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The patient with acute gastrointestinal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Rebecca Maindonald, Adrian Jugdoyal
Alcohol: ethanol is oxidised to acetaldehyde, but as this is unstable, it is further metabolised to acetic acid utilising the enzyme alcohol dehydrogenase. This, in turn, collaborates with a further enzyme (ACSS2) to form Acetyl-CoA, which is then available for cellular metabolism.
The patient with acute gastrointestinal problems
Published in Ian Peate, Helen Dutton, Acute Nursing Care, 2014
Alcohol – ethanol is oxidised to acetaldehyde, but as this is unstable it is further metabolised to acetic acid utilising the enzyme alcohol dehydrogenase. This in turn collaborates with a further enzyme (ACSS2) to form Acetyl-CoA which is then available for cellular metabolism.
Recent progress in the development of nanomaterials targeting multiple cancer metabolic pathways: a review of mechanistic approaches for cancer treatment
Published in Drug Delivery, 2023
Ling Zhang, Bing-Zhong Zhai, Yue-Jin Wu, Yin Wang
The function of acetate and acetate-metabolizing enzymes in cancer cells has recently been demonstrated (Schug et al., 2016). Both substrates could be oxidized when 13 C-glucose and 13 C-acetate were infused into mice with orthotopic glioblastomas. However, in plasma, the tumors oxidized more quickly than the nearby normal brain tissues did. Acetate oxidation has been seen in metastatic brain tumors, suggesting that this pathway is a common characteristic of tumors in the brain (Mashimo et al., 2014). Infusion of a similar mixture of 13 C-glucose and 13 C-acetate in human patients also revealed extensive acetate oxidation in gliomas and brain metastases. An Acyl-CoA Synthetase Short Chain 2 (ACSS2) deficient mouse model was used to examine the role of this enzyme in tumor growth (Huang et al., 2018). These embryonic fibroblasts lacking ACSS2 are unable to use exogenous acetate for lipogenesis and histone acetylation. Furthermore, ACSS2 knockout in two hepatocellular carcinoma models lessens the tumor burden (Huang et al., 2018; Bidkhori et al., 2018). According to the selective ACSS2 inhibitors hypothesis, targeting acetate metabolism may have a potent therapeutic effect in some types of cancer (Olson et al., 2016). Given the importance of the aforementioned cancer metabolic pathways, nanoparticles can be used to target specific metabolic sections in these pathways to identify potential cancer therapeutic strategies.
Gene expression profiling of rat livers after continuous whole-body exposure to low-dose rate of gamma rays
Published in International Journal of Radiation Biology, 2018
Acetyl-CoA is at the center of lipid metabolism. Cytosolic acetyl-CoA synthesis, which is essential for de novo lipogenesis, was reduced in response to the low-dose-rate radiation. The cytosolic pool of acetyl-CoA is mainly supplied by two different ATP-dependent reactions: cleavage of citrate, which is generated from TCA cycle, into oxaloacetate and acetyl-CoA by ATP citrate lyase (ACLY) or the ligation of acetate and CoA by acetyl-CoA synthetase (ACSS) (Schug et al. 2015). Both ACLY and ACSS2, the cytosolic ACSS, were transcriptionally down-regulated in this study. Another pathway in producing cytosolic acetyl-CoA was through converting acetoacetate to acetoacetyl-CoA by acetoacetyl-CoA synthetase (AACS) and subsequently to acetyl-CoA by acetyl-CoA acetyltransferase 2 (ACAT2). This acetyl-CoA synthesis was also decreased as both Aacs and Acat2 genes were down-regulated.