Tools and techniques for illuminating the cell biology of zinc

Pratt, Evan P.S.; Damon, Leah J.; Anson, Kelsie J.; Palmer, Amy E.

doi:10.1016/j.bbamcr.2020.118865

Cited by 51 publications

(40 citation statements)

References 126 publications

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“…Thus, investigating zinc and calcium in relation to one another may provide new insights into the mechanisms by which these ions work together to contribute to mitochondrial defects such as mitochondrial permeability transition. Excitingly, the development of various novel tools and methods for detecting cytosolic and mitochondrial zinc [ 260 ], as well as more selective and fast chelators [ 20 ], may allow us to investigate the effects of zinc on mitochondria with greater specificity and accuracy than ever before. Prior use of FluoZin-3 in tandem with the calcium indicator fura-2FF has been particularly useful for determining the simultaneous effects of zinc and calcium [ 189 , 190 , 261 ].…”

Section: Discussionmentioning

confidence: 99%

The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction

Liu

Gale

Reynolds³

et al. 2021

Biomedicines

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Zinc is a highly abundant cation in the brain, essential for cellular functions, including transcription, enzymatic activity, and cell signaling. However, zinc can also trigger injurious cascades in neurons, contributing to the pathology of neurodegenerative diseases. Mitochondria, critical for meeting the high energy demands of the central nervous system (CNS), are a principal target of the deleterious actions of zinc. An increasing body of work suggests that intracellular zinc can, under certain circumstances, contribute to neuronal damage by inhibiting mitochondrial energy processes, including dissipation of the mitochondrial membrane potential (MMP), leading to ATP depletion. Additional consequences of zinc-mediated mitochondrial damage include reactive oxygen species (ROS) generation, mitochondrial permeability transition, and excitotoxic calcium deregulation. Zinc can also induce mitochondrial fission, resulting in mitochondrial fragmentation, as well as inhibition of mitochondrial motility. Here, we review the known mechanisms responsible for the deleterious actions of zinc on the organelle, within the context of neuronal injury associated with neurodegenerative processes. Elucidating the critical contributions of zinc-induced mitochondrial defects to neurotoxicity and neurodegeneration may provide insight into novel therapeutic targets in the clinical setting.

show abstract

Section: Discussionmentioning

confidence: 99%

The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction

Liu

Gale

Reynolds³

et al. 2021

Biomedicines

View full text Add to dashboard Cite

show abstract

“…Thus, investigating zinc and calcium in relation to one another may provide new insights into the mechanisms by which these ions work together to contribute to mitochondrial defects such as mitochondrial permeability transition. Excitingly, the development of various novel tools and methods for detecting cytosolic and mitochondrial zinc [255], as well as more selective and fast chelators [20] may allow us to investigate the effects of zinc on mitochondria with greater specificity and accuracy than ever before. Prior use of FluoZin-3 in tandem with the calcium indicator fura-2FF has been particularly useful for determining the simultaneous effects of zinc and calcium because FluoZin-3 is not sensitive to calcium [186,187,256].…”

Section: Discussionmentioning

confidence: 99%

The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction

Liu

Gale

Reynolds³

et al. 2021

Preprint

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Zinc is a highly abundant cation in the brain, where it is essential for cellular function, including transcription, enzymatic activity, and cell signaling. However, zinc can also trigger injurious cascades in neurons, contributing to the pathology of neurodegenerative diseases. Mitochondria, critical for meeting the high energy demands of the central nervous system (CNS), are a principal target of the deleterious actions of zinc. An increasing body of work suggests that intracellular zinc, can, under certain circumstances, contribute to neuronal damage by inhibiting mitochondrial energy processes, including dissipation of the mitochondrial membrane potential, leading to ATP depletion. Additional consequences of zinc-mediated mitochondrial damage include reactive oxygen species (ROS) generation, mitochondrial permeability transition, and calcium deregulation. Zinc can also induce mitochondrial fission, resulting in mitochondrial fragmentation, as well as inhibition of mitochondrial motility. Here, we review the known mechanisms responsible for the deleterious actions of zinc on the organelle, within the context of neuronal injury associated with neurodegenerative processes. Elucidating the critical contributions of zinc-induced mitochondrial defects to neurotoxicity and neurodegeneration may provide insight into novel therapeutic targets in the clinical setting.

show abstract

“…In addition to its role in protein function, Zn acts as a second messenger in mammalian systems, being involved in processes such as insulin secretion, immune system function, neurotransmitter signaling, and egg fertilization (Ghafghazi et al, 1981;Hirano et al, 2008;Fukada et al, 2011;Que et al, 2015). It was proposed that intracellular and extracellular fluctuations in labile Zn 2+ ions can act in biological signaling and in the regulation of signaling cascades in animals (Pratt et al, 2021). Zn also performs important functions in vertebrate immunity.…”

Section: Introduction-why Zinc?mentioning

confidence: 99%

Zinc in plants: Integrating homeostasis and biofortification

et al. 2022

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Zinc plays many essential roles in life. As a strong Lewis acid that lacks redox activity under environmental and cellular conditions, the Zn 2+ cation is central in determining protein structure and catalytic function of nearly 10% of most eukaryotic proteomes. While specific functions of zinc have been elucidated at a molecular level in a number of plant proteins, wider issues abound with respect to the acquisition and distribution of zinc by plants. An important challenge is to understand how plants balance between Zn supply in soil and their own nutritional requirement for zinc, particularly where edaphic factors lead to a lack of bioavailable zinc or, conversely, an excess of zinc that bears a major risk of phytotoxicity. Plants are the ultimate source of zinc in the human diet, and human Zn deficiency accounts for over 400 000 deaths annually. Here, we review the current understanding of zinc homeostasis in plants from the molecular and physiological perspectives. We provide an overview of approaches pursued so far in Zn biofortification of crops. Finally, we outline a ''push-pull'' model of zinc nutrition in plants as a simplifying concept. In summary, this review discusses avenues that can potentially deliver wider benefits for both plant and human Zn nutrition.

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Tools and techniques for illuminating the cell biology of zinc

Cited by 51 publications

References 126 publications

The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction

The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction

The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction

Zinc in plants: Integrating homeostasis and biofortification

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