Comparison of the duration of spermatogenesis between male rodents and humans

Adler, I.‐D.

doi:10.1016/0027-5107(95)00223-5

Cited by 147 publications

(113 citation statements)

References 9 publications

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“…Sperm were collected from the cauda epididymis 6 wk after the end of the exposure period. ESTR mutations require DNA replication, and this interval permits sperm that were at the spermatogonial cell stage during exposure, which is the last stage at which DNA replication occurs during spermatogenesis (15), to reach the epididymis. ESTR mutation frequencies in two independent sham-exposed groups were 1.5% (range, 0.8-2.9%) and 1.3% (range, 0.9-1.7%), respectively.…”

Section: Resultsmentioning

confidence: 99%

Sidestream tobacco smoke is a male germ cell mutagen

Marchetti

Rowan-Carroll

Williams

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Active cigarette smoking increases oxidative damage, DNA adducts, DNA strand breaks, chromosomal aberrations, and heritable mutations in sperm. However, little is known regarding the effects of second-hand smoke on the male germ line. We show here that short-term exposure to mainstream tobacco smoke or sidestream tobacco smoke (STS), the main component of secondhand smoke, induces mutations at an expanded simple tandem repeat locus (Ms6-hm) in mouse sperm. We further show that the response to STS is not linear and that, for both mainstream tobacco smoke and STS, doses that induced significant increases in expanded simple tandem repeat mutations in sperm did not increase the frequencies of micronucleated reticulocytes and erythrocytes in the bone marrow and blood of exposed mice. These data show that passive exposure to cigarette smoke can cause tandem repeat mutations in sperm under conditions that may not induce genetic damage in somatic cells. Although the relationship between noncoding tandem repeat instability and mutations in functional regions of the genome is unclear, our data suggest that paternal exposure to second-hand smoke may have reproductive consequences that go beyond the passive smoker.DNA mutation | micronuclei | germline | spermatogenesis D espite years of intense public campaigns to limit and reduce tobacco consumption, smoking is still widespread, and its health effects remain a significant public concern. Approximately 35% of men of reproductive age in the United States smoke cigarettes (1), and there is extensive evidence to suggest that tobacco smoking can result in abnormal reproductive outcomes such as spontaneous abortions and birth defects (2). Men who smoke are at high risk for several semen abnormalities, including reduced motility, sperm DNA damage such as DNA breaks and adducts, and chromosomal abnormalities (3). In mice, exposure to mainstream tobacco smoke (MTS) induces germ-line mutations in expanded simple tandem repeats (ESTR) that can be transmitted to the progeny, causing irreversible modifications in the genome of the offspring (4). Recently, the International Agency for Research on Cancer concluded that there is enough evidence to link paternal smoking in humans with increased risk of childhood cancer, suggesting that tobacco smoking causes heritable germ cell mutation in humans (5).Exposure to second-hand smoke also remains widespread, with an estimated 40% of nonsmokers being exposed to secondhand smoke (6). Much less is known about the health effects of second-hand (or passive) smoking, although evidence is rapidly accumulating that exposure to second-hand smoke can be as harmful and hazardous to human health as active smoking (6, 7), and that there may be no risk-free level of exposure (8). Sidestream tobacco smoke (STS), the main component of secondhand smoke, is a complex mixture of more than 4,000 chemicals, including at least 50 known carcinogens (8). Qualitative differences between MTS-the smoke inhaled by active smokers-and STS are small; however, some toxicants...

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Section: Resultsmentioning

confidence: 99%

Sidestream tobacco smoke is a male germ cell mutagen

Marchetti

Rowan-Carroll

Williams

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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“…A cycle of the male spermatogenesis from stem cells to ejaculating spermatozoa takes around 40 days for the mouse and 70 days for humans (Adler, 1996). In the former, epididymal and testicular spermatozoa last for 4-6 and 6 days, respectively.…”

Section: Minisatellite Mutation and Male Spermatogenesismentioning

confidence: 99%

“…It may also be due to the difference in the stages of spermatids at the time of irradiation. Mating of males at 3 weeks after irradiation corresponds to the late spermatocyte to early spermatid stage (Adler, 1996;Barber et al, 2000). At this stage, germ cells still retain a capacity to repair double-strand breaks, but replication and recombination of DNA does not take place.…”

