…”

Section: Estrogen Metabolites and Mutations In Dnamentioning

confidence: 99%

Cancer Morbidity in Rheumatoid Arthritis: Role of Estrogen Metabolites

Khan

2013

BioMed Research International

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Estrogen metabolites have been implicated in rheumatoid arthritis (RA) and cancer, although the mechanism remains unestablished. Some estrogen metabolites, which are used for the assessment of cancer risk, play an important role in RA. The pathways by which malignancies associated with RA remain elusive. Possible mechanism involves enzymatic or nonenzymatic oxidation of estrogen into catecholestrogen metabolites through semiquinone and quinone redox cycle to produce free radicals that can cause DNA modifications. Modifications of DNA alter its immunogenicity and trigger various immune responses leading to elevated levels of cancer and RA antibodies. However, the role of different estrogen metabolites as a mediator of immune response cannot be ruled out in various immune-related diseases.

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Effects of Estrogens on Microtubule Assembly: Significance for Aneuploidy

Cited by 6 publications

References 11 publications

Endocrine Disruptors Acting on Estrogen and Androgen Pathways Cause Reproductive Disorders through Multiple Mechanisms: A Review

Endocrine Disruptors Acting on Estrogen and Androgen Pathways Cause Reproductive Disorders through Multiple Mechanisms: A Review

Chapter 4: Estrogens as Endogenous Genotoxic Agents--DNA Adducts and Mutations

Cancer Morbidity in Rheumatoid Arthritis: Role of Estrogen Metabolites

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