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State-of-the-Art Bioactives and Nutraceuticals in USA (Closed)

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Collection Editor
Department of Physiology & Developmental Biology and the Neuroscience Center, Brigham Young University, Provo, UT, USA
Interests: dermatology; testosterone; estrogens; steroids; endocrine disruption; reproductive endocrinology; molecular endocrinology; neuroendocrinology; stress physiology; reproductive biology
Special Issues, Collections and Topics in MDPI journals

Topical Collection Information

Dear Colleagues,

This Topical Collection aims to publish contributions that report on novel research findings regarding bioactive compounds and nutraceutical products in USA. We welcome submissions and studies on nutritional applications using biological, chemical, cellular, molecular, and immunological methods. Topics include but are not limited to:

  • The discovery and/or use of novel bioactive natural products;
  • The role of these products as active ingredients, supportive biochemical and molecular actions, functional foods, and hence potential physiological mediation for enhanced human nutrition and potential improvement of health;
  • The use of in vitro and in vivo bioactivity research using cell lines and animal models as exemplars of human physiology;
  • Clinical research examining novel bioactive natural products including nutrition, human disorders/disease covering aging, endocrine and metabolism and/or the microbiome axes (such as gut, skin, brain, lung, etc.), for advancing the understanding of biological interactions and/or the improvement of human health and wellbeing.

The only limitation is the main part of the study must be carried out in the USA or by researchers from the USA.

Importantly, the exact composition of active ingredient(s) of natural origin extracts, biosynthesis, or preparation must be reported in the submitted research manuscript, since papers describing the effects of mixed extraction from natural origin are not in the scope of the journal.

Prof. Dr. Edwin Lephart
Collection Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the collection website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • bioactive
  • nutraceutical
  • nutrient
  • health
  • diet
  • functional food
  • obesity
  • diabetes
  • cancer
  • cardiovascular and cerebrovascular diseases
  • vitamins
  • proteins
  • peptides
  • polysaccharides
  • carotenoids
  • polyphenols
  • phytosterols and isoflavones
  • saponins
  • phytic acid
  • probiotics
  • prebiotics
  • enzymes
  • flavonoids
  • caffeine
  • carnitine
  • choline
  • creatine
  • dithiolthiones
  • phytoestrogens
  • glucosinolates

Published Papers (6 papers)

2023

Jump to: 2022

12 pages, 1758 KiB  
Article
In Vitro Assessment of Gold Nanoparticles on Telomerase Activity and Telomere Length in Human Fibroblasts
by Xuesheng Han, Alice Hirschel, Menelaos Tsapekos, Diego Perez and David Vollmer
Int. J. Mol. Sci. 2023, 24(18), 14273; https://doi.org/10.3390/ijms241814273 - 19 Sep 2023
Cited by 1 | Viewed by 1644
Abstract
Telomerase activity coincides with lengthening of the ends of chromosomes known as telomeres. Telomere length is used as a marker for cellular aging. Telomeres shorten over time as cells divide, and certain bioactive compounds such as gold nanoparticles (AuNPs) may slow the shortening [...] Read more.
Telomerase activity coincides with lengthening of the ends of chromosomes known as telomeres. Telomere length is used as a marker for cellular aging. Telomeres shorten over time as cells divide, and certain bioactive compounds such as gold nanoparticles (AuNPs) may slow the shortening of telomeres by increasing telomerase activity. The objective of the present study is to assess the effect of AuNPs on telomerase activity and telomere length in human fibroblasts. Telomerase activity was measured using enzyme-linked immunosorbent assay (ELISA) in primary human lung fibroblasts (IMR90) and using quantitative PCR-based telomeric repeat amplification protocol (Q-TRAP) in primary human dermal fibroblasts, neonatal (HDFn). Telomere length was determined by Telomere Analysis Technology (TAT®)assay in HDFn. In IMR90, all AuNP treatments showed significant increases in telomerase activity when compared to earlier passages. HDFn treated with AuNPs at 0 ppm, 0.05 ppm, 0.5 ppm, or 5 ppm did not show significant differences in telomerase activity compared to the control group. Significant differences in telomere length in HDFn were observed at 2 weeks of 0.05 and 0.5 ppm AuNPs under oxidative culture conditions as compared to the control group. The study showed preliminary evidence that AuNPs may increase telomerase activity and decelerate the shortening of telomeres in human fibroblasts, suggesting its potential anti-aging effects, which warrants further investigation. Full article
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2022

