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Nutrition, the Mediterranean Diet and Selected Supplements for the Prevention and Treatment of Coronary Heart Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
SFA also have variable effects on serum lipids and lipid subfractions, hepatic LDL receptor activity, nonalcoholic liver disease (NAFLD), thrombosis, release of tissue plasminogen activator, macrophage foam cell formation and growth, TLRs (TLR 2 and TLR 4) interactions, nuclear factor (NF-kB) cytokine gene expression, NADPH oxidase, detoxification of radical oxygen species (ROS), activity of catalase, glutathione peroxidase (GPx), superoxide dismutase (SOD 1), thioredoxin reductase (TxNRD1) and the genetic ability to desaturate SFA to monounsaturated fatty acids (MUFA) [31–41]. Stearate (C-18) has minimal effect on CHD risk and serum lipids due to its rapid desaturation to MUFA by stearoyl-CoA Δ-9-desaturase (SCD), which is genetically determined [31–33]. The dietary SFA intake may not correlate with the measured SFA content in serum cholesterol esters and erythrocytes, resulting in a discrepancy in the ability to accurately predict CHD risk based on the “real” SFA status of an individual [31,36–38]. High SFA content in serum cholesterol esters and erythrocytes, not high SFA intake, more accurately predicts CHD risk [36]. Endogenous SFA synthesis, especially that of palmitic acid (16:0) from carbohydrates, contributes to the SFA status. Increased dietary intake of refined carbohydrates with low dietary consumption of SFA spares SFA due to the de novo synthesis of SFA from refined carbohydrates. A diet with reduced carbohydrate intake allows SFA to be utilized directly for energy production. Long-chain fatty acids (LCFA) enhance gastrointestinal growth of gram negative bacteria (GNB) and lipopolysaccharide (LPS) uptake, inflammation and immune activation of T-cells which will increase gastrointestinal permeability, the risk of endotoxemia and infection from a variety of pathobionts at a dysfunctional microbial-epithelial interface [31,36–40].
The level of S-glutathionylated protein is a predictor for metastasis in colorectal cancer and correlated with those of Nrf2/Keap1 pathway
Published in Biomarkers, 2021
Liang-Che Chang, Chung-Wei Fan, Wen-Ko Tseng, Chung-Ching Hua
Glutathionylation, proceeded by GSH under oxidative stress (Zhang et al.2018), inhibits most metabolic pathways resulting in the diversion of fuels towards NADPH-producing pathways and the inhibition of ROS production (Mailloux 2020). S-glutathionylation may reflect the cellular adaption to cell stress like ROS (Townsend 2007). The formation of intermolecular disulphide chains in Keap1 can be blocked by the TXN/GSH system, especially by TXNRD (Cebula et al.2015, Fourquet et al.2010). In cluster dendrogram, Keap1, TXNRD1 and SGP had proximity in all except the normal tissues without metastasis. TXNRD1 is vital to the TXN system and works in concert with Keap1 to regulate Nrf2 activation (Cebula et al.2015), which is essential for cellular response to ROS (Sykiotis and Bohmann 2010) that affects protein S-glutathionylation (Zhang et al.2018). The T/N ratio of SGP level was a negative predictor for metastasis in CRC. The protein levels of TXN had proximity close to none of the others in all the tissues, and the results may suggest the presence of oxidative stress-independent impacts of TXNRD1 on the Nrf2/Keap1 pathway (Cebula et al.2015) in CRC. ROS is essential for creating the immunosuppressive microenvironment for field cancerisation and metastasis (Chaiswing et al.2018, Liao et al.2019). Further in-depth studies of protein S-glutathionylation are needed to define its roles other than as a surrogate for the cellular adaption of ROS in CRC metastasis.
Radiosensitizing Potential of Curcumin in Different Cancer Models
Published in Nutrition and Cancer, 2020
Mechanisms that suppress tumorigenesis after irradiation treatment are generally diverse and interrelated, involving modulation of cellular signal transduction pathways that ultimately lead to cell death (1, 33). Ionizing radiation enhances production of free radicals, reactive oxygen species (ROS), which play a crucial role in cell signaling and cause damage to the DNA inducing double-stranded breaks (2, 34). After that, DNA damage response pathway is actuated by activating the proteins related to DNA reparation, ie., ataxia telangiectasia mutated, ATM and DNA-dependent protein kinase, DNA-PK (22, 34). Therefore, use of natural phytochemicals that augment ROS generation and suppress DNA repair machinery could be important in regulation of radiation-induced cell death (2, 22). However, it is well accepted that due to higher basal production of ROS, the intrinsic level of oxidative stress is greater in malignant cells than normal cells, allowing cancer cells to develop enhanced endogenous antioxidant capacity that makes them more resistant to exogenous oxidative attacks (14, 24,25). The upregulation of antioxidant enzymes, such as thioredoxin reductase-1 (TxnRd1), has been indeed reported in numerous human tumor types (14). Thus, besides potentiation of ROS production, inhibition of key antioxidant proteins by nontoxic natural agents could also contribute to augmentation of radioresponse in cancerous cells.
Insights into cancer and neurodegenerative diseases through selenoproteins and the connection with gut microbiota – current analytical methodologies
Published in Expert Review of Proteomics, 2019
Ana Arias-Borrego, Belén Callejón-Leblic, Marta Calatayud, José Luis Gómez-Ariza, Maria Carmen Collado, Tamara García-Barrera
On the other hand, thioredoxin reductases (TrxR) are important selenoproteins for redox homeostasis capable of reducing disulfide bonds [51]. The expression of these selenoproteins can protect against malignant transformation [62] and inhibit tumor progression and metastasis [51]. TXNRD1 promotes tumor growth, DNA replication, and tumorigenicity and its downregulation increases the sensitivity of cancer cells to some chemotherapy drugs suggesting its potential use as target for anticancer agents [63].