Zinc, redox regulation and brain development
3
Issued Date
2026-08-01
Resource Type
ISSN
08915849
eISSN
18734596
Scopus ID
2-s2.0-105036247109
Pubmed ID
41935706
Journal Title
Free Radical Biology and Medicine
Volume
251
Start Page
137
End Page
154
Rights Holder(s)
SCOPUS
Bibliographic Citation
Free Radical Biology and Medicine Vol.251 (2026) , 137-154
Suggested Citation
Adamo A.M., Supasai S., Salvador G.A., Liu X., Mackenzie G.G., Oteiza P.I. Zinc, redox regulation and brain development. Free Radical Biology and Medicine Vol.251 (2026) , 137-154. 154. doi:10.1016/j.freeradbiomed.2026.03.075 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/116456
Title
Zinc, redox regulation and brain development
Corresponding Author(s)
Other Contributor(s)
Abstract
Zinc is a component of the antioxidant defense system. Its functions protecting biological systems from oxidation are exerted at multiple levels including competing with redox active metals for binding sites, dynamically interacting with thiol groups and inducing metallothionein (MT) expression, regulating oxidant production, and increasing antioxidant defenses in part via NRF2 modulation. Zinc also directly and indirectly modulates redox regulated signaling cascades. Zinc deficits can affect not only the capacity of cells to defend against oxidative challenges but also alter redox signaling that modulate key cellular processes. Zinc is essential at different stages of development given its capacity to regulate key participating processes, e.g. cell proliferation, differentiation and survival. In the developing brain, the adverse consequences of a decrease in zinc availability depend on the severity and the timing of the deficiency. While gestational severe zinc deficiency causes teratogenesis in the brain and several other organs, mild zinc deficiency has significant deleterious consequences on the neural stem cell pool, neurogenesis, oligodendrogenesis, and astrogliogenesis in the offspring. Alterations in neuron, oligodendrocyte and astrocyte number, neuronal specification and myelination associated with zinc deficits in early development persist into adulthood, affecting behavior and motor performance. This review will focus on the role of zinc on brain development and on the interconnection between zinc and the redox tone in shaping different windows of neurodevelopment.