Category: 97-67-6

Lim, Juhyeon published the artcilePhosphoenolpyruvate depletion mediates both growth arrest and drug tolerance of Mycobacterium tuberculosis in hypoxia, Recommanded Product: (S)-2-hydroxysuccinic acid, the main research area is Mycobacterium hypoxia phosphoenolpyruvate growth inhibition drug tolerance; drug tolerance; metabolic remodeling; phosphoenolpyruvate; synthetic lethality; tuberculosis.

Mycobacterium tuberculosis (Mtb) infection is difficult to treat because Mtb spends the majority of its life cycle in a nonreplicating (NR) state. Since NR Mtb is highly tolerant to antibiotic effects and can mutate to become drug resistant (DR), our conventional tuberculosis (TB) treatment is not effective. Thus, a novel strategy to kill NR Mtb is required. Accumulating evidence has shown that repetitive exposure to sublethal doses of antibiotics enhances the level of drug tolerance, implying that NR Mtb is formed by adaptive metabolic remodeling. As such, metabolic modulation strategies to block the metabolic remodeling needed to form NR Mtb have emerged as new therapeutic options. Here, we modeled in vitro NR Mtb using hypoxia, applied isotope metabolomics, and revealed that phosphoenolpyruvate (PEP) is nearly completely depleted in NR Mtb. This near loss of PEP reduces PEP-carbon flux toward multiple pathways essential for replication and drug sensitivity. Inversely, supplementing with PEP restored the carbon flux and the activities of the foregoing pathways, resulting in growth and heightened drug susceptibility of NR Mtb, which ultimately prevented the development of DR. Taken together, PEP depletion in NR Mtb is associated with the acquisition of drug tolerance and subsequent emergence of DR, demonstrating that PEP treatment is a possible metabolic modulation strategy to resensitize NR Mtb to conventional TB treatment and prevent the emergence of DR.

Proceedings of the National Academy of Sciences of the United States of America published new progress about Drug tolerance. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Recommanded Product: (S)-2-hydroxysuccinic acid.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Dani, Vivek D. published the artcileComparison of metabolomic responses of earthworms to sub-lethal imidacloprid exposure in contact and soil tests, SDS of cas: 97-67-6, the main research area is Eisenia metabolomic response imidacloprid contact soil test; Contact exposure; Eisenia fetida; Energy disruption; Gluconeogenesis; Neonicotinoids; Soil exposure.

Eisenia fetida earthworms were exposed to sub-lethal levels of imidacloprid for 48 h via contact filter paper tests and soil tests. After the exposure, 1H NMR (NMR) metabolomics was used to measure earthworm sub-lethal responses by analyzing the changes in the polar metabolite profile. Maltose, glucose, malate, lactate/threonine, myo-inositol, glutamate, arginine, lysine, tyrosine, leucine, and phenylalanine relative concentrations were altered with imidacloprid exposure in soil. In addition to these metabolites (excluding leucine and phenylalanine), fumarate, ATP, inosine, betaine, scyllo-inositol, glutamine, valine, tryptophan, alanine, tyrosine, and isoleucine relative concentrations shifted with imidacloprid exposure during contact tests. Overall, imidacloprid exposure in soil induces a less pronounced response in metabolites glucose, maltose, fumarate, adenosine-5′-triphosphate (ATP), inosine, scyllo-inositol, lactate/threonine, and tyrosine in comparison to the response observed via contact tests. Thus, our study highlights that tests in soil can result in a different metabolic response in E. fetida and demonstrates the importance of different modes of exposure and the extent of metabolic perturbation in earthworms. Our study also emphasizes the underlying metabolic disruption of earthworms after acute sub-lethal exposure to imidacloprid.

Environmental Science and Pollution Research published new progress about Eisenia fetida. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, SDS of cas: 97-67-6.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Zhang, Hao published the artcileThe enhanced mechanisms of Hansschlegelia zhihuaiae S113 degrading bensulfuron-methyl in maize rhizosphere by three organic acids in root exudates, Name: (S)-2-hydroxysuccinic acid, the main research area is bensulfuronmethyl degradation organic acid root exudate maize rhizosphere Hansschlegelia; Bensulfuron-methyl; Chemotactic response; Hansschlegelia zhihuaiae S113; Maize rhizosphere; Organic acids.