Section: Minisatellite Mutation and Male Spermatogenesismentioning

confidence: 99%

Induced genomic instability in irradiated germ cells and in the offspring; reconciling discrepancies among the human and animal studies

Niwa

2003

Oncogene

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Many studies confirmed that radiation induces genomic instability in whole-body systems. However, the results of the studies are not always consistent with each other. Attempts are made in the present review to resolve the discrepancies. Many of the studies in human and experimental animals utilize the length change mutation of minisatellite sequences as a marker of genomic instability. Minisatellite sequences frequently change their length, and the data obtained by conventional Southern blotting give rather qualitative information, which is sometimes difficult to scrutinize quantitatively. This is the problem inevitably associated with the study of minisatellite mutations and the source of some conflicts among studies in humans and mice. Radiation induction of genomic instability has also been assessed in whole-body experimental systems, using other markers such as the mouse pink-eyed unstable allele and the specific pigmentation loci of medaka fish (Oryzias latipes). Even though there are some contradictions, all these studies have demonstrated that genomic instability is induced in the germ cells of irradiated parents, especially of males, and in offspring born to them. Among these, transmission of genomic instability to the second generation of irradiated parents is limited to the mouse minisatellite system, and awaits further clarification in other experimental systems.

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“…It is still not clear whether these protective mechanisms sufficiently protect the integrity of germ cell DNA upon exposure to B[a]P, but failure of these defense mechanisms may lead to increased levels of DNA damage and possibly germ line mutations. Moreover, the vulnerability of germ cells to the persistence of DNA damage is known to change during spermatogenesis [Adler, 1996], and depends on DNA synthesis and cell proliferation in both the mitotic and meiotic stages. During these early stages, dividing sperm cells are still DNA repair proficient and seem to be well protected.…”

Section: Introductionmentioning

confidence: 99%

DNA adduct kinetics in reproductive tissues of DNA repair proficient and deficient male mice after oral exposure to benzo(a)pyrene

Verhofstad

Oostrom

Benthem

et al. 2009

Environ and Mol Mutagen

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Benzo(a)pyrene (B[a]P) can induce somatic mutations, whereas its potential to induce germ cell mutations is unclear. There is circumstantial evidence that paternal exposure to B[a]P can result in germ cell mutations. Since DNA adducts are thought to be a prerequisite for B[a]P induced mutations, we studied DNA adduct kinetics by 32 P-postlabeling in sperm, testes and lung tissues of male mice after a single exposure to B[a]P (13 mg/kg bw, by gavage). To investigate DNA adduct formation at different stages of spermatogenesis, mice were sacrificed at Day 1, 4, 7, 10, 14, 21, 32, and 42 after exposure. In addition, DNA repair deficient (Xpc 2/2 ) mice were used to study the contribution of nucleotide excision repair in DNA damage removal. DNA adducts were detectable with highest levels in lung followed by sperm and testis. Maximum adduct levels in the lung and testis were observed at Day 1 after exposure, while adduct levels in sperm reached maximum levels at 1 week after exposure. Lung tissue and testis of Xpc 2/2 mice contained significantly higher DNA adduct levels compared to wild type (Wt) mice over the entire 42 day observation period (P < 0.05). Differences in adduct half-life between Xpc 2/2 and Wt mice were only observed in testis. In sperm, DNA adduct levels were significantly higher in Xpc 2/2 mice than in Wt mice only at Day 42 after exposure (P 5 0.01). These results indicate that spermatogonia and testes are susceptible for the induction of DNA damage and rely on nucleotide excision repair for maintaining their genetic integrity. Environ. Mol. Mutagen. 51:123-129, 2010. V V C 2009 Wiley-Liss, Inc.

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Comparison of the duration of spermatogenesis between male rodents and humans

Cited by 147 publications

References 9 publications

Sidestream tobacco smoke is a male germ cell mutagen

Sidestream tobacco smoke is a male germ cell mutagen

Induced genomic instability in irradiated germ cells and in the offspring; reconciling discrepancies among the human and animal studies

DNA adduct kinetics in reproductive tissues of DNA repair proficient and deficient male mice after oral exposure to benzo(a)pyrene

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