			Home About us Contact

Paternal Exposure (paternal + exposure)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	50%

Selected Abstracts

Paternal exposures: Altered sex ratios.

BIRTH DEFECTS RESEARCH, Issue 1 2001

No abstract is available for this article. [source]

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

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2 2010
Nicole Verhofstad
Abstract 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 32P-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,/,) 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,/, 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,/, and Wt mice were only observed in testis. In sperm, DNA adduct levels were significantly higher in Xpc,/, mice than in Wt mice only at Day 42 after exposure (P = 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. 2010. © 2009 Wiley-Liss, Inc. [source]

Paternal transmission of genetic damage: findings in animals and humans

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 3 2000
Martin H. Brinkworth
The concept that mutations can be induced in the male germ-line and result in adverse effects in the offspring has achieved only limited acceptance despite considerable theoretical appeal. This is partly because fetal malformations are generally perceived to be induced solely as a result of maternally mediated events during gestation and partly because the low incidence of the end-points concerned make experimental approaches costly and time-consuming. Nonetheless, a substantial body of work relating to the hypothesis has accumulated in the last 20 years, which has never been reviewed in its entirety. A consideration of the available evidence indicates that preconceptional paternal exposure to mutagens (particularly radiation, cyclophosphamide and ethylnitrosourea) can indeed, under certain conditions, have adverse effects on offspring. The results suggest two principal mechanisms by which such effects may be induced: the induction of germ-line genomic instability or the suppression of germ cell apoptosis. [source]

Parental exposure to lead and small for gestational age births

AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 6 2006
Pau-Chung Chen MD
Abstract Background Previous studies about the effect of lead exposure on adverse birth outcomes are still inconsistent and few studies estimate the relationship between parental lead exposure and small for gestational age (SGA) infants. An occupational cohort study to assess whether parental lead exposure would be related to decreased birth weight and shortened gestational ages of their offspring was conducted. Whether higher lead exposure doses would increase risks of low birth weight (LBW), preterm delivery, and SGA births was also investigated. Methods A Program to Reduce Exposure by Surveillance System,Blood Lead Levels (Press-BLLS) was established in Taiwan in July 1993. The names of workers exposed to lead was collected from this occupational blood-lead notification database. The birth outcomes of their offspring were determined by linking to the Taiwan birth registration database from 1993 to 1997. Only singleton births whose parental blood-lead concentrations were tested during pregnancy or prior to conception, or within a 1-year span before these two periods were included. Results Among 1,611 eligible births, 72 births were LBW, 74 were preterm deliveries, and 135 were SGA. Maternal blood-lead concentrations (PbBs) equal to or more than 20 µg/dl had a higher risk of mothering a SGA child (risk ratio (RR),=,2.15; 95% confidence interval (CI), 1.15,3.83). Conclusions Additional evidence of the effects of lead on adverse birth outcomes, especially for SGA births is reported. Maternal exposure to lead plays a more important role in the adverse effect on birth outcome than does paternal exposure. Am. J. Ind. Med. 2006. © 2006 Wiley-Liss, Inc. [source]