ArticleFree radical biology & medicine2011
A deficit in zinc availability can cause alterations in tubulin thiol redox status in cultured neurons and in the developing fetal rat brain.
Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Neurodevelopmental Consequences of Dietary Zinc Deficiency: A Status Report.Biological trace element research · 2023Review
- Molecular Insight into the Regulation of Vimentin by Cysteine Modifications and Zinc Binding.Antioxidants (Basel, Switzerland) · 2021Article
- Severe Zinc Deficiency Causes the Loss and Apoptosis of Olfactory Ensheathing Cells (OECs) and Olfactory Deficit.Journal of molecular neuroscience : MN · 2021Article
- Environment-Based Impairment in Mineral Nutrient Status and Heavy Metal Contents of Commonly Consumed Leafy Vegetables Marketed in Kyrgyzstan: a Case Study for Health Risk Assessment.Biological trace element research · 2021Article
- Effect of Maternal Marginal Zinc Deficiency on Development, Redox Status, and Gene Expression Related to Oxidation and Apoptosis in an Avian Embryo Model.Oxidative medicine and cellular longevity · 2021Article
- Zinc Differentially Modulates the Assembly of Soluble and Polymerized Vimentin.International journal of molecular sciences · 2020Article
- Early Developmental Marginal Zinc Deficiency Affects Neurogenesis Decreasing Neuronal Number and Altering Neuronal Specification in the Adult Rat Brain.Frontiers in cellular neuroscience · 2019Article
- Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide Pathology.Oxidative medicine and cellular longevity · 2018Review
- Zinc deficiency affects the STAT1/3 signaling pathways in part through redox-mediated mechanisms.Redox biology · 2017Article
- Upregulated Expression of Karyopherin α2 is Involved in Neuronal Apoptosis Following Intracerebral Hemorrhage in Adult Rats.Cellular and molecular neurobiology · 2016Article
- Regulation of cytoskeletal dynamics by redox signaling and oxidative stress: implications for neuronal development and trafficking.Frontiers in cellular neuroscience · 2015Review
- Copper-uptake is critical for the down regulation of synapsin and dynamin induced by neocuproine: modulation of synaptic activity in hippocampal neurons.Frontiers in aging neuroscience · 2014Article
- Zinc and the aging brain.Genes & nutrition · 2014Article
- A zinc transporter gene required for development of the nervous system.Communicative & integrative biology · 2013Article
- Decreased zinc availability affects glutathione metabolism in neuronal cells and in the developing brain.Toxicological sciences : an official journal of the Society of Toxicology · 2013Article
- Zinc and the modulation of redox homeostasis.Free radical biology & medicine · 2012Review
- An update on toxicology of aluminum phosphide.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2012Article
- In utero oxidative stress epigenetically programs antioxidant defense capacity and adulthood diseases.Antioxidants & redox signaling · 2012Review
- Zinc and the ERK kinases in the developing brain.Neurotoxicity research · 2012Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Zinc (Zn) deficiency during early development can result in multiple brain abnormalities and altered neuronal functions. In rats, a gestational deficit of Zn can affect the fetal brain cytoskeleton and signaling cascades involved in cellular processes that are central to brain development. In this paper, we tested the hypothesis that oxidative stress is involved in Zn deficiency-induced altered tubulin dynamics and the associated dysregulation of transcription factor NF-κB. For this purpose, we used two cell culture models (rat cortical neurons, human IMR-32 neuroblastoma cells) and an animal model of Zn deficiency. A low rate of in vitro tubulin polymerization, an increase in tubulin oligomers, and a higher protein cysteine oxidation were observed in the Zn-deficient neuronal cells and in gestation day 19 fetal brains obtained from dams fed marginal-Zn diets throughout pregnancy. These alterations could be prevented by treating the Zn-deficient cells with the reducing agent tris(2-carboxyethyl)phosphine or by the presence of N-acetylcysteine (NAC) and α-lipoic acid (LA). Consistent with the above, Zn deficiency-induced tubulin-mediated alterations in transcription factor NF-κB nuclear translocation were prevented by treating IMR-32 cells with LA and NAC. Binding of the NF-κB protein p50, dynein, and karyopherin α (components of the NF-κB transport complex) to β-tubulin as well as the expression of NF-κB-dependent genes (Bcl-2, cyclin D1, and c-myc) was also restored by the addition of LA and NAC to Zn-deficient cells. In conclusion, a deficit in Zn viability could affect early brain development through: (1) an induction of oxidative stress, (2) tubulin oxidation, (3) altered tubulin dynamics, and (4) deregulation of signals (e.g., NF-κB) involved in critical developmental events.
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