Iron is required for normal cell growth and proliferation. However, excess iron is potentially harmful, as it can catalyse the formation of toxic reactive oxygen species (ROS) via Fenton chemistry. For this reason, cells have evolved highly regulated mechanisms for controlling intracellular iron levels. Chief among these is the sequestration of iron in ferritin. Ferritin is a 24 subunit protein composed of two subunit types, termed H and L. The ferritin H subunit has a potent ferroxidase activity that catalyses the oxidation of ferrous iron, whereas ferritin L plays a role in iron nucleation and protein stability. In the present study we report that increased synthesis of both subunits of ferritin occurs in HeLa cells exposed to oxidative stress. An increase in the activity of iron responsive element binding proteins in response to oxidative stress was also observed. However, this activation was transient, allowing ferritin protein induction to subsequently proceed. To assess whether ferritin induction reduced the accumulation of ROS, and to test the relative contribution of ferritin H and L subunits in this process, we prepared stable transfectants that overexpressed either ferritin H or ferritin L cDNA under control of a tetracycline-responsive promoter. We observed that overexpression of either ferritin H or ferritin L reduced the accumulation of ROS in response to oxidant challenge.
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July 2001
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Research Article|
June 25 2001
Ferritin and the response to oxidative stress
Kouichi ORINO;
Kouichi ORINO
1
∗Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
†The Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
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Lori LEHMAN;
Lori LEHMAN
†The Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
‡Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
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Yoshiaki TSUJI;
Yoshiaki TSUJI
†The Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
‡Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
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Hitoshi AYAKI;
Hitoshi AYAKI
†The Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
‡Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
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Suzy V. TORTI;
Suzy V. TORTI
2
∗Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
†The Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
2To whom correspondence should be addressed (e-mail storti@wfubmc.edu).
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Frank M. TORTI
Frank M. TORTI
†The Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
‡Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
§Department of Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157, U.S.A.
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Biochem J (2001) 357 (1): 241–247.
Article history
Received:
January 15 2001
Revision Received:
March 08 2001
Accepted:
April 10 2001
Citation
Kouichi ORINO, Lori LEHMAN, Yoshiaki TSUJI, Hitoshi AYAKI, Suzy V. TORTI, Frank M. TORTI; Ferritin and the response to oxidative stress. Biochem J 1 July 2001; 357 (1): 241–247. doi: https://doi.org/10.1042/bj3570241
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