The residues of bensulfuron-Me (BSM), a sulfonylurea herbicide, in soil have caused serious damage to the rotation of susceptible crops. Many studies have reported that the removal of BSM in soil was achieved by adding degrading bacteria. However, the mechanisms used by bacteria to degrade BSM in the crop rhizosphere remain unclear. In this study, a BSM-degrading bacterium, Hansschlegelia zhihuaiae S113, was applied to investigate the enhancement of effects mediated by organic acids during the bioremediation of BSM-contaminated maize rhizosphere soil. Organic acids, such as -malic acid, tartaric acid, and fumaric acid, identified in maize root exudates, significantly stimulated the expression of cheA, which encoded the histidine kinase in strain S113 and contributed to the chemotactic response. This process accelerated the accumulation of strain S113 around the maize roots and promoted the colonization process on maize roots. The growth of strain S113 was significantly increased by -malic acid but not tartaric acid or fumaric acid. After the S113 suspension was root-irrigated to BSM-contaminated soil, the d. of strain S113 colonizing root surfaces and in rhizosphere soil reached 1.1 x 104 cells/g for roots and 4.9 x 104 cells/g in dry soil at 15 d, leading to 80.9% BSM degradation efficiency. The treatment with the addition of a mixture of S113 and -malic acid completely degraded BSM in rhizosphere soil due to the strong attraction and growth promotion of strain S113 by -malic acid, with a higher efficiency than that with the extra addition of fumaric acid (89.7%) or tartaric acid (87.0%). This paper revealed the enhancement effects of organic acids identified in root exudates for the in situ bioremediation of BSM-contaminated rhizosphere soil.

Ecotoxicology and Environmental Safety published new progress about Bioremediation. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Name: (S)-2-hydroxysuccinic acid.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Vazquez-Martinez, Olivia published the artcileMitochondrial Oxidation of the Cytoplasmic Reducing Equivalents at the Onset of Oxidant Stress in the Isoproterenol-Induced Rat Myocardial Infarction, Synthetic Route of 97-67-6, the main research area is myocardial infarction mitochondrial oxidation cytoplasm NADH oxidant stress; cardiac infarction; isoproterenol; malate-aspartate shuttle; oxidative stress; sequential alterations.

We have developed and characterized a model of isoproterenol (ISO)-induced myocardial necrosis, identifying three stages of cardiac damage: a pre-infarction (0-12 h), infarction (24 h), and post-infarction period (48-96 h). Using this model, we have previously found alterations in calcium homeostasis and their relationship with oxidant stress in mitochondria, which showed deficient oxygen consumption and coupled ATP synthesis. Therefore, the present study was aimed at assessing the mitochondrial ability to transport and oxidize cytoplasmic reducing equivalent (NADH), correlating the kinetic parameters of the malate-aspartate shuttle, oxidant stress, and mitochondrial functionality. Our results showed only discreet effects during the cardiotoxic ISO action on the endogenous malate-aspartate shuttle activity, suggesting that endogenous mitochondrial NADH oxidation capacity (Nohl dehydrogenase) was not affected by the cellular stress. On the contrary, the reconstituted system showed significant enhancement in maximal capacity of the malate-aspartate shuttle activity only at later times (post-infarction period), probably as a compensatory part of cardiomyocytes′ response to the metabolic and functional consequences of the infarcted tissue. Therefore, these findings support the notion that heart damage associated with myocardial infarction suffers a set of sequential biochem. and metabolic modifications within cardiomyocytes, where mitochondrial activity, controlling the redox state, could play a relevant role.

Antioxidants published new progress about Cardiac injury. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Synthetic Route of 97-67-6.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Norris, Marie K. published the artcileTutorial: Triheptanoin and Nutrition Management for Treatment of Long-Chain Fatty Acid Oxidation Disorders, Recommanded Product: (S)-2-hydroxysuccinic acid, the main research area is triheptanoin nutrition management treatment long chain fatty acid oxidation; anaplerotic; carnitine-acylcarnitine translocase deficiency; fatty acid oxidation disorder; medical nutrition therapy; triheptanoin; very long-chain acyl-CoA dehydrogenase deficiency.

