TY - JOUR
T1 - Activation of ornithine decarboxylase protects against methylmercury toxicity by increasing putrescine
AU - Sato, Masayuki
AU - Toyama, Takashi
AU - Lee, Jin Yong
AU - Miura, Nobuhiko
AU - Naganuma, Akira
AU - Hwang, Gi Wook
N1 - Funding Information:
This work was supported by a Grant-in-Aid for Scientific Research from the Japanese Society for the Promotion of Science (#15H05714, #16H02961).
Funding Information:
This work was supported by a Grant-in-Aid for Scientific Research from the Japanese Society for the Promotion of Science ( #15H05714 , #16H02961 ).
Publisher Copyright:
© 2018
PY - 2018/10/1
Y1 - 2018/10/1
N2 - We previously reported significantly increased level of putrescine, a polyamine, in the brains of mice administered methylmercury. Moreover, addition of putrescine to culture medium reduced methylmercury toxicity in C17.2 mouse neural stem cells. In this study, the role of ornithine decarboxylase (ODC), an enzyme involved in putrescine synthesis, in response to methylmercury toxicity was investigated. Methylmercury increased ODC activity in mouse cerebrum and cerebellum, but this increase was hardly observed in the kidney and liver, where methylmercury accumulated at a high concentration. In the cerebrum and cerebellum, increased putrescine was observed with methylmercury administration. Methylmercury increased ODC activity in C17.2 cells, but this was almost completely abolished in the presence of an ODC inhibitor. Methylmercury also increased the level of ODC protein in mouse brain and C17.2 cells. In addition, C17.2 cells pretreated with ODC inhibitor showed higher methylmercury sensitivity than control cells. These results suggest that the increased ODC activity by methylmercury is involved in the increase in putrescine level, and ODC plays an important role in the reduction of methylmercury toxicity. This is the first study to provide evidence that increased ODC activity may be a protective response against methylmercury-induced neurotoxicity.
AB - We previously reported significantly increased level of putrescine, a polyamine, in the brains of mice administered methylmercury. Moreover, addition of putrescine to culture medium reduced methylmercury toxicity in C17.2 mouse neural stem cells. In this study, the role of ornithine decarboxylase (ODC), an enzyme involved in putrescine synthesis, in response to methylmercury toxicity was investigated. Methylmercury increased ODC activity in mouse cerebrum and cerebellum, but this increase was hardly observed in the kidney and liver, where methylmercury accumulated at a high concentration. In the cerebrum and cerebellum, increased putrescine was observed with methylmercury administration. Methylmercury increased ODC activity in C17.2 cells, but this was almost completely abolished in the presence of an ODC inhibitor. Methylmercury also increased the level of ODC protein in mouse brain and C17.2 cells. In addition, C17.2 cells pretreated with ODC inhibitor showed higher methylmercury sensitivity than control cells. These results suggest that the increased ODC activity by methylmercury is involved in the increase in putrescine level, and ODC plays an important role in the reduction of methylmercury toxicity. This is the first study to provide evidence that increased ODC activity may be a protective response against methylmercury-induced neurotoxicity.
KW - Methylmercury
KW - Ornithine Decarboxylase
KW - Putrescine
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U2 - 10.1016/j.taap.2018.08.002
DO - 10.1016/j.taap.2018.08.002
M3 - Article
C2 - 30081057
AN - SCOPUS:85051130569
SN - 0041-008X
VL - 356
SP - 120
EP - 126
JO - Toxicology and Applied Pharmacology
JF - Toxicology and Applied Pharmacology
ER -