Preconditioning with subneurotoxic allyl nitrile: Protection against allyl nitrile neurotoxicity

• Tanii, Hideji

• Higashi, T.

• Saijoh, Kiyofumi

抄録

金沢大学医薬保健研究域医学系

High-dose cruciferous allyl nitrile can induce behavioral abnormalities in rodents, while repeated exposure to allyl nitrile at subneurotoxic levels can increase phase 2 detoxification enzymes in many tissues, although the brain has not been investigated yet. In the present study, we examined the effect of 5 days repeated exposure to subneurotoxic allyl nitrile (0-400 μmol/kg/day) on the brain. Elevated glutathione S-transferase activity was recorded in the striatum, hippocampus, medulla oblongata plus pons, and cortex. Enhancement of quinone reductase activity was observed in the medulla oblongata plus pons, hippocampus, and cortex. In the medulla oblongata plus pons, elevated glutathione levels were recorded. Following repeated subneurotoxic allyl nitrile exposure (0-400 μmol/kg/day), mice were administered a high-dose allyl nitrile (1.2 mmol/kg) which alone led to appearance of behavioral abnormalities. Compared with the 0 μmol/kg/day group, animals in the 200 and 400 μmol/kg/day pre-treatment groups exhibited decreased behavioral abnormalities and elevated GABA-positive cell counts in the substantia nigra pars reticulata and the interpeduncular nucleus. These data suggest that repeated exposure to subneurotoxic levels of allyl nitrile can induce phase 2 enzymes in the brain, which together with induction in other tissues, may contribute to protection against allyl nitrile neurotoxicity. © 2009 Elsevier Ltd. All rights reserved.

収録刊行物

• Food and Chemical Toxicology

  Food and Chemical Toxicology 48 (2), 750-754, 2010-02-01

  Elsevier

キーワード

• γ-Aminobutyric acid
• Allyl nitrile
• Behavioral abnormalities
• Glutathione
• Glutathione S-transferase
• Quinone reductase

詳細情報

• CRID: 1050001335948221952
• NII論文ID: 120001828362
• NII書誌ID: AA10627174
• ISSN: 02786915
• DOI: 10.1016/j.fct.2009.12.010
• Web Site: http://hdl.handle.net/2297/20342
• Web Site: https://api.elsevier.com/content/article/PII:S0278691509005924?httpAccept=text/xml
• Web Site: https://api.elsevier.com/content/article/PII:S0278691509005924?httpAccept=text/plain
• 本文言語コード: en
• 資料種別: journal article
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