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Calvin M. Foltz

Bio: Calvin M. Foltz is an academic researcher from United States Public Health Service. The author has contributed to research in topics: Selenium in biology & Selenium. The author has an hindex of 4, co-authored 4 publications receiving 1878 citations.


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Journal ArticleDOI
TL;DR: The development of new organochalcogens with higher thiol-peroxidase activity that can use other non-toxic thiol reducing agents, such as N-acetylcysteine instead of glutathione, will permit the investigation of the co-administration of organochAlcogens and thiols as a formulation for antioxidant therapy.
Abstract: The organoselenium and organotellurium compounds have been described as promising pharmacological agents in view of their unique biological properties. Glutathione peroxidase mimic, antioxidant activity and thioredoxin reductase inhibition are some of the properties reviewed here. On the other hand, little is known about the molecular toxicological effects of organoselenium and organotellurium compounds. Most of our knowledge arose from research on inorganic selenium and tellurium. However, the ability to oxidize sulfhydryl groups from biological molecules can be involved both in their pharmacological properties and in their toxicological effects. In fact, exposition to high doses of organoselenium or to low doses of organotellurium causes the depletion of endogenous reduced glutathione in a variety of tissues. Thus, the design of compounds that cause low depletion of glutathione and react with specific targeted proteins, controlling specific metabolic pathways, will represent an important progress in understanding the field of organochalcogen compounds. Furthermore, the development of new organochalcogens with higher thiol-peroxidase activity that can use other non-toxic thiol reducing agents, such as N-acetylcysteine instead of glutathione, will permit the investigation of the co-administration of organochalcogens and thiols as a formulation for antioxidant therapy.

1,572 citations

Journal ArticleDOI
TL;DR: The aulh,o~s described an incorpora t ion o f in t raper imne~ ly injee~ted '~s Se in to a IVrOtein f ract ion w N e h after partial puMfieafion showed GSH peroxidase a ctiVi:ty.

1,252 citations

Journal ArticleDOI
28 Nov 2003
TL;DR: Recent advances in the understanding of the plant's ability to metabolize Se into volatile Se forms (phytovolatilization) are discussed, along with the application of phytoremediation for the cleanup of Se contaminated environments.
Abstract: Plants vary considerably in their physiological response to selenium (Se). Some plant species growing on seleniferous soils are Se tolerant and accumulate very high concentrations of Se (Se accumulators), but most plants are Se nonaccumulators and are Se-sensitive. This review summarizes knowledge of the physiology and biochemistry of both types of plants, particularly with regard to Se uptake and transport, biochemical pathways of assimilation, volatilization and incorporation into proteins, and mechanisms of toxicity and tolerance. Molecular approaches are providing new insights into the role of sulfate transporters and sulfur assimilation enzymes in selenate uptake and metabolism, as well as the question of Se essentiality in plants. Recent advances in our understanding of the plant's ability to metabolize Se into volatile Se forms (phytovolatilization) are discussed, along with the application of phytoremediation for the cleanup of Se contaminated environments.

1,243 citations

Journal ArticleDOI
TL;DR: In this paper, the authors provide a critical analysis of the current molecular mechanisms and regulatory networks of ferroptosis, the potential physiological functions of the potential therapeutic roles, and its pathological roles, together with a potential for therapeutic targeting.
Abstract: The research field of ferroptosis has seen exponential growth over the past few years, since the term was coined in 2012. This unique modality of cell death, driven by iron-dependent phospholipid peroxidation, is regulated by multiple cellular metabolic pathways, including redox homeostasis, iron handling, mitochondrial activity and metabolism of amino acids, lipids and sugars, in addition to various signalling pathways relevant to disease. Numerous organ injuries and degenerative pathologies are driven by ferroptosis. Intriguingly, therapy-resistant cancer cells, particularly those in the mesenchymal state and prone to metastasis, are exquisitely vulnerable to ferroptosis. As such, pharmacological modulation of ferroptosis, via both its induction and its inhibition, holds great potential for the treatment of drug-resistant cancers, ischaemic organ injuries and other degenerative diseases linked to extensive lipid peroxidation. In this Review, we provide a critical analysis of the current molecular mechanisms and regulatory networks of ferroptosis, the potential physiological functions of ferroptosis in tumour suppression and immune surveillance, and its pathological roles, together with a potential for therapeutic targeting. Importantly, as in all rapidly evolving research areas, challenges exist due to misconceptions and inappropriate experimental methods. This Review also aims to address these issues and to provide practical guidelines for enhancing reproducibility and reliability in studies of ferroptosis. Finally, we discuss important concepts and pressing questions that should be the focus of future ferroptosis research.

1,243 citations