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Naturally Occurring Histone Deacetylase (HDAC) Inhibitors in the Treatment of Cancers
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Sujatha Puttalingaiah, Murthy V. Greeshma, Mahadevaswamy G. Kuruburu, Venugopal R. Bovilla, SubbaRao V. Madhunapantula
Allyl sulphides, which are derived from Allium sativum L. (garlic), are known to inhibit HDAC activity in cancer cells (Nian et al., 2009b). In general, the metabolites of organo-sulphur allyl mercaptan (AM), organo-selenium compound β-methylselenopyruvate (MSP) and α-keto-γ-methylselenobutyrate (KMSB) have been shown to exhibit better HDAC inhibitory activity than the native compounds (Lee et al., 2009). MSP and KMSB are α-keto acid metabolites of Se-methylselenocysteine (MSC) and selenomethionine (SM), respectively. Computational studies suggested that these metabolites fit into the active site of HDAC enzymes and chelate catalytic Zn²⁺ via sulfhydryl group (AM) or keto acid group (MSP and KMSB). Further, these compounds induce cell cycle arrest and apoptosis via p21WAF1-mediated mechanism in human colon cancer cells (Nian et al., 2009a). A study by Nian et al. (2008) reported that allyl mercaptan inhibits the HDAC activity in HT29 human colon adenocarcinoma cell lines (Nian et al., 2008).
Orthomolecular Parenteral Nutrition Therapy
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
Arturo O'Byrne-Navia, Arturo O'Byrne-De Valdenebro
This phenomenon hasn't been clearly understood, while the information on Se biology is not yet complete and many questions remain unanswered about the cellular and genetic interactions of Se (Hatfield and Gladyshev 2009). Some have pointed to the very slight differences between the two forms of Se supplement. It is clear that both forms contain mainly selenomethionine, but SeEnY also contains little amounts of other sulfur compounds like gamma-glutamyl Se-methylselenocysteine and methylselenocysteine, which some have postulated as responsible for anticancer effects observed in the NPC trial. Apart from that, there are some discrete pro-oxidant properties of selenite, which is an Se species with potential contribution to ROS-mediated apoptosis. Malignant cells usually exist under mild oxidative conditions and many of them can be more vulnerable to oxidative stress than normal cells. There is some research toward the development of oncologic medications based on selenite that utilize oxidative damage as its main anticancer mechanism. These hypotheses were put to test in a recent trial that was able to demonstrate a different biochemical antioxidative profile derived from the use of SeEnY versus SeMet in a randomized trial with healthy volunteers (Richie et al. 2014).
Selenium
Published in Judy A. Driskell, Ira Wolinsky, Sports Nutrition, 2005
L. Mallory Boylan, Julian E. Spallholz
Selenium in nutritional supplements includes organic forms such as selenomethionine and Se-methylselenocysteine and inorganic forms such as sodium selenite and sodium selenate. Another Se supplement is high-Se broccoli, which contains primarily Se-methylselenocysteine. Selenium-yeast is also used frequently as a Se supplement and the selenocompounds in this product have been reported to vary widely with a selenomethionine content ranging from 16.0–62.6%. There have been efforts to have a standard of 85% of the Se as selenomethionine by some companies.7 All of the supplements are useful in correcting selenium GSHPx deficiency, but selenomethionine is incorporated in a nonspecific manner into tissue proteins in place of methionine, as methionine-tRNA does not distinguish between the two amino acids.7 Thus, less Se may be available for cancer chemoprevention or other functions when the Se in supplements is provided predominantly as selenomethionine.
The effects of combined selenium nanoparticles and radiation therapy on breast cancer cells in vitro
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Feng Chen, Xiao Hong Zhang, Xiao Dan Hu, Pei Dang Liu, Hai Qian Zhang
Recently, selenium, a trace element, has attracted great interest due to its important health effects, especially the effects related to the immune reaction and cancer prevention activity [8,9]. Results of epidemiological, pre-clinical and clinical studies indicated that selenium can reduce risk of a series of cancers, such as liver, mammary, prostate, colon and lung cancer [10,11]. Clinical studies also showed that plasma selenium level in cancer patients was dramatically reduced during radiotherapy [12]. Some molecular selenium compounds, such as sodium selenite, selenomethionine and methylselenocysteine, have more effective anti-cancer activity at high dosage [13–15]. As an anti-tumour agent and essential microelement, the effective dose of selenium is close to the toxic range, which immensely limits its clinical application [16,17]. However, selenium nanoparticles (Nano-Se) attract increasing attention due to its excellent bioavailability, high biological activity and low toxicity [18,19]. The toxicity reported for elemental selenium (Se0) at nano-size is lower than selenite (Se+2 or Se+4) ions; therefore, selenium nanoparticles may be a good candidate to replace other types of selenium in nutritional supplements or pharmaceutical dosage types [20]. Therefore, it is possible that Nano-Se can be utilized as a radiation sensitizer to improve radiotherapy effects and reduce side effects.
Altered gut microbial profile is associated with abnormal metabolism activity of Autism Spectrum Disorder
Published in Gut Microbes, 2020
Zhou Dan, Xuhua Mao, Qisha Liu, Mengchen Guo, Yaoyao Zhuang, Zhi Liu, Kun Chen, Junyu Chen, Rui Xu, Junming Tang, Lianhong Qin, Bing Gu, Kangjian Liu, Chuan Su, Faming Zhang, Yankai Xia, Zhibin Hu, Xingyin Liu
The equilibrium between reduced and oxidized forms of glutathione (GSH and GSSG, respectively) is the primary determinant of intracellular redox status,54 which may play an essential role in this pathogenesis of ASD.55 Systemic deficits of glutathione and cysteine in ASD have been reported by Frustaci et al.56 Consistent with this finding, the current study found that the level of the intermediate product, Methylselenocysteine Se-oxide and 3-(Uracil-1-yl)-L-alanine from intermediate derivative of L-alanine were elevated in ASD group, which may further lead to a decrease in selenocysteine and the abnormal reaction of glutathione. Gut microbes in the gastrointestinal tract compete for nutrient resources in the usual symbiotic way; however, gut dysbiosis may interfere with nutrient resources. Thus, the current study suggested constipated ASD may be related to the failure of gastrointestinal epithelium to absorb antioxidant nutrients such as cysteine or selenocysteine. Recently, Wang et al. reported that alterations in the gut glutamate metabolism were associated with changes in gut microbiota composition in ASD children,57 but the differential metabolites shown in the Wang et al. study showed no difference between the ASD and TD groups of the current study, which imply the complexity of the pathological mechanism of ASD. These inconsistent and altered metabolites also reflect the limitation of the analysis method, since fecal metabolism analysis does not fully reveal the true metabolic state of the host. Thus, future studies that focus on the associated analysis of the urine metabolism with fecal microbiota metabolites are suggested to better understand the metabolite role in the pathological mechanism of autism.
Effect of Dietary Methylseleninic Acid and Se-Methylselenocysteine on Carcinogen-Induced, Androgen-Promoted Prostate Carcinogenesis in Rats
Published in Nutrition and Cancer, 2022
Maarten C. Bosland, Michael J. Schlicht, Yibin Deng, Junxuan Lü
SeMet did not prevent the development of prostate cancer when we tested dietary feeding (13) in the rat MNU plus testosterone model (14) and in the testosterone plus estradiol model in NBL rats (15), showing the predictive value of these two models. However, we have shown that daily oral bolus administration of next-generation selenium forms, especially methylseleninic acid (MSeA) and Se-methylselenocysteine (MSeC), inhibits prostate carcinogenesis in the TRAMP mouse model (16) and growth of human prostate cancer cells xenografted in immunodeficient mice (17). Lee et al. (18) showed that intraperitoneal injections of MSeC inhibited the growth of xenografted LNCaP cells in nude mice. We have recently also reported that MSeA suppresses progression of high grade prostatic intraepithelial neoplasia to adenocarcinoma in pten-deficient mice (19). The idea that these next-generation selenium compounds might be active in preventing prostate cancer is based on the assumption that methylselenol is an In Vivo metabolite pool with anticancer activity (20) and that the presumed methylselenol precursors MSeA and MSeC thus would have preventive efficacy (21, 22). One favored hypothetical mechanism is an enhanced generation of methylselenol pool by next-generation selenium compounds at intake levels exceeding the nutritional requirement to saturate selenoproteins. The activities attributed to increased methylselenol pool that include G1 arrest and caspase-mediated apoptosis of cancer cells, suppression of androgen receptor signaling and PSA expression by prostate cancer cells, suppression of angiogenic factor expression such as VEGF by cancer cells, and for angiogenesis response, the suppression of mitogen-stimulated endothelial proliferation, and MMP-2 expression and secretion by vascular endothelial cells, etc. (20–24).