Category: 434-16-2

Zhang, Jiahe; Shi, Jiaqi; Han, Shuo; Zheng, Pai; Chen, Zhangjian; Jia, Guang published the artcile< Titanium dioxide nanoparticles induced reactive oxygen species (ROS) related changes of metabolomics signatures in human normal bronchial epithelial (BEAS-2B) cells>, Name: (3S,9S,10R,13R,14R,17R)-10,13-Dimethyl-17-((R)-6-methylheptan-2-yl)-2,3,4,9,10,11,12,13,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol, the main research area is titanium dioxide nanoparticle reactive oxygen species bronchial epithelial; Lipid metabolism; Liquid chromatography; Metabolomics; Reactive oxygen pecies; Titanium dioxide nanoparticles.

Titanium dioxide often enters the respiratory tract in the form of nano-dust in occupational sites. Metabolomics may be a promising method for studying the toxicol. of nano titanium dioxide. The intention of this study was to explore the possible impact of titanium dioxide nanoparticles (TiO2 NPs) on the metabolomics signatures of human normal bronchial epithelial (BEAS-2B) cells and to search for investigate the role of reactive oxygen species (ROS). In this study, BEAS-2B cells were treated by TiO2 NPs (0, 25, 50 and 100μg/mL) for 48 h. The metabolites extracted from BEAS-2B cells were determined by untargeted metabolomics technique, and the differential metabolites and metabolic pathways were discovered by using multivariate anal. Intracellular ROS was detected by DCFH-DA probe and flow cytometry method. Machine learning was used to explore the relationship between ROS and metabolomics changes. Totