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The cell and tissues
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
In the presence of oxygen, the pyruvic acid moves into the mitochondria and is converted into acetyl coenzyme A (acetyl CoA) and enters the Krebs or citric acid cycle. This part of the process produces the hydrogen ions that will combine with oxygen in the next phase. It is the Krebs cycle that produces the carbon dioxide that we exhale. During the cycle, the coenzyme A is released and the pick-up molecule, oxaloacetic acid, is regenerated, ready for the next cycle. During the cycle, molecules that are the building blocks for non-essential amino acids and fatty acids are produced. It can therefore be seen that this is a very efficient energy production system.
Introduction and Method
Published in Christopher Cumo, Ancestral Diets and Nutrition, 2020
Chemistry reveals additional insights into diet. Information comes from photosynthesis because plants use carbon dioxide (CO2) differently depending on their origins in temperate regions or the tropics. Temperate plants—for example, potatoes (Solanum tuberosum), wheat, rye, barley, oats, lentils, chickpeas, soybeans, and peas—transform the carbon dioxide they absorb into phosphoglyceric acid (C3H7O7P), a compound with three carbons, by a pathway known as C3. All fruit trees and some plants that arose in the tropics—for example, sweet potatoes (Ipomoea batatas), tomatoes, and Phaseolus beans—are also C3. In contrast, other tropical plants—for example, sugarcane, corn, millet, and sorghum—use carbon dioxide to make oxaloacetic acid (C4H4O5), a four-carbon molecule, by the C4 pathway. Corn’s tropical origins may surprise readers who know it is grown in Canada, but this hardiness resulted from selection by American Indians, who expanded the grass’ geography over innumerable generations. C3 plants represent roughly 85 percent of florae.75
Propionic acidemia
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
When propionyl CoA accumulates, other metabolic products are found in the blood and urine. The predominant compound is 3-hydroxypropionic acid; others include tiglic acid, tiglyglycine, butanone, and propionylglycine. In addition, the unusual metabolite methylcitrate is formed by condensation of propionyl CoA and oxaloacetic acid [65]. This compound is an end product of metabolism and is very stable, resistant to conditions of shipment and bacterial contamination. In our hands, it is the most reliable chemical indicator of the presence of this disorder. It is useful in prenatal diagnosis, as well as the initial diagnosis. Odd chain fatty acids may accumulate in body lipids as a consequence of synthesis from propionyl CoA. They may be demonstrated and quantified in erythrocytes [66]. 3-Ureidopropionate is found in the urine [67], a consequence of propionate inhibition of ureidopropionase. The manifestations of patients with inherited deficiency of this enzyme of pyrimidine metabolism are reminiscent of those of propionic acidemic patients with changes in the basal ganglia, and there is in vitro evidence that ureidopropionate is neurotoxic [68]. 2-Methyl-3-oxovaleric acid, a product of self-condensation of two molecules of propionyl CoA, has been a useful metabolite for Lehnert and colleagues [14] for the diagnosis of propionic acidemia. Its reduction yields 3-hydroxy 2-methylvaleric acid. Hyperlysinemia or hyperlysinuria encountered in propionic acidemia [14] appears to reflect study during hyperammonemia, during which lysine accumulates.
Novel targets and inhibitors of the Mycobacterium tuberculosis cytochrome bd oxidase to foster anti-tuberculosis drug discovery
Published in Expert Opinion on Drug Discovery, 2023
Amaravadhi Harikishore, Vikneswaran Mathiyazakan, Kevin Pethe, Gerhard Grüber
Recent studies from Hards et al. show [54], that a derivative of the FDA approved drug amiloride, referred to as HM2-16F (2× MIC50), showed synergy with Telacebec (10×MIC50) by inhibition of the mycobacterial cyt-bd oxidase and potentiated the actions of Telacebec or its analog TB47 [54]. HM2-16F displayed a potent bactericidal activity (MIC 4 µM) toward Mtb cultures. The compound blocked the entry of oxaloacetic acid into the Krebs cycle and weakly inhibited the F- ATP synthase. The molecule also showed potent inhibition of OCR by 58.8% at 1×MIC50 in M. smegmatis IMVs. This effect was much more dominant with complete inhibition of OCR in presence of TB47 in M. smegmatis IMVs [54]. Metabolomic profiling of HM2-16F treated Mtb cultures highlighted, that respiration was blocked with a concomitant increase of cellular reductive stress [54].
A novel hepatoprotective activity of Alangium salviifolium in mouse model
Published in Drug and Chemical Toxicology, 2022
Preeti Dhruve, Mohd Nauman, Raosaheb K. Kale, Rana P. Singh
The effects observed in terms of biochemical parameters were further proved by histochemical studies, where BEA was able to restore the morphology of damaged liver tissue comparable to normal. Morphology of CCl4-treated group showed loss of tissue integrity, necrosis, and increased infiltration of membrane while all these parameters were moderately decreased in BEA receiving groups. These observations provide the evidence for the protective effect of A. salviifolium on liver. Previous study reported that ethanol extract of leaves of A. salviifolium causes a significant decrease in serum alkaline phosphatase, serum glutamate oxaloacetic acid transaminase, and glutamate pyruvic transaminase which were found to be elevated due to CCl4-induced liver damage (Parameshwar and Reddy 2015).
BCG-induced trained immunity in macrophage: reprograming of glucose metabolism
Published in International Reviews of Immunology, 2020
Yuntong Liu, Shu Liang, Ru Ding, Yuyang Hou, Feier Deng, Xiaohui Ma, Tiantian Song, Dongmei Yan
Pyruvate is converted to acetyl-CoA in mitochondria by PDH, then condenses with oxaloacetic acid and enter into TCA cycle to produce citrate. In addition, cells utilize acetyl-CoA, rather than pyruvate, to generate NAD+ in order to inhibit OXPHOS and promote aerobic glycolysis.76 Glutamine metabolism provides the source for LPS-induced increase in succinate generation, via anaplerosis proceeding through α-ketoglutarate (α-KG), as well as via the γ-aminobutyric acid (GABA) shunt.47 Citrate has been shown to be an inflammatory signal, leading to the production of three key pro-inflammatory mediators: NO, ROS and prostaglandins (PGs). Citrate is transported to the cytoplasm and exchange with malate through citrate carrier (CIC). In the cytoplasm, citrate acts as a key regulator of energy metabolism, inhibiting glycolysis and TCA cycle while promoting lipid synthesis and glycosynthesis. It produces oxaloacetic acid and acetyl-CoA. Acetyl-CoA is used for the biosynthesis of fatty acids, and oxanoacetic acid can produce NADPH by generating malate and pyruvate.84 It is known that NADPH participates in NO and ROS production. Studies have shown that long-term activated monocytes in the absence of glucose can enhance their transport activity by acetylating CIC, promoting citrate efflux and maintaining NADPH, which is inadequate supplied by PPP. This process is accompanied by the depletion of malate and the conversion of citrate into glutamate,85 so whether this process can explain the accumulation of glutamate and malate induced by BCG remains to be further studied.