Enhanced NADPH oxidases and reactive oxygen species in the mechanism of methanol-initiated protein oxidation and embryopathies in vivo and in embryo culture.

Archives of Toxicology
Lutfiya Miller-PinslerP G Wells

Abstract

Methanol (MeOH) teratogenicity in rodents may be mediated in part by reactive oxygen species (ROS), the source of which is unknown. To determine if MeOH enhances embryonic ROS-producing NADPH oxidases (NOXs), p22phox mRNA and protein and oxidatively damaged protein were measured in gestational day 12 MeOH-exposed CD-1 mouse embryos with or without pretreatment with the free radical spin trap phenylbutylnitrone (PBN) or the NOX inhibitor diphenyleneiodonium chloride (DPI). MeOH exposure upregulated p22phox mRNA and protein expression, and enhanced protein oxidation, within 3-6 h. Compared to embryos exposed to MeOH alone, PBN and DPI pretreatment decreased MeOH-enhanced p22phox mRNA expression, DPI but not PBN blocked p22phox protein expression, and both blocked protein oxidation. To assess developmental relevance, mouse embryos were exposed in culture for 24 h to MeOH or vehicle with or without pretreatment with PBN, DPI, or the prostaglandin H synthase (PHS) inhibitor eicosatetraynoic acid (ETYA), and evaluated for abnormalities. ETYA did not prevent MeOH embryopathies, despite blocking phenytoin embryopathies (ROS-initiating positive control), precluding bioactivation of MeOH or its metabolites by PHS. Concentration-dependent...Continue Reading

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Citations

Oct 7, 2015·Archives of Toxicology·Philip Pallmann, Ludwig A Hothorn
Jan 2, 2015·Ecotoxicology and Environmental Safety·Keqiang Wei, Junxian Yang
Sep 2, 2016·Reproductive Toxicology·J Nicole Sweeting, Peter G Wells
Jun 28, 2016·Birth Defects Research. Part C, Embryo Today : Reviews·Peter G WellsLutfiya Miller-Pinsler
Dec 13, 2016·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Yongfeng GuoLi Sun
Jan 24, 2019·Stem Cells and Development·Nikola SobočanFloriana Bulić-Jakuš
Apr 30, 2019·Birth Defects Research·Shama BhatiaPeter G Wells

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