Patients with severe long-chain fatty acid oxidation disorders (LC-FAODs) experience serious morbidity and mortality despite traditional dietary management including medium-chain triglyceride (MCT)-supplemented, low-fat diets. Triheptanoin is a triglyceride oil that is broken down to acetyl-CoA (CoA) and propionyl-CoA, which replenishes deficient tricarboxylic acid cycle intermediates. We report the complex medical and nutrition management of triheptanoin therapy initiated emergently for 3 patients with LC-FAOD. Triheptanoin (Ultragenyx Pharmaceutical, Inc, Novato, CA, USA) was administered to 3 patients with LC-FAOD on a compassionate-use basis. Triheptanoin was mixed with non-MCT-containing low-fat formula. Patients were closely followed with regular cardiac and laboratory monitoring. Cardiac ejection fraction normalized after triheptanoin initiation. Patients experienced fewer hospitalizations related to metabolic crises while on triheptanoin. Patient 1 has tolerated oral administration without difficulty since birth. Patients 2 and 3 experienced increased diarrhea. Recurrent breakdown of the silicone gastrostomy tube occurred in patient 3, whereas the polyurethane nasogastric tube for patient 2 remained intact. Patient 3 experiences recurrent episodes of elevated creatine kinase levels and muscle weakness associated with illness. Patient 3 had chronically elevated C10-acylcarnitines while on MCT supplementation, which normalized after initiation of triheptanoin and discontinuation of MCT oil. Triheptanoin can ameliorate acute cardiomyopathy and increase survival in patients with severe LC-FAOD. Substituting triheptanoin for traditional MCT-based treatment improves clin. outcomes. MCT oil might be less effective in carnitine-acylcarnitine translocase deficiency patients compared with other FAODs and needs further investigation.

JPEN, Journal of Parenteral and Enteral Nutrition published new progress about Cardiomyopathy. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Recommanded Product: (S)-2-hydroxysuccinic acid.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Prestes, Alessandro de Souza published the artcileMethylglyoxal disrupts the functionality of rat liver mitochondria, SDS of cas: 97-67-6, the main research area is liver mitochondria superoxide phosphorylation bioenergetics methylglyoxal; High-resolution respirometry; Methylglyoxal; Mitochondria; Oxidative stress.

Methylglyoxal (MG) is a reactive metabolite derived from different physiol. pathways. Its production can be harmful to cells via glycation reactions of lipids, DNA, and proteins. But, the effects of MG on mitochondrial functioning and bioenergetic responses are still elusive. Then, the effects of MG on key parameters of mitochondrial functionality were examined here. Isolated rat liver mitochondria were exposed to 0.1-10 mM of MG to determine its toxicity in the mitochondrial viability, membrane potential (Δψm), swelling and the superoxide (O·-2) production Besides, mitochondrial oxidative phosphorylation parameters were analyzed by high-resolution respiratory (HRR) assay. In this set of experiments, routine state, PM state (pyruvate/malate), oxidative phosphorylation (OXPHOS), LEAK respiration, electron transport system (ETS) and oxygen residual (ROX) states were evaluated. HRR showed that PM state, OXPHOS CI-Linked, LEAK respiration, ETS CI/CII-Linked and ETS CII-Linked/ROX were significantly inhibited by MG exposure. MG also inhibited the complex II activity, and decreased Δψm and the viability of mitochondria. Taken together, our data indicates that MG is an inductor of mitochondrial dysfunctions and impairs important steps of respiratory chain, effects that can alter bioenergetics responses.

Chemico-Biological Interactions published new progress about Cell viability. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, SDS of cas: 97-67-6.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Zhao, Jianjian published the artcileArene-perfluoroarene interaction induced chiroptical inversion and precise ee% detection of chiral acids in a benzimidazole-involved ternary coassembly, Name: (S)-2-hydroxysuccinic acid, the main research area is pyrenecarboxylate octafluoronaphthalene hydrogen bond chiral recognition CD.

Flexible regulation of chirality and handedness of chiral functional materials and quant. sensing of natural chiral compounds remains a considerable challenge. Herein, an achiral fluorescent 1-pyrenecarboxylic acid-benzimidazole derivative (PBI) was synthesized and its chiroptical properties upon coassembly with chiral acids (TA and MA) and octafluoronaphthalene (OFN) through hydrogen bonds between benzimidazole and chiral acids as well as an arene-perfluoroarene (AP) interaction between a pyrene moiety and OFN were systemically studied. The binary assemblies of PBI/TA and PBI/MA displayed opposite chiroptical properties including CD and circularly polarized luminescence (CPL) signals. Interestingly, the handedness of CPL was further inverted in ternary assemblies due to the synergistic effect of the AP interaction and hydrogen bonds. Besides, the highly accurate chiral sensing of chiral acids via binary assemblies was successfully achieved with a high correlation coefficient This work provides a simple method for regulating the handedness of chiroptical active materials and quant. sensing of chiral acids through orthogonal multiple component coassemblies.

Nanoscale published new progress about Binary systems. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Name: (S)-2-hydroxysuccinic acid.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

MacCannell, Amanda D. V. published the artcileSexual dimorphism in adipose tissue mitochondrial function and metabolic flexibility in obesity, Safety of (S)-2-hydroxysuccinic acid, the main research area is gene expression sexual dimorphism adipose tissue metabolic flexibility obesity.

