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Amino Acid Metabolism and Disease 2.0

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (20 February 2024) | Viewed by 11707

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Dr. Maria A. Pajares

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Centro de Investigaciones Biológicas Margarita Salas (CSIC), Ramiro de Maeztu 9, 28040 Madrid, Spain
Interests: amino acid metabolism; one-carbon metabolism; sulfur amino acids and liver disease; homocysteine and hearing loss; structure/function relationships; redox stress; cysteine modifications
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Special Issue Information

Dear Colleagues,

The current Special Issue is the continuation of our 2021 Special Issue “Amino Acid Metabolism and Disease”.

Amino acids are better known as the building blocks of proteins, but their role extends to the synthesis of other key compounds for the function of any organism and even the post-translational modification of proteins. Among these additional roles, a special place is reserved for the synthesis of S-adenosylmethionine, which seems to be involved in as many reactions as ATP, but also for the synthesis of neurotransmitters, glutathione, and nucleotides. Pathways of amino acid metabolism are interconnected to recycle essential amino acids, thus guaranteeing their supply during unfavorable conditions, but also with energy metabolism. Vitamins and cations are important for enzymes in these routes, further linking amino acid metabolism to nutrition, an aspect to be considered in pathological states where patients tend to change their habits or decrease their daily food ingestion. Moreover, human mutations in genes involved in amino acid metabolism are constantly being discovered, studied, and linked to a variety of outcomes, including major and rare diseases. This Special Issue focuses on these additional roles of amino acids, how pathological impairments of their metabolism impact cell function, and whether they can be prevented or ameliorated by drugs and/or nutritional interventions.

Dr. Maria A. Pajares
Guest Editor

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Keywords

amino acid transport
essential amino acids
hearing loss
liver disease
mutations
neurological disorders
oligomerization state
post-translational modifications
protein–protein interactions
structure/function relationships
sulfur amino acids

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Published Papers (5 papers)

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Research

Jump to: Review

11 pages, 655 KiB

Open AccessArticle

The Variability of Tryptophan Metabolism in Patients with Mixed Type of Irritable Bowel Syndrome

by Jan Chojnacki, Paulina Konrad, Marta Mędrek-Socha, Aleksandra Kaczka, Aleksandra Błońska, Radosław Zajdel, Cezary Chojnacki and Anita Gąsiorowska

Int. J. Mol. Sci. 2024, 25(5), 2550; https://doi.org/10.3390/ijms25052550 - 22 Feb 2024

Cited by 2 | Viewed by 992

Abstract

Patients with a mixed type of irritable bowel syndrome (IBS-M) experience constipation and diarrhea, which alternate between weeks or months. The pathogenesis of this syndrome is still little understood. The aim of the study was mainly to evaluate the urinary excretion of selected tryptophan (TRP) metabolites during the constipation and diarrhea periods of this syndrome. In 36 patients with IBS-M and 36 healthy people, serum serotonin level was measured by ELISA and urinary levels of 5-hydroxyindoleacetic acid (5-HIAA), kynurenine (KYN) and indican (3-IS) were determined using the LC-MS/MS method. The levels of all above metabolites were higher in the patient group, and increased significantly during the diarrheal period of IBS-M. In particular, the changes concerned 5-HIAA (3.67 ± 0.86 vs. 4.59 ± 0.95 mg/gCr, p < 0.001) and 3-IS (80.2 ± 17.4 vs. 93.7 ± 25.1 mg/g/Cr, p < 0.001). These changes coexisted with gut microbiome changes, assessed using hydrogen-methane and ammonia breath tests. In conclusion, the variability of TRP metabolism and the gut microbiome may cause the alternation of IBS-M symptoms. Full article

(This article belongs to the Special Issue Amino Acid Metabolism and Disease 2.0)

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15 pages, 2589 KiB

Open AccessArticle

Arginine Is a Novel Drug Target for Arginine Decarboxylase in Human Colorectal Cancer Cells

by Xinlei Wei, Ho-Yin Chow, Hiu-Chi Chong, Siu-Lun Leung, Mei-Ki Ho, Man-Yuen Lee and Yun-Chung Leung

Int. J. Mol. Sci. 2023, 24(18), 13741; https://doi.org/10.3390/ijms241813741 - 6 Sep 2023

Cited by 3 | Viewed by 1895

Abstract

Colorectal cancer (CRC) has been proven to be highly reliant on arginine availability. Limiting arginine-rich foods or treating patients with arginine-depleting enzymes arginine deiminase (ADI) or arginase can suppress colon cancer. However, arginase and ADI are not the best drug candidates for CRC. Ornithine, the product of arginase, can enhance the supply of polyamine, which favors CRC cell growth, while citrulline, the product of ADI, faces the problem of arginine recycling due to the overexpression of argininosuccinate synthetase (ASS). Biosynthetic arginine decarboxylase (ADC), an enzyme that catalyzes the conversion of arginine to agmatine and carbon dioxide, may be a better choice as it combines both arginine depletion and suppression of intracellular polyamine synthesis via its product agmatine. ADC has anti-tumor potential yet has received much less attention than the other two arginine-depleting enzymes. In order to gain a better understanding of ADC, the preparation and the anti-cancer properties of this enzyme were explored in this study. When tested in vitro, ADC inhibited the proliferation of three colorectal cancer cell lines regardless of their ASS cellular expression. In contrast, ADC had a lesser cytotoxic effect on the human foreskin fibroblasts and rat primary hepatocytes. Further in vitro studies revealed that ADC induced S and G2/M phase cell-cycle arrest and apoptosis in HCT116 and LoVo cells. ADC-induced apoptosis in HCT116 cells followed the mitochondrial apoptotic pathway and was caspase-3-dependent. With all results obtained, we suggest that arginine is a potential target for treating colorectal cancer with ADC, and the anti-cancer properties of ADC should be more deeply investigated in the future. Full article

