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Cyanogenic Glycosides
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Sulfanegen (as the sodium or triethanolamine salt) generates 3-mercaptopyruvic acid (3-MP), an intermediate in cysteine metabolism, and acts as a decoy receptor for cyanide. As sulfanegen is water soluble, it can be administered intramuscularly (IM).
The Role of Light and Electromagnetic Fields in Maintaining Vascular Health
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
The gaseous signaling molecules, hydrogen sulfide and nitric oxide, are tightly coupled in human physiology. Cystathionine γ lyase (CSE) is a major source of hydrogen sulfide gas through cysteine metabolism. Mice engineered to be deficient in CSE (CSE knockout mice) have reduced levels of sulfide in the blood along with significant increases in oxidative stress [32]. Perhaps surprisingly, they also have reduced bioavailability of nitric oxide associated with impaired eNOS functioning. CSE knockout mice showed a reduction in nitrite levels, attributed to impaired phosphorylation of eNOS, leading to susceptibility to myocardial injury. Thus, hydrogen sulfide gas plays an essential role in promoting the release of nitric oxide, which, as we've seen, will lead to a stripping of the extracellular matrix glycoproteins.
Microbial contribution to the caloric restriction-triggered regulation of the intestinal levels of glutathione transferases, taurine, and bile acid
Published in Gut Microbes, 2021
András Gregor, Marc Pignitter, Slave Trajanoski, Sandra Auernigg-Haselmaier, Veronika Somoza, Jürgen König, Kalina Duszka
As we published before,37 CR elevates free taurine and taurine conjugates in the mucosa of jejunum and ileum. In the current study, the levels of GSH-taurine conjugates showed a tendency toward increased levels in CR mice; yet, not statistically significantly. The depletion of microbiota minimized the difference between CR and ad libitum fed mice in the mucosa of the jejunum (Figure 2l-n) and ileum (Figure 2o-r, Suppl fig S2 F-I) in terms of GSH-taurine conjugate, other taurine conjugates, and free taurine. Further, the mRNA expression of taurine transporter TauT, which was increased in the ileum of CR mice, was not different between AT and AT CR animals (Figure 3a). In agreement with the expression pattern of TauT and our previous publication,37 CR reduced the levels of taurine and its conjugates in the mice’s feces (Suppl fig S2 J-K). In the liver, the expression of genes associated with BA synthesis (Cyp7a1) and transport (Ntcp) as well as cysteine metabolism (cysteine sulfonate decarboxylase; Csd) was regulated by CR and not by microbiota depletion (Figure 3b-d). Importantly, antibiotics treatment did not impact the expression of any of the measured genes in ad libitum fed mice.
Molecular insights into cancer drug resistance from a proteomics perspective
Published in Expert Review of Proteomics, 2019
Yao An, Li Zhou, Zhao Huang, Edouard C. Nice, Haiyuan Zhang, Canhua Huang
Pancreatic cancer is the fifth most common cause of cancer mortality worldwide due to both a lack of methods for early diagnosis and poor prognosis [83]. Gemcitabine is a first-line chemotherapeutic drug for pancreatic cancer. However, intrinsic or acquired resistance to gemcitabine leads to the failure of gemcitabine treatment [84]. A label-free quantification strategy was designed to investigate changes between a normal pancreatic duct cell line (HPDE), an intrinsic gemcitabine-resistant cell line (PANC-1) and a sensitive human pancreatic adenocarcinoma cell line (BxPC3). The experiment found 787 differentially expressed proteins. Bioinformatic analysis subsequently identified 15 markers of epithelial-to-mesenchymal transition (EMT) and 13 EMT-related proteins, such as CDH1 and CTNNB1. In addition, eight of these proteins were involved in glutathione and cysteine metabolism. These results indicate that EMT and glutathione metabolism are associated with intrinsic gemcitabine resistance in pancreatic cancer cell lines [85].
Research on the hepatotoxicity mechanism of citrate-modified silver nanoparticles based on metabolomics and proteomics
Published in Nanotoxicology, 2018
Jiabin Xie, Wenying Dong, Rui Liu, Yuming Wang, Yubo Li
Cysteine catabolism mainly proceeds the oxidation of cysteine sulfate. In the cysteine dioxygenase (CDO) catalytic reaction, dioxyl is added to cysteine to form a cysteine sulfinic acid, which is further converted to alanine (Ueki et al. 2011). Alanine enters the liver through the blood, combining with deamination and releasing ammonia to synthesize urea, which is an important biological function of liver cells. Since AgNP-cit decreases the alanine content, urea synthesis is obstructed in the liver, causing liver damage (Su et al. 2017). Meanwhile, the methionine content was significantly reduced in the cysteine and methionine metabolic pathways, suggesting that cysteine and methionine metabolism was abnormal and that the liver was seriously injured by the effects of AgNP-cit (Dominy, Hwang, and Stipanuk 2007). AgNP-cit up-regulated L-serine dehydratase/L-threonine deaminase and phosphoglycerate mutase, and down-regulated cysteine dioxygenase, alanine, isoleucine and methionine in the liver, which are involved in oxidation, and deamination. This led to abnormalities of glycine, serine and threonine metabolism, cysteine, and methionine metabolism, thus resulting in liver damage.