The prevalence of obesity is growing globally. Adiposity increases the risk for metabolic syndrome, type 2 diabetes and cardiovascular disease. Adipose tissue distribution influences systemic metabolism and impacts metabolic disease risk. The link between sexual dimorphisms of adiposity and metabolism is poorly defined. We hypothesise that depot-specific adipose tissue mitochondrial function contributes to the sexual dimorphism of metabolic flexibility in obesity. Male and female mice fed high fat diet (HFD) or standard diet (STD) from 8-18 wk of age underwent whole animal calorimetry and high-resolution mitochondrial respirometry anal. on adipose tissue depots. To determine translatability we used RT-qPCR to examine key brown adipocyte-associated gene expression: peroxisome proliferator-activated receptor co-activator 1α, Uncoupling protein 1 and cell death inducing DFFA like effector a in brown adipose tissue (BAT) and s.c. adipose tissue (sWAT) of 18-wk-old mice and sWAT from human volunteers. Male mice exhibited greater weight gain compared to female mice when challenged with HFD. Relative to increased body mass, the adipose to body weight ratio for BAT and sWAT depots was increased in HFD-fed males compared to female HFD-fed mice. Oxygen consumption, energy expenditure, respiratory exchange ratio and food consumption did not differ between males and females fed HFD. BAT mitochondria from obese females showed increased Complex I & II respiration and maximal respiration compared to lean females whereas obese males did not exhibit adaptive mitochondrial BAT respiration. Sexual dimorphism in BAT-associated gene expression in sWAT was also associated with Body Mass Index in humans. We show that sexual dimorphism of weight gain is reflected in mitochondrial respiration anal. Female mice have increased metabolic flexibility to adapt to changes in energy intake by regulating energy expenditure through increased complex II and maximal mitochondrial respiration within BAT when HFD challenged and increased proton leak in sWAT mitochondria.

International Journal of Obesity published new progress about Adipose tissue. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Safety of (S)-2-hydroxysuccinic acid.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Simmen, Frank A. published the artcileMalic enzyme 1 (ME1) in the biology of cancer: it is not just intermediary metabolism, Safety of (S)-2-hydroxysuccinic acid, the main research area is review malic enzyme cancer biol intermediary metabolism; NADPH; cancer; glutathione; hyperinsulinemia; malic enzyme; thioredoxin.

Malic enzyme 1 (ME1) is a cytosolic protein that catalyzes the conversion of malate to pyruvate while concomitantly generating NADPH from NADP. Early studies identified ME1 as a mediator of intermediary metabolism primarily through its participatory roles in lipid and cholesterol biosynthesis. ME1 was one of the first identified insulin-regulated genes in liver and adipose and is a transcriptional target of thyroxine. Multiple studies have since documented that ME1 is pro-oncogenic in numerous epithelial cancers. In tumor cells, the reduction of ME1 gene expression or the inhibition of its activity resulted in decreases in proliferation, epithelial-to-mesenchymal transition and in vitro migration, and conversely, in promotion of oxidative stress, apoptosis and/or cellular senescence. Here, we integrate recent findings to highlight ME1’s role in oncogenesis, provide a rationale for its nexus with metabolic syndrome and diabetes, and raise the prospects of targeting the cytosolic NADPH network to improve therapeutic approaches against multiple cancers.

Journal of Molecular Endocrinology published new progress about Adipose tissue. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Safety of (S)-2-hydroxysuccinic acid.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Bikman, Benjamin T. published the artcileA high-carbohydrate diet lowers the rate of adipose tissue mitochondrial respiration, Synthetic Route of 97-67-6, the main research area is adipose tissue mitochondrial respiration diet rate.

Adipocyte mitochondrial respiration may influence metabolic fuel partitioning into oxidation vs. storage, with implications for whole-body energy expenditure. Although insulin has been shown to influence mitochondrial respiration, the effects of dietary macronutrient composition have not been well characterized. The aim of this exploratory study was to test the hypothesis that a high-carbohydrate diet lowers the oxygen flux of adipocyte mitochondria ex vivo. Among participants in a randomized-controlled weight-loss maintenance feeding trial, those consuming a high-carbohydrate diet (60% carbohydrate as a proportion of total energy, n = 10) had lower rates of maximal adipose tissue mitochondrial respiration than those consuming a moderate-carbohydrate diet (40%, n = 8, p = 0.039) or a low-carbohydrate diet (20%, n = 9, p = 0.005) after 10 to 15 wk. This preliminary finding may provide a mechanism for postulated calorie-independent effects of dietary composition on energy expenditure and fat deposition, potentially through the actions of insulin on fuel partitioning.

European Journal of Clinical Nutrition published new progress about Adipose tissue. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Synthetic Route of 97-67-6.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts