紀要論文 酸化ストレスを抑制するミトコンドリア局在マンガンスーパーオキサイドディスムターゼの機能
サンカ ストレス オ ヨクセイ スル ミトコンドリア キョクザイ マンガン スーパーオキサイド ディスムターゼ ノ キノウ
Beyond the function of Manganese superoxide dismutase in oxidative stress

犬童, 寛子  ,  インドウ, ヒロコ  ,  INDO, Hiroko P.

36pp.25 - 33 , 2016-03-25 , 鹿児島大学 , カゴシマ ダイガク , Kagoshima University
ISSN:03897834
NII書誌ID(NCID):AN0035442X
内容記述
It is well known that reactive oxygen species (ROS) causes various redox related diseases. Recent studies have shown that peroxidant molecules, such as hydrogen peroxide, work actively as signaling molecules in cancer cells. Superoxide is considered to be a major factor in oxidant toxicity, and mitochondria are the major source of superoxide. The reaction of superoxide generated from mitochondria with nitric oxide is faster than superoxide catalyzed reaction, and produces peroxynitrite. Then, peroxynitrite produces hydroxyl radicals and nitrogen dioxide, and oxidizes and nitrates DNAs, lipids and proteins, etc., and induces cell death. Thus, based on research conducted after Fridovich’s seminal studies, we now propose a modified superoxide theory. Manganese superoxide dismutase (MnSOD), which scavenges superoxide anions generated from mitochondria, is an important enzyme in cellular homeostasis, cellular defense and functional dynamics. MnSOD expression and/or activity is generally lower in cancer cells than in their normal cell counterparts, while other studies demonstrate that cancer tissues possess elevated MnSOD expression compared to normal tissues. It suggests that regulation of MnSOD may confer differential outcomes in the protection of normal and cancer cells against agents that cause oxidative stress. Furthermore, expression and/or the activity of MnSOD may affect the antioxidant capacity and overall health of cells by altering mitochondrial metabolism, leading to the development and progression of cancer. It might be suggested that altered MnSOD activity on the mitochondrial metabolism in cancer cells is a key factor of cancer treatment strategy.
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http://ir.kagoshima-u.ac.jp/bitstream/10232/26738/2/歯学部紀要-第36巻_p25-33.pdf

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