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Changes in expression levels of oxidative stress-related genes in mouse epididymides by neonatal exposure to low-dose decabromodiphenyl ether.

ABSTRACT: Decabromodiphenyl ether (decaBDE), one of the polybrominated diphenyl ethers (PBDEs), is the most well-known flame retardant and is used worldwide. In a previous study, we identified adverse effects of neonatal decaBDE exposure on mouse epididymides, such as decreased epididymal weight. On the other hand, neonatal exposure to diethylstilbestrol (DES), an artificial estrogenic compound, also causes several adverse effects on epididymides. DES exposure results in decreased epididymal weight, morphological abnormalities, and permanent alterations in the expression levels of several genes. The molecular mechanisms underlying the harmful effects of decaBDE exposure remain unclear. Many studies have reported that PBDEs have estrogenic activity, which may contribute to the induction of the adverse effects of decaBDE exposure. We aimed to examine the effects of neonatal decaBDE exposure on epididymides. Our data showed that (1) no histological change was observed on epididymal tissues from neonatal decaBDE exposure, unlike the effect of DES, (2) decaBDE exposure did not induce the alterations in gene expression observed with DES exposure; instead alterations in gene expression of certain oxidative stress-related genes were observed, and (3) the expression of ubiquitin C increased in decaBDE-exposed mouse epididymides. Our present data suggest the possibility that increased oxidative stress plays a role in the harmful effects observed in mouse epididymides after decaBDE-exposure.

SUBMITTER: Nakamoto M

PROVIDER: S-EPMC5904619 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature

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Changes in expression levels of oxidative stress-related genes in mouse epididymides by neonatal exposure to low-dose decabromodiphenyl ether.

Nakamoto Makoto M Miyaso Hidenobu H Komiyama Masatoshi M Matsuno Yoshiharu Y Mori Chisato C

Reproductive medicine and biology 20131231 3

Decabromodiphenyl ether (decaBDE), one of the polybrominated diphenyl ethers (PBDEs), is the most well-known flame retardant and is used worldwide. In a previous study, we identified adverse effects of neonatal decaBDE exposure on mouse epididymides, such as decreased epididymal weight. On the other hand, neonatal exposure to diethylstilbestrol (DES), an artificial estrogenic compound, also causes several adverse effects on epididymides. DES exposure results in decreased epididymal weight, morph ...[more]

PMID: 29699156

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Project description:Chlorpyrifos (CPF) is a widely used organophosphorus insecticide (OP) and putative developmental neurotoxicant in humans. The acute toxicity of CPF is elicited by acetylcholinesterase (AChE) inhibition. We characterized dose-related (0.1, 0.5, 1 and 2mg/kg) gene expression profiles and changes in cell signaling pathways 24h following acute CPF exposure in 7-day-old rats. Microarray experiments indicated that approximately 9% of the 44,000 genes were differentially expressed following either one of the four CPF dosages studied (546, 505, 522, and 3,066 genes with 0.1, 0.5, 1.0 and 2.0mg/kg CPF). Genes were grouped according to dose-related expression patterns using K-means clustering while gene networks and canonical pathways were evaluated using Ingenuity Pathway Analysis®. Twenty clusters were identified and differential expression of selected genes was verified by RT-PCR. The four largest clusters (each containing from 276 to 905 genes) constituted over 50% of all differentially expressed genes and exhibited up-regulation following exposure to the highest dosage (2mg/kg CPF). The total number of gene networks affected by CPF also rose sharply with the highest dosage of CPF (18, 16, 18 and 50 with 0.1, 0.5, 1 and 2mg/kg CPF). Forebrain cholinesterase (ChE) activity was significantly reduced (26%) only in the highest dosage group. Based on magnitude of dose-related changes in differentially expressed genes, relative numbers of gene clusters and signaling networks affected, and forebrain ChE inhibition only at 2mg/kg CPF, we focused subsequent analyses on this treatment group. Six canonical pathways were identified that were significantly affected by 2mg/kg CPF (MAPK, oxidative stress, NFΚB, mitochondrial dysfunction, arylhydrocarbon receptor and adrenergic receptor signaling). Evaluation of different cellular functions of the differentially expressed genes suggested changes related to olfactory receptors, cell adhesion/migration, synapse/synaptic transmission and transcription/translation. Nine genes were differentially affected in all four CPF dosing groups. We conclude that the most robust, consistent changes in differential gene expression in neonatal forebrain across a range of acute CPF dosages occurred at an exposure level associated with the classical marker of OP toxicity, AChE inhibition. Disruption of multiple cellular pathways, in particular cell adhesion, may contribute to the developmental neurotoxicity potential of this pesticide.

Dataset Information

Changes in expression levels of oxidative stress-related genes in mouse epididymides by neonatal exposure to low-dose decabromodiphenyl ether.

Publications

Changes in expression levels of oxidative stress-related genes in mouse epididymides by neonatal exposure to low-dose decabromodiphenyl ether.

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