Abstract
Zinc (Zn) deficiency, a frequent condition in human populations, induces oxidative stress and subsequently activates/inhibits oxidant-sensitive transcription factors that can affect cell function, proliferation and survival leading to disease. Zn deficiency-triggered oxidative stress could affect cell signaling, including: (1) transcription factors containing Zn finger motifs, and (2) other oxidant-sensitive transcription factors (NF-κB and AP-1). The Zn finger motif in the Zn finger transcription factors is mainly a DNA binding domain. Cysteine residues coordinate the Zn ion folding structural domains that participate in intermolecular interactions. Oxidative stress can impair the DNA-binding activity of Zn finger transcription factor, by oxidizing the cysteine residues and therefore altering the secondary structure of the protein. AP-1 is generally activated in Zn deficiency that can occur secondary to an increase in cellular H2O2, followed by activation of MAPKs p38 and JNK. The role of AP-1 in Zn deficiency-associated pathology remains to be established. The cytosolic steps of the NF-κB cascade are activated by oxidants in Zn deficiency. However, an impaired nuclear transport of the active transcription factor leads to a low expression of NF-κB-dependent genes that could be involved in multiple aspects of Zn deficiency associated pathology. In summary, Zn deficiency induces oxidative stress that can both, lead to tissue oxidative damage and/or to the modulation of select signaling cascades. Their role in the pathology of Zn deficiency remains to be defined.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 245-255 |
| Number of pages | 11 |
| Journal | Molecular Aspects of Medicine |
| Volume | 26 |
| Issue number | 4-5 SPEC. ISS. |
| DOIs | |
| State | Published - Aug 2005 |
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Keywords
- AP-1
- Cell signaling
- NF-κB
- Oxidative stress
- Zinc
- Zinc deficiency
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Molecular Medicine
Cite this
Zinc, oxidant-triggered cell signaling, and human health. / Oteiza, Patricia I.; Mackenzie, Gerardo.
In: Molecular Aspects of Medicine, Vol. 26, No. 4-5 SPEC. ISS., 08.2005, p. 245-255.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Zinc, oxidant-triggered cell signaling, and human health
AU - Oteiza, Patricia I.
AU - Mackenzie, Gerardo
PY - 2005/8
Y1 - 2005/8
N2 - Zinc (Zn) deficiency, a frequent condition in human populations, induces oxidative stress and subsequently activates/inhibits oxidant-sensitive transcription factors that can affect cell function, proliferation and survival leading to disease. Zn deficiency-triggered oxidative stress could affect cell signaling, including: (1) transcription factors containing Zn finger motifs, and (2) other oxidant-sensitive transcription factors (NF-κB and AP-1). The Zn finger motif in the Zn finger transcription factors is mainly a DNA binding domain. Cysteine residues coordinate the Zn ion folding structural domains that participate in intermolecular interactions. Oxidative stress can impair the DNA-binding activity of Zn finger transcription factor, by oxidizing the cysteine residues and therefore altering the secondary structure of the protein. AP-1 is generally activated in Zn deficiency that can occur secondary to an increase in cellular H2O2, followed by activation of MAPKs p38 and JNK. The role of AP-1 in Zn deficiency-associated pathology remains to be established. The cytosolic steps of the NF-κB cascade are activated by oxidants in Zn deficiency. However, an impaired nuclear transport of the active transcription factor leads to a low expression of NF-κB-dependent genes that could be involved in multiple aspects of Zn deficiency associated pathology. In summary, Zn deficiency induces oxidative stress that can both, lead to tissue oxidative damage and/or to the modulation of select signaling cascades. Their role in the pathology of Zn deficiency remains to be defined.
AB - Zinc (Zn) deficiency, a frequent condition in human populations, induces oxidative stress and subsequently activates/inhibits oxidant-sensitive transcription factors that can affect cell function, proliferation and survival leading to disease. Zn deficiency-triggered oxidative stress could affect cell signaling, including: (1) transcription factors containing Zn finger motifs, and (2) other oxidant-sensitive transcription factors (NF-κB and AP-1). The Zn finger motif in the Zn finger transcription factors is mainly a DNA binding domain. Cysteine residues coordinate the Zn ion folding structural domains that participate in intermolecular interactions. Oxidative stress can impair the DNA-binding activity of Zn finger transcription factor, by oxidizing the cysteine residues and therefore altering the secondary structure of the protein. AP-1 is generally activated in Zn deficiency that can occur secondary to an increase in cellular H2O2, followed by activation of MAPKs p38 and JNK. The role of AP-1 in Zn deficiency-associated pathology remains to be established. The cytosolic steps of the NF-κB cascade are activated by oxidants in Zn deficiency. However, an impaired nuclear transport of the active transcription factor leads to a low expression of NF-κB-dependent genes that could be involved in multiple aspects of Zn deficiency associated pathology. In summary, Zn deficiency induces oxidative stress that can both, lead to tissue oxidative damage and/or to the modulation of select signaling cascades. Their role in the pathology of Zn deficiency remains to be defined.
KW - AP-1
KW - Cell signaling
KW - NF-κB
KW - Oxidative stress
KW - Zinc
KW - Zinc deficiency
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UR - http://www.scopus.com/inward/citedby.url?scp=24144483524&partnerID=8YFLogxK
U2 - 10.1016/j.mam.2005.07.012
DO - 10.1016/j.mam.2005.07.012
M3 - Article
C2 - 16115673
AN - SCOPUS:24144483524
VL - 26
SP - 245
EP - 255
JO - Molecular Aspects of Medicine
JF - Molecular Aspects of Medicine
SN - 0098-2997
IS - 4-5 SPEC. ISS.
ER -