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Exposure to benzyl butyl phthalate (BBP) leads to increased double-strand break formation and germline dysfunction in Caenorhabditis elegans

ABSTRACT: Exposure to benzyl butyl phthalate (BBP) leads to increased double-strand break formation and germline dysfunction in Caenorhabditis elegans

PROVIDER: PRJNA1102026 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28740108_1.fastq.gz	Fastqsanger.gz
	SRR28740108_2.fastq.gz	Fastqsanger.gz
	SRR28740109_1.fastq.gz	Fastqsanger.gz
	SRR28740109_2.fastq.gz	Fastqsanger.gz
	SRR28740110_1.fastq.gz	Fastqsanger.gz

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Exposure to benzyl butyl phthalate (BBP) leads to increased double-strand break formation and germline dysfunction in Caenorhabditis elegans

Project description:Endocrine disrupting chemicals (EDCs) have been linked to various health problems including effects on reproductive health. Benzyl butyl phthalate (BBP) is a commonly used plasticizer found in many consumer products that has been shown to act as an EDC and affect human reproduction and development. However, how it might impact the germline and affect the specialized cell division program of meiosis, which results in the formation of haploid gametes (i.e. eggs and sperm), remained unclear. Here, using the nematode C. elegans, we show that BBP exposure at levels within the range of what is detected in humans, impairs accurate chromosome segregation which can result in aneuploidy. Similar to mammals, BBP exposure in C. elegans results in a non-monotonic dose response, whereby lower doses result in the strongest effects, and BBP is efficiently metabolized, underscoring the use of this model system for gaining mechanistic insights into how this EDC impacts the germline. BBP results in increased levels of DNA double-strand breaks (DSBs), activation of a DNA damage checkpoint, and altered chromosome morphology in exposed germlines. We propose that BBP exposure alters gene expression and results in increased oxidative stress, resulting in increased DSBs, thereby compromising chromosome morphology and accurate segregation.

2024-09-24 | GSE264361 | GEO

Exposure to Benzyl butyl phthalate deteriorates oocyte quality by inducing oxidative stress-related apoptosis and DNA damage in mice

Project description:Benzyl butyl phthalate (BBP) is a chemical softener and plasticizer commonly used in toys, food packaging, wallpaper, detergents, and shampoos. The estrogenic actions of BBP have detrimental effects on humans and animals. This study investigated the specific influence of BBP on mouse oocyte maturation using in vitro and in vivo models. The results indicated that BBP exposure disrupted spindle organization, chromosomal arrangement, and the distribution of cortical actin, and led to the failure of oocyte meiotic maturation and early embryo development. Singe-cell transcriptome analysis found that BBP exposure altered the expression levels of 588 genes, most associated with mitochondria-related oxidative stress. Further analysis demonstrated that the detrimental effects of BBP involved the disruption of mitochondrial function and oxidative stress-induced early apoptosis. Nicotinamide mononucleotide supplementation reduced the adverse effects of BBP. Collectively, these findings revealed a mechanism of BBP-induced toxicity on female reproduction, and showed that nicotinamide mononucleotide provides an effective treatment for BBP actions.

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Gene expression data from splenocytes of 3 week-old offspring after maternal exposure to benzyl butyl phthalate (BBP)

Project description:The prenatal and early postnatal period is highly sensitive to environmental exposures that may interfere with the developmental programming of the immune system leading to an altered disease risk in later life. To clarify the role of early influences in activation or exacerbation of autoimmune diseases like rheumatoid arthritis (RA) we investigated the effect of maternal exposure during the prenatal and weaning period of DBA/1 mice to the plasticizer benzyl butyl phthalate (BBP) on the development of RA in the offspring. Using a mild collagen-induced arthritis (CIA) model, maternal BBP-exposure increased both the prevalence and the severity of RA in the progeny compared to un-exposed dams. Additionally, maternal BBP exposure led to elevated serum IgG1 and IgG2a level in the offspring and increased the IFN-? and IL-17 release from collagen-re-stimulated spleen cells. Transcriptome analysis of splenoytes isolated from 3-week-old pups before RA-induction revealed considerable changes in gene expression in the offspring from BBP-exposed dams. Among them were regulator of G-protein signaling 1 (rgs1), interleukin-7 receptor (il-7r) and CXC chemokine 4 (cxcr4), all genes that have previously been described as associated with RA pathology. In summary, our results demonstrate that perinatal exposure to BBP increases the susceptibility of the offspring to RA, probably via a phthalate-induced disturbed regulation of RA-relevant genes or signalling pathways.

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Gene expression data from splenocytes of 3 week-old offspring after maternal exposure to benzyl butyl phthalate (BBP)

Project description:Gene expression data from splenocytes of 3 week-old offspring after maternal exposure to benzyl butyl phthalate (BBP)

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Exposure to Benzyl butyl phthalate deteriorates oocyte quality by inducing oxidative stress-related apoptosis and DNA damage in mice

Project description:Exposure to Benzyl butyl phthalate deteriorates oocyte quality by inducing oxidative stress-related apoptosis and DNA damage in mice

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p53 binding during the DNA double-strand break response

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2017-08-02 | GSE101737 | GEO

CGH of Drosophila Follicle Cell Amplicons in double-strand break repair mutants

Project description:CGH of stage 13 amplifying follicle cells to measure changes in replication fork progression in double-strand break repair mutants Comparative genomic hybridization was performed to compare amplification gradients of stage 13 follicle cells from several double-strand break repair mutants to wild type (OrR) gradients. Two-three replicates were done for each genotype.

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RecG Directs DNA Synthesis During Double-Strand Break Repair [ChIP-seq]

Project description:In the bacterium Escherichia coli, RecG directs DNA synthesis during the repair of DNA double-strand breaks by homologous recombination. Examination of RecA binding during double-strand break repair in Escherichia coli in the presence and absence of RecG protein

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