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    Paternal Exposure to Environmental Chemical Stress Affects Male Offspring's Hepatic Mitochondria.

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    Authors
    Godschalk, Roger
    Remels, Alex
    Hoogendoorn, Camiel
    van Benthem, Jan
    Luijten, Mirjam
    Duale, Nur
    Brunborg, Gunnar
    Olsen, Ann-Karin
    Bouwman, Freek G
    Munnia, Armelle
    Peluso, Marco
    Mariman, Edwin
    van Schooten, Frederik Jan
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    Type
    Article
    Language
    en
    
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    Title
    Paternal Exposure to Environmental Chemical Stress Affects Male Offspring's Hepatic Mitochondria.
    Published in
    Toxicol Sci 2018; 162(1):241-50
    Publiekssamenvatting
    Preconceptional paternal exposures may affect offspring's health, which cannot be explained by mutations in germ cells, but by persistent changes in the regulation of gene expression. Therefore, we investigated whether pre-conceptional paternal exposure to benzo[a]pyrene (B[a]P) could alter the offspring's phenotype. Male C57BL/6 mice were exposed to B[a]P by gavage for 6 weeks, 3× per week, and were crossed with unexposed BALB-c females 6 weeks after the final exposure. The offspring was kept under normal feeding conditions and was sacrificed at 3 weeks of age. Analysis of the liver proteome by 2D-gel electrophoresis and mass spectrometry indicated that proteins involved in mitochondrial function were significantly downregulated in the offspring of exposed fathers. This down-regulation of mitochondrial proteins was paralleled by a reduction in mitochondrial DNA copy number and reduced activity of citrate synthase and β-hydroxyacyl-CoA dehydrogenase, but in male offspring only. Surprisingly, analysis of hepatic mRNA expression revealed a male-specific up-regulation of the genes, whose proteins were downregulated, including Aldh2 and Ogg1. This discrepancy could be related to several selected microRNA (miRNA)'s that regulate the translation of these proteins; miRNA-122, miRNA-129-2-5p, and miRNA-1941 were upregulated in a gender-specific manner. Since mitochondria are thought to be a source of intracellular reactive oxygen species, we additionally assessed oxidatively-induced DNA damage. Both 8-hydroxy-deoxyguanosine and malondialdehyde-dG adduct levels were significantly reduced in male offspring of exposed fathers. In conclusion, we show that paternal exposure to B[a]P can regulate mitochondrial metabolism in offspring, which may have profound implications for our understanding of health and disease risk inherited from fathers.
    DOI
    10.1093/toxsci/kfx246
    PMID
    29145655
    URI
    http://hdl.handle.net/10029/621755
    ae974a485f413a2113503eed53cd6c53
    10.1093/toxsci/kfx246
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