Mammalian male germ cell cytogenetics

Albanese, R.

doi:10.1093/mutage/2.2.79

Cited by 32 publications

(5 citation statements)

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“…With the exception of diepoxybutane, these studies generally reported a linear or nearly linear increase in the frequencies of chromosomal aberrations, providing further evidence for the diminished repair of sperm lesions in postmeiotic germ cells. The time‐response studies (Albanese, 1987; Matsuda et al, 1989c, 1989d; Marchetti et al, 2001, 2004) show patterns of sensitivity for the induction of paternally‐transmitted chromosomal aberrations that overlap the pattern of sensitivity for dominant lethality: namely, the highest frequencies of chromosomal aberrations are found after exposure of postmeiotic germ cells, and very few mutagens induced significant increases after treatment of meiotic germ cells or spermatogonia.…”

Section: Methods For Investigating Paternally‐transmitted Chromosomalmentioning

confidence: 99%

Mechanisms and consequences of paternally‐transmitted chromosomal abnormalities

Marchetti

Wyrobek

2005

Birth Defects Research Pt C

119

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Paternally transmitted chromosomal damage has been associated with pregnancy loss, developmental and morphological defects, infant mortality, infertility, and genetic diseases in the offspring including cancer. There is epidemiological evidence linking paternal exposure to occupational or environmental agents with an increased risk of abnormal reproductive outcomes.There is also a large body of literature on germ cell mutagenesis in rodents showing that treatment of male germ cells with mutagens has dramatic consequences on reproduction producing effects such as those observed in human epidemiological studies. However, we know very little about the etiology, transmission and early embryonic consequences of paternallyderived chromosomal abnormalities. The available evidence suggests that: 1) there are distinct patterns of germ cell-stage differences in the sensitivity of induction of transmissible genetic damage with male postmeiotic cells being the most sensitive; 2) cytogenetic abnormalities at first metaphase after fertilization are critical intermediates between paternal exposure and abnormal reproductive outcomes; and, 3) there are maternally susceptibility factors that may have profound effects on the amount of sperm DNA damage that is converted into chromosomal aberrations in the zygote and directly affect the risk for abnormal reproductive outcomes.

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Section: Methods For Investigating Paternally‐transmitted Chromosomalmentioning

confidence: 99%

Mechanisms and consequences of paternally‐transmitted chromosomal abnormalities

Marchetti

Wyrobek

2005

Birth Defects Research Pt C

119

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“…Exposure of mammalians to mutagenic agents may cause genetic alterations in germ cells and lead to reproductive disorders. It has been estimated that up to 50% of fetal death, 30% of mental retardation, 20% of congenital defects and 2% of total male infertility are associated with chromosomal aberrations (Alder et al 1978, Bloom and Paul 1981, Hook 1982, Albanese 1987.…”

Section: Discussionmentioning

confidence: 99%

Cytogenetic Studies on Two Drugs for Natural Relief of Prostatic Disorders

Ahmed

Othman

2004

CYTOLOGIA

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Pepon and prostoplex, new drugs containing natural substances, are used in the treatment of prostatic disorders. The cytogenetic effects of these drugs were tested in mice's bone marrow and spermatocytes cells at two doses comparable to propose human therapeutic and double therapeutic doses. The results revealed that the total numbers of structural chromosomal aberrations in mice's bone marrow, with or without gap, were significantly increased at pϽ0.01 for pepon and at pϽ0.05 for prostoplex at therapeutic doses. Whereas at double therapeutic doses, the two drugs showed highly significant increases in the total numbers of structural chromosomal aberrations compared with controls. The frequency of total chromosomal aberrations in mice's spermatocytes was increased at significant level pϽ0.01 for both drugs at therapeutic doses. At double therapeutic doses, pepon and postoplex increased the total chromosomal aberrations in spermatocyte cells at highly significant level pϽ0.001. In conclusion, the cytogenetic analysis of pepon and prostoplex revealed that the two drugs have adverse effect on somatic and germinal materials at therapeutic dose. Also, our results are considered as a caution for the treatment with these two drugs at double therapeutic doses, which have mutagenic effect on somatic and germinal materials.

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“…High levels of aberrations were produced in early embryos derived from spermatozoa exposed at the spermatozoa and/or spermatid stages to all the alkylating agents tested (busulfan, cyclophosphamide, melphalan, and mitomycin C) and to radiation (Table S7). The topoisomerase inhibitor etoposide was strongly and selectively mutagenic toward spermatocytes, and the antimetabolite, 5‐fluorouracil, produced modest levels of mutations in spermatocytes and spermatids. Most of the drugs failed to produce transmissible chromosomal aberrations in differentiating spermatogonia, suggesting that this effect would also be low in stem spermatogonia.…”

Section: Animal Data On Mutations In Spermatozoa At Various Time Poinmentioning

confidence: 99%

Risks of genetic damage in offspring conceived using spermatozoa produced during chemotherapy or radiotherapy

Meistrich

2020

Andrology

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Background: Men who have just started cytotoxic therapy for cancer are uncertain and concerned about whether spermatozoa collected or pregnancies occurring during therapy might be transmitting genetic damage to offspring. There are no comprehensive guidelines on the risks of different doses of the various cytotoxic, and usually genotoxic, antineoplastic agents. Objectives:To develop a schema showing the risks of mutagenic damage when spermatozoa, exposed to various genotoxic agents during spermatogenesis, are collected or used to produce a pregnancy. Materials and methods:A comprehensive literature review was performed updating the data on genetic and epigenetic effects of genotoxic agents on animal and human spermatozoa exposed during spermatogenic development.Results: Relevant data on human spermatozoa and offspring are extremely limited, but there are extensive genetic studies in experimental animals that define sensitivities for specific drugs and times. The animal data were extrapolated to humans based on the stage when the cells were exposed and the relative kinetics of spermatogenesis and were consistent with the limited human data. In humans, alkylating agents and radiation should already induce a high risk of mutations in spermatozoa produced within 1 or 2 weeks after initiation of therapy. Topoisomerase II inhibitors and possibly microtubule inhibitors produce the greatest risk at weeks 5-7 of therapy.Nucleoside analogs, antimetabolites, and bleomycin exert their mutagenic effects on spermatozoa collected at 7-10 weeks of therapy. Discussion and conclusions:A schema showing the time from initiation of therapy at which specific antineoplastic agents can cause significant levels of genetic damage in conceptuses and live offspring was developed. The estimates and methods for computing the level of such risk from an individual patient's treatment regimen will enable patients and counselors to make informed decisions on the use of spermatozoa or continuation of a pregnancy. K E Y W O R D Schemotherapy, radiotherapy, mutations, chromosome aberrations, human, animal models

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Mammalian male germ cell cytogenetics

Cited by 32 publications

References 0 publications

Mechanisms and consequences of paternally‐transmitted chromosomal abnormalities

Mechanisms and consequences of paternally‐transmitted chromosomal abnormalities

Cytogenetic Studies on Two Drugs for Natural Relief of Prostatic Disorders

Risks of genetic damage in offspring conceived using spermatozoa produced during chemotherapy or radiotherapy

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