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At least 55 records · Page 3Linked to original sources
PubMed1987

Cyclophosphamide: effects of paternal exposure on the brain chemistry of the F1 progeny.

The effects of acute and chronic cyclophosphamide (CP) exposure to male rats on several neurotransmitter enzymes have been examined in various brain regions of the F1 progeny at 90 d old. The acute postmeiotic CP exposure to male rats induced significant biphasic changes in the choline acetyltransferase (ChAT) activity in various brain regions of F1 progeny; significant decreases in the cerebellar acetylcholinesterase (AChE) activity of the male (47%) and the female (14%) F1 progeny, and moderate decrease (26%) in the hippocampal AChE activity in the female F1 progeny; and a moderate increase (29%) in the temporo-cortical glutamic acid decarboxylase (GAD) activity of the female F1 rats. The chronic CP-exposed male rats resulted in a slight but significant decrease (16%) in the temporo-cortical ChAT activity in the female F1 progeny; a marked increase (51%) in the hypothalamic AChE activity in the male F1 progeny; and a marked decrease (32%) in cerebellar GAD activity and a slight increase (13%) in the striatal GAD activity in the female F1 progeny. These enzymatic changes in the adult brain of F1 progeny of CP-treated males may be associated with the behavioral abnormalities observed previously. Results suggest that these neurochemical parameters may be useful markers for analysis of the potential neurotoxicity of CP.

Acetylcholinesterase↗
PubMed1991

Paternal exposure to radiation and offspring cancer in mice: reanalysis and new evidence.

Parental exposure to radiation could induce various kinds of tumors in the next generation. In ICR mice, a large and significant increase of adult types tumor was observed in the F1 offspring after X-ray exposure at spermatozoa and spermatid stages, and less clear increase was observed after spermatogonial exposure. Mature oocytes were resistant upto 1 Gy, but very sensitive to tumor induction at higher doses. While there was no difference in the tumor incidence between acute and fractionated (0.36 Gy at 2 hr intervals) irradiation at post-gonial stages, a large reduction of tumor incidence was observed after spermatogonial and mature oocyte exposure, suggesting some repairs of X-ray damages in these germ cells. Acute lymphocytic leukemia was not induced in ICR and LT mice after spermatogonial exposure, while a large increase of adult type cancers was observed in F1 offspring. However, 1.9-3.2 fold and 4.5-7.4 fold increases of leukemia incidence were observed in ICR and LT mice, when spermatozoa stage was treated with the X-ray doses of 0.36-5.04 Gy and 3.6-5.04 Gy, respectively, indicating the large difference in the sensitivity of developing germ cells to leukemia induction by radiation in the F1 offspring. In contrast to ICR and LT mice, N5 strain developed about 10 or 18 times higher incidence of leukemia in the offspring after spermatogonial or spermatozoa exposure to 5.04 Gy of X-rays, respectively, showing a marked difference in the sensitivity to the leukemia induction by radiation between mouse strains.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Infant leukemia and paternal exposure to motor vehicle exhaust fumes.

The children of fathers who work in gas stations, automobile or truck repair, and aircraft maintenance appear to be at increased risk for acute leukemia during their first year of life. The odds ratio was found to be about 2.5 overall, but risk appears to be greater for female offspring. A decline in sex ratio was observed for the three decades of the study, with the lowest ratio observed from 1969 through 1978. These preliminary findings suggest that exposure to one or more of the components of exhaust fumes might be of etiologic importance for this malignancy. The limitations of this investigation are discussed.

Acute Disease↗
PubMed1994

Spermatogenic and mutagenic damage after paternal exposure to systemic indium-114m.

The cytotoxic and mutagenic consequences of systemic administration of 114mIn have been examined. Adult male rats were dosed intraperitoneally with 14.8 or 3.7 MBq/kg 114mIn. Approximately 0.25% of the injected radioactivity was localized within the testis by 24 h and was retained with an effective half-life of 49.5 days. Breeding studies were started 3 days after injection, males being housed with two females for seven consecutive mating trials of 19 days, separated by 2 days. Indium-114m caused a reduction in litter size and an increase in the incidence of pre- and postimplantation losses and dominant lethal mutations. These effects became evident from 24 days but were most marked between 87-126 days after treatment and persisted up to 147 days. When animals were mated 200 days after treatment, no significant changes were observed. In a parallel study, administration of 14.8 MBq/kg 114mIn resulted in decreased testis and epididymal weight and sperm reserves. Maximal reduction occurred between 87-108 days after injection followed by recovery toward control values, but neither organ had reached normal levels at 200 days. A single dose of 3.7 MBq/kg, however, had no effect on reproductive organ weight or sperm content. Male F1 progeny from the 14.8 MBq/kg group of the second mating period (commencing at 24 days) displayed decreased testis weights and sperm content and provoked a higher incidence of dominant lethal mutations. This effect was not observed in male progeny from any other time or the alternative dose level.

Animals↗
PubMed2004

Allele-specific germ cell epimutation in the spacer promoter of the 45S ribosomal RNA gene after Cr(III) exposure.