(This article belongs to the Special Issue Amino Acid Metabolism and Disease 2.0)

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13 pages, 1464 KiB

Open AccessArticle

The Greater Impact of Paternal, Compared to Maternal, Hereditary Background on Depressive-Like Behavior in Wistar Kyoto Rats with Different Amino Acid Metabolism in the Pup Brain

by Tsubasa Ihara, Mizuki Hamada and Mitsuhiro Furuse

Int. J. Mol. Sci. 2023, 24(4), 4199; https://doi.org/10.3390/ijms24044199 - 20 Feb 2023

Cited by 1 | Viewed by 1762

Abstract

In the pathogenesis of depression, heredity is believed to be a major factor. However, the mechanism by which heredity contributes to the onset of depression is not fully understood. Wistar Kyoto (WKY) rats have been used as an animal model for depression because of their increased depression-like behavior compared to Wistar (WIS) rats. In the present study, pups crossbred from WKY × WIS rats were used to evaluate locomotor activity in an open field test (OFT) and depression-like behavior in a forced swimming test (FST), with a focus on amino acid metabolism. Pups in the WKY♂ × WKY♀ group showed lower locomotor activity in the OFT and higher depression-like behavior in the FST than those in the WIS♂ × WIS♀ group. In addition, multiple regression analysis showed that the paternal strain had a greater effect than the maternal strain on locomotor activity and depression-like behavior in OFT and FST, respectively. Several amino acids in the brainstem, hippocampus, and striatum were significantly decreased through the influence of the WKY paternal strain, but not the WKY maternal strain. Based on these data from comparing WKY and WIS rats, we hypothesize that the hereditary effects of the WKY paternal strain on behavioral tests are partially caused by dysregulation of the amino acid metabolism in the brain. Full article

(This article belongs to the Special Issue Amino Acid Metabolism and Disease 2.0)

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Review

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32 pages, 2394 KiB

Open AccessReview

Appraising the Role of Astrocytes as Suppliers of Neuronal Glutathione Precursors

by Dolores Pérez-Sala and María A. Pajares

Int. J. Mol. Sci. 2023, 24(9), 8059; https://doi.org/10.3390/ijms24098059 - 29 Apr 2023

Cited by 7 | Viewed by 2241

Abstract

The metabolism and intercellular transfer of glutathione or its precursors may play an important role in cellular defense against oxidative stress, a common hallmark of neurodegeneration. In the 1990s, several studies in the Neurobiology field led to the widely accepted notion that astrocytes produce large amounts of glutathione that serve to feed neurons with precursors for glutathione synthesis. This assumption has important implications for health and disease since a reduction in this supply from astrocytes could compromise the capacity of neurons to cope with oxidative stress. However, at first glance, this shuttling would imply a large energy expenditure to get to the same point in a nearby cell. Thus, are there additional underlying reasons for this expensive mechanism? Are neurons unable to import and/or synthesize the three non-essential amino acids that are the glutathione building blocks? The rather oxidizing extracellular environment favors the presence of cysteine (Cys) as cystine (Cis), less favorable for neuronal import. Therefore, it has also been proposed that astrocytic GSH efflux could induce a change in the redox status of the extracellular space nearby the neurons, locally lowering the Cis/Cys ratio. This astrocytic glutathione release would also increase their demand for precursors, stimulating Cis uptake, which these cells can import, further impacting the local decline of the Cis/Cys ratio, in turn, contributing to a more reduced extracellular environment and subsequently favoring neuronal Cys import. Here, we revisit the experimental evidence that led to the accepted hypothesis of astrocytes acting as suppliers of neuronal glutathione precursors, considering recent data from the Human Protein Atlas. In addition, we highlight some potential drawbacks of this hypothesis, mainly supported by heterogeneous cellular models. Finally, we outline additional and more cost-efficient possibilities by which astrocytes could support neuronal glutathione levels, including its shuttling in extracellular vesicles. Full article

(This article belongs to the Special Issue Amino Acid Metabolism and Disease 2.0)

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27 pages, 9199 KiB

Open AccessReview

Chlorine Dioxide: Friend or Foe for Cell Biomolecules? A Chemical Approach

by Celia María Curieses Andrés, José Manuel Pérez de la Lastra, Celia Andrés Juan, Francisco J. Plou and Eduardo Pérez-Lebeña

Int. J. Mol. Sci. 2022, 23(24), 15660; https://doi.org/10.3390/ijms232415660 - 10 Dec 2022

Cited by 8 | Viewed by 3660

Abstract

This review examines the role of chlorine dioxide (ClO₂) on inorganic compounds and cell biomolecules. As a disinfectant also present in drinking water, ClO₂ helps to destroy bacteria, viruses, and some parasites. The Environmental Protection Agency EPA regulates the maximum concentration of chlorine dioxide in drinking water to be no more than 0.8 ppm. In any case, human consumption must be strictly regulated since, given its highly reactive nature, it can react with and oxidize many of the inorganic compounds found in natural waters. Simultaneously, chlorine dioxide reacts with natural organic matter in water, including humic and fulvic acids, forming oxidized organic compounds such as aldehydes and carboxylic acids, and rapidly oxidizes phenolic compounds, amines, amino acids, peptides, and proteins, as well as the nicotinamide adenine dinucleotide NADH, responsible for electron and proton exchange and energy production in all cells. The influence of ClO₂ on biomolecules is derived from its interference with redox processes, modifying the electrochemical balances in mitochondrial and cell membranes. This discourages its use on an individual basis and without specialized monitoring by health professionals. Full article

(This article belongs to the Special Issue Amino Acid Metabolism and Disease 2.0)

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