Jump to: 2023

16 pages, 3152 KiB  
Article
Exploring GPR109A Receptor Interaction with Hippuric Acid Using MD Simulations and CD Spectroscopy
by Dipendra Bhandari, Sangita Kachhap, Geet Madhukar, Kiran Kumar Adepu, Andriy Anishkin, Jin-Ran Chen and Sree V. Chintapalli
Int. J. Mol. Sci. 2022, 23(23), 14778; https://doi.org/10.3390/ijms232314778 - 26 Nov 2022
Viewed by 1788
Abstract
Previous research has indicated that various metabolites belonging to phenolic acids (PAs), produced by gut microflora through the breakdown of polyphenols, help in promoting bone development and protecting bone from degeneration. Results have also suggested that G-protein-coupled receptor 109A (GPR109A) functions as a [...] Read more.
Previous research has indicated that various metabolites belonging to phenolic acids (PAs), produced by gut microflora through the breakdown of polyphenols, help in promoting bone development and protecting bone from degeneration. Results have also suggested that G-protein-coupled receptor 109A (GPR109A) functions as a receptor for those specific PAs such as hippuric acid (HA) and 3-(3-hydroxyphenyl) propionic acid (3-3-PPA). Indeed, HA has a molecular structural similarity with nicotinic acid (niacin) which has been shown previously to bind to GPR109A receptor and to mediate antilipolytic effects; however, the binding pocket and the structural nature of the interaction remain to be recognized. In the present study, we employed a computational strategy to elucidate the molecular structural determinants of HA binding to GPR109A and GPR109B homology models in understanding the regulation of osteoclastogenesis. Based on the docking and molecular dynamics simulation studies, HA binds to GPR109A similarly to niacin. Specifically, the transmembrane helices 3, 4 and 6 (TMH3, TMH4 and TMH6) and Extracellular loop 1 and 2 (ECL1 and ECL2) residues of GRP109A; R111 (TMH3), K166 (TMH4), ECL2 residues; S178 and S179, and R251 (TMH6), and residues of GPR109B; Y87, Y86, S91 (ECL1) and C177 (ECL2) contribute for HA binding. Simulations and Molecular Mechanics Poisson-Boltzmann solvent accessible area (MM-PBSA) calculations reveal that HA has higher affinity for GPR109A than for GPR109B. Additionally, in silico mutation analysis of key residues have disrupted the binding and HA exited out from the GPR109A protein. Furthermore, measurements of time-resolved circular dichroism spectra revealed that there are no major conformational changes in the protein secondary structure on HA binding. Taken together, our findings suggest a mechanism of interaction of HA with both GPR109A and GPR109B receptors. Full article
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26 pages, 1949 KiB  
Article
Naphthoquinones Oxidize H2S to Polysulfides and Thiosulfate, Implications for Therapeutic Applications
by Kenneth R. Olson, Kasey J. Clear, Paul J. Derry, Yan Gao, Zhilin Ma, Nathaniel M. Cieplik, Alyssa Fiume, Dominic J. Gaziano, Stephen M. Kasko, Kathleen Narloch, Cecilia L. Velander, Ifeyinwa Nwebube, Collin J. Pallissery, Ella Pfaff, Brian P. Villa, Thomas A. Kent, Gang Wu and Karl D. Straub
Int. J. Mol. Sci. 2022, 23(21), 13293; https://doi.org/10.3390/ijms232113293 - 31 Oct 2022
Cited by 4 | Viewed by 2007
Abstract
1,4-Napththoquinones (NQs) are clinically relevant therapeutics that affect cell function through production of reactive oxygen species (ROS) and formation of adducts with regulatory protein thiols. Reactive sulfur species (RSS) are chemically and biologically similar to ROS and here we examine RSS production by [...] Read more.
