التفاصيل البيبلوغرافية
| العنوان: |
Superoxide dismutase as a target of clioquinol-induced neurotoxicity. |
| المؤلفون: |
Kawamura, Kazuyuki1 kawamura@tokusima.hosp.go.jp, Kuroda, Yukiko2, Sogo, Masako2, Fujimoto, Miki2, Inui, Toshio1, Mitsui, Takao1,2 |
| المصدر: |
Biochemical & Biophysical Research Communications. Sep2014, Vol. 452 Issue 1, p181-185. 5p. |
| مصطلحات موضوعية: |
*SUPEROXIDE dismutase, *IODOCHLORHYDROXYQUIN, *NEUROTOXICOLOGY, *SUBACUTE myelooptic neuropathy, *SPINAL cord diseases, *PERIPHERAL nervous system, *OPTIC nerve diseases, *TOXICOLOGY |
| مستخلص: |
Subacute myelo-optico-neuropathy (SMON) is a progressive neurological disorder affecting the spinal cord, peripheral nerves and optic nerves. Although it has been assumed that SMON was caused by intoxication of clioquinol, the mechanism underlying clioquinol-induced neurotoxicity is not fully understood. This study aimed to clarify the relevance of oxidative stress to clioquinol-induced neurotoxicity and the cause of the enhanced oxidative stress. Clioquinol induced cell death in human-derived neuroblastoma cell line, SH-SY5Y, in a dose-dependent manner. This process was accompanied by activation of caspase-3 and enhanced production of reactive oxygen species (ROS). We examined whether clioquinol inhibited the activity of superoxide dismutase-1 (SOD1), based on its metal chelating properties. Clioquinol inhibited activities of purified SOD1 in a dose-dependent manner. Cytosolic SOD activities were also inhibited in SH-SY5Y cells treated with clioquinol. Finally, addition of exogenous SOD1 to the culture significantly reduced enhanced ROS production and cell death induced by clioquinol in SH-SY5Y cells. These findings suggested that enhanced oxidative stress caused by inhibition of SOD1 undelay clioquinol-induced neurotoxicity and was relevant to the pathogenesis of SMON. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
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