Paternal exposure of mice to Cr(III) causes increased tumor risk in offspring; an epigenetic mechanism has been hypothesized. Representational difference analysis of gene methylation in sperm revealed hypomethylation in the 45S ribosomal RNA (rRNA) gene after Cr(III) exposure, compared with controls. The most striking effects were seen in the rRNA spacer promoter, a region in the intergenic region of rRNA gene clusters that can influence transcription. Methylation of the rRNA spacer promoter has not been studied heretofore. Sperm DNAs from Cr(III)-treated and control mice were modified by the bisulfite method followed by PCR amplification of the spacer promoter, including 27 CpG sites. Cloning and dideoxy sequencing identified sequence variants (T or G at base -2214) in the spacer promoter. The T allele had less DNA methylation than the G allele in control mice (17 of 17 clones vs. 42 of 72 clones, P = 0.0004). In spite of diversity of sperm DNA methylation patterns, the DNA clones from Cr(III)-exposed mice had fewer methylated CpG sites, by an average of 19% (P < 0.0001). This difference was limited to the G allele. The pyrosequencing technique was applied to quantify the percentage of methylation directly from amplified PCR products. Strikingly, for nine CpG sites including the spacer promoter core region, hypomethylation was highly significant in the Cr(III)-treated group (paired T test, P < 0.0001). Thus, one allele of the 45S rRNA spacer promoter is hypomethylated in sperm germ cells after Cr(III) exposure. This epimutation may lead to increase of tumor risk in the offspring.

Alleles↗
PubMed2005

Epigenetic programming in the preimplantation rat embryo is disrupted by chronic paternal cyclophosphamide exposure.

Preconceptional paternal exposure to cyclophosphamide, a widely used anticancer agent, leads to increases in embryo loss, malformations, and behavioral deficits in offspring; these abnormalities are transmissible to subsequent generations [Auroux, M., Dulioust, E., Selva, J. & Rince, P. (1990) Mutat. Res. 229, 189-200]. Little information exists on the mechanisms underlying this male-mediated developmental toxicity. We assessed the impact of paternal cyclophosphamide exposure on the dynamic regulation of histone H4 acetylation at lysine 5 and DNA methylation in preimplantation rat embryos. Zygotes sired by drug-treated males displayed advanced developmental progression, increased pronuclear areas, and disruption of the epigenetic programming of both parental genomes. Early postfertilization zygotic pronuclei were hyperacetylated; by mid-zygotic development, male pronuclei were dramatically hypomethylated, whereas female pronuclei were hypermethylated. Micronuclei were substantially elevated, and histone H4 acetylation at lysine 5 localization to the nuclear periphery was disrupted in two-cell embryos fertilized by cyclophosphamide-exposed spermatozoa. This finding demonstrates that paternal exposure to this drug induces aberrant epigenetic programming in early embryos. We hypothesize that disturbances in epigenetic programming contribute to heritable instabilities later in development, emphasizing the importance of epigenetic risk assessment after chemotherapy.

Acetylation↗
PubMed2000

Parental occupational exposure to magnetic fields and childhood cancer (Sweden).

OBJECTIVES: To test the hypothesis that parental occupational exposure to magnetic fields before conception and during pregnancy increases the risk of cancer in the offspring. METHODS: The study is designed as a cohort study based on a population of 235,635 children born shortly after two different censuses in Sweden. The children were followed from birth to 14 years and cases of cancer were identified in the Swedish cancer registry. The parents' occupational titles in the censuses were linked to a job-exposure matrix with information about magnetic field levels in different occupations. The cancer incidence among the exposed was compared to that among the unexposed using Cox proportional hazards modeling. RESULTS: There was no association between childhood cancer and maternal occupational magnetic field exposure. Paternal exposure was associated with an increased risk of childhood leukemia, with a relative risk of 2.0 (95% CI 1.1-3.5) for exposures > or = 0.30 microT. A decreased risk was found for brain tumors (RR = 0.5; 95% CI 0.3-1.0). CONCLUSIONS: The results do not support previous findings of an increased risk of childhood brain tumors associated with paternal occupational exposure to magnetic fields. The finding for childhood leukemia has to be interpreted with caution.

Adolescent↗
PubMed1991

Effects of paternal occupational exposure on spontaneous abortions.

BACKGROUND: Paternal exposure to mutagenic agents has been suggested to affect pregnancy outcome adversely. METHODS: A nationwide data base of medically diagnosed spontaneous abortions and other pregnancies and national census data was used to evaluate the effects of men's occupational exposures on risk of spontaneous abortion in 99,186 pregnancies in Finland. Census data from the years 1975 and 1980 provided information about the occupation, industry, and socioeconomic status. A job-exposure classification was developed to classify women and their husbands according to possible occupational exposures on the basis of their occupational title and industry. RESULTS: In 10% of the pregnancies, the husband was exposed to one or more of the mutagens, and the rate of spontaneous abortion was unaffected (OR = 1.0). Of the 25 specific mutagenic exposures evaluated, paternal exposure to four (ethylene oxide, rubber chemicals, solvents used in refineries, and solvents used in the manufacturing of rubber products) was associated with an increased relative risk of spontaneous abortion. In addition, the risk of spontaneous abortion was higher among wives of rubber products workers than among unexposed men. CONCLUSIONS: Although there is some biological rationale for the findings of this study, these findings need to be confirmed by studies in which individual exposures can be measured directly.

Abortion, Spontaneous↗