DNA methylation change involved in doxorubicin-induced testicular toxicity in mice
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ABSTRACT:
PROVIDER: PRJNA433228 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6677970_1.fastq.gz | Fastqsanger.gz | |||
| SRR6677970_2.fastq.gz | Fastqsanger.gz | |||
| SRR6677971_1.fastq.gz | Fastqsanger.gz | |||
| SRR6677971_2.fastq.gz | Fastqsanger.gz | |||
| SRR6677972_1.fastq.gz | Fastqsanger.gz |
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Project description:Testicular toxicity is one of the frequent adverse effects of cancer chemotherapy and the problem is that there is no effective biomarker. To find effective biomarkers, we focused on epigenetic mechanisms of male germline. Therefore, our study investigated the DNA methylation status of male germline under the testicular toxicity induced by doxorubicin(DXR), a widely used anticancer agent. We established mouse models of initial stage of testicular toxicity and testicular pre-toxicity by administrating 0.2 mg/kg and 0.02 mg/kg of DXR twice a week for 5 weeks. Western blotting analysis revealed the protein expression levels of DNA methyltransferases DNMT3a and DNMT3b were decreased in both the DXR administration groups. Consistently, comprehensive DNA methylation analysis of sperm DNA using MBD-seq revealed that the majority of methylation changes induced by DXR administration were hypomethylation. This study showed the possibility of early diagnosis of testicular toxicity by examining DNA methylation status of sperm.
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Project description:Using an ex-vivo testicular culture from rats, we carried out transcriptomic experiments to identify the pathway of toxicity ellicited by the fungicides carbendazim, iprodione alone or in combination. we used commercial Agilent Microarray GE 4x44K Rat (V3) Gene Expression Microarray (G2514F) AMADID : 028282
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Project description:In the present study, the effects of prenatal exposure to bisphenol A (BPA) and diethyl hexyl phthalate (DEHP) on male reproductive system of offspring were examined by a tissue-specific microarray and gene annotation with Medical Subject Headings (MeSH) indicative of testicular components. The aim of this study was to investigate the validity of microarray analysis with MeSH as a method for obtaining and evaluating an overview of testicular toxicity mechanisms in maternally exposed specimens. Pregnant mice were treated with BPA or DEHP by subcutaneous administration on days 7 and 14 of pregnancy. Tissue and blood samples were collected from 6-week-old male offspring. Testes were subjected to gene expression analysis using quantitative RT-PCR and cDNA microarray (testis2). To interpret the microarray data, genes were classified using MeSH related to the functions of testis and sperm. As a result, MeSH categories related to androgen of dysregulated genes and Sertoli cells of downregulated genes were only enriched in BPA-treated groups. These results were consistent with the observations in the sperm properties and histological examination of testes. This article concludes that 1) microarray analysis of expression changes of genes associated with testicular function and spermatogenetic process, and 2) a method using MeSH to extract common terms among dysregulated genes, are useful for predicting an overview of the testicular and reproductive toxicity of prenatal exposure to chemical substances.
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Project description:Using an ex-vivo testicular culture from rats, we carried out transcriptomic experiments to identify the pathway of toxicity ellicited by the fungicides carbendazim, iprodione alone or in combination. we used commercial Agilent Microarray GE 4x44K Rat (V3) Gene Expression Microarray (G2514F) AMADID : 028282 Cultures were performed with and without fungicides. When required, CBZ, IPR or mixture was added beginning from day 2, at 50 nM or 500 nM for CBZ and at 50 nM or 500 nM for IPR; 50 nM each or 500 nM each for the mixture. For microarray experiments, three different pools of seminiferous tubules were exposed to two concentrations of CBZ, IPR or their mixture (50 nM and 500 nM) or to complete medium with vehicle (control cells) for 7, 14, and 21 days. Each condition of exposure to fungicides was compared with control cells at the same time point.
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