1,4-Napththoquinones (NQs) are clinically relevant therapeutics that affect cell function through production of reactive oxygen species (ROS) and formation of adducts with regulatory protein thiols. Reactive sulfur species (RSS) are chemically and biologically similar to ROS and here we examine RSS production by NQ oxidation of hydrogen sulfide (H2S) using RSS-specific fluorophores, liquid chromatography-mass spectrometry, UV-Vis absorption spectrometry, oxygen-sensitive optodes, thiosulfate-specific nanoparticles, HPLC-monobromobimane derivatization, and ion chromatographic assays. We show that NQs, catalytically oxidize H2S to per- and polysulfides (H2Sn, n = 2–6), thiosulfate, sulfite and sulfate in reactions that consume oxygen and are accelerated by superoxide dismutase (SOD) and inhibited by catalase. The approximate efficacy of NQs (in decreasing order) is, 1,4-NQ ≈ juglone ≈ plumbagin > 2-methoxy-1,4-NQ ≈ menadione >> phylloquinone ≈ anthraquinone ≈ menaquinone ≈ lawsone. We propose that the most probable reactions are an initial two-electron oxidation of H2S to S0 and reduction of NQ to NQH2. S0 may react with H2S or elongate H2Sn in variety of reactions. Reoxidation of NQH2 likely involves a semiquinone radical (NQ·−) intermediate via several mechanisms involving oxygen and comproportionation to produce NQ and superoxide. Dismutation of the latter forms hydrogen peroxide which then further oxidizes RSS to sulfoxides. These findings provide the chemical background for novel sulfur-based approaches to naphthoquinone-directed therapies. Full article
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13 pages, 4204 KiB  
Article
Myoglobin–Pyruvate Interactions: Binding Thermodynamics, Structure–Function Relationships, and Impact on Oxygen Release Kinetics
by Kiran Kumar Adepu, Dipendra Bhandari, Andriy Anishkin, Sean H. Adams and Sree V. Chintapalli
Int. J. Mol. Sci. 2022, 23(15), 8766; https://doi.org/10.3390/ijms23158766 - 6 Aug 2022
Cited by 1 | Viewed by 1794
Abstract
Myoglobin (Mb), besides its roles as an oxygen (O2) carrier/storage protein and nitric oxide NO scavenger/producer, may participate in lipid trafficking and metabolite binding. Our recent findings have shown that O2 is released from oxy-Mb upon interaction with lactate (LAC, [...] Read more.
Myoglobin (Mb), besides its roles as an oxygen (O2) carrier/storage protein and nitric oxide NO scavenger/producer, may participate in lipid trafficking and metabolite binding. Our recent findings have shown that O2 is released from oxy-Mb upon interaction with lactate (LAC, anerobic glycolysis end-product). Since pyruvate (PYR) is structurally similar and metabolically related to LAC, we investigated the effects of PYR (aerobic glycolysis end-product) on Mb using isothermal titration calorimetry, circular dichroism, and O2-kinetic studies to evaluate PYR affinity toward Mb and to compare the effects of PYR and LAC on O2 release kinetics of oxy-Mb. Similar to LAC, PYR interacts with both oxy- and deoxy-Mb with a 1:1 stoichiometry. Time-resolved circular dichroism spectra revealed that there are no major conformational changes in the secondary structures of oxy- or deoxy-Mb during interactions with PYR or LAC. However, we found contrasting results with respect to binding affinities and substrate preference, where PYR has higher affinity toward deoxy-Mb when compared with LAC (which prefers oxy-Mb). Furthermore, PYR interaction with oxy-Mb releases a significantly lower amount of O2 than LAC. Taken together, our findings support the hypothesis that glycolytic end-products play a distinctive role in the Mb-rich tissues by serving as novel regulators of O2 availability, and/or by impacting other activities related to oxy-/deoxy-Mb toggling in resting vs. exercised or metabolically activated conditions. Full article
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15 pages, 3029 KiB  
Article
Myoglobin Interaction with Lactate Rapidly Releases Oxygen: Studies on Binding Thermodynamics, Spectroscopy, and Oxygen Kinetics
by Kiran Kumar Adepu, Dipendra Bhandari, Andriy Anishkin, Sean H. Adams and Sree V. Chintapalli
Int. J. Mol. Sci. 2022, 23(9), 4747; https://doi.org/10.3390/ijms23094747 - 26 Apr 2022
Cited by 7 | Viewed by 2365
Abstract
Myoglobin (Mb)-mediated oxygen (O2) delivery and dissolved O2 in the cytosol are two major sources that support oxidative phosphorylation. During intense exercise, lactate (LAC) production is elevated in skeletal muscles as a consequence of insufficient intracellular O2 supply. The [...] Read more.
Myoglobin (Mb)-mediated oxygen (O2) delivery and dissolved O2 in the cytosol are two major sources that support oxidative phosphorylation. During intense exercise, lactate (LAC) production is elevated in skeletal muscles as a consequence of insufficient intracellular O2 supply. The latter results in diminished mitochondrial oxidative metabolism and an increased reliance on nonoxidative pathways to generate ATP. Whether or not metabolites from these pathways impact Mb-O2 associations remains to be established. In the present study, we employed isothermal titration calorimetry, O2 kinetic studies, and UV-Vis spectroscopy to evaluate the LAC affinity toward Mb (oxy- and deoxy-Mb) and the effect of LAC on O2 release from oxy-Mb in varying pH conditions (pH 6.0–7.0). Our results show that LAC avidly binds to both oxy- and deoxy-Mb (only at acidic pH for the latter). Similarly, in the presence of LAC, increased release of O2 from oxy-Mb was detected. This suggests that with LAC binding to Mb, the structural conformation of the protein (near the heme center) might be altered, which concomitantly triggers the release of O2. Taken together, these novel findings support a mechanism where LAC acts as a regulator of O2 management in Mb-rich tissues and/or influences the putative signaling roles for oxy- and deoxy-Mb, especially under conditions of LAC accumulation and lactic acidosis. Full article
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42 pages, 4552 KiB  
Review
Micronutrient Improvement of Epithelial Barrier Function in Various Disease States: A Case for Adjuvant Therapy
by Katherine M. DiGuilio, Elizabeth Rybakovsky, Reza Abdavies, Romy Chamoun, Colleen A. Flounders, Ariel Shepley-McTaggart, Ronald N. Harty and James M. Mullin
Int. J. Mol. Sci. 2022, 23(6), 2995; https://doi.org/10.3390/ijms23062995 - 10 Mar 2022
Cited by 7 | Viewed by 4748
Abstract
The published literature makes a very strong case that a wide range of disease morbidity associates with and may in part be due to epithelial barrier leak. An equally large body of published literature substantiates that a diverse group of micronutrients can reduce [...] Read more.
The published literature makes a very strong case that a wide range of disease morbidity associates with and may in part be due to epithelial barrier leak. An equally large body of published literature substantiates that a diverse group of micronutrients can reduce barrier leak across a wide array of epithelial tissue types, stemming from both cell culture as well as animal and human tissue models. Conversely, micronutrient deficiencies can exacerbate both barrier leak and morbidity. Focusing on zinc, Vitamin A and Vitamin D, this review shows that at concentrations above RDA levels but well below toxicity limits, these micronutrients can induce cell- and tissue-specific molecular-level changes in tight junctional complexes (and by other mechanisms) that reduce barrier leak. An opportunity now exists in critical care—but also medical prophylactic and therapeutic care in general—to consider implementation of select micronutrients at elevated dosages as adjuvant therapeutics in a variety of disease management. This consideration is particularly pointed amidst the COVID-19 pandemic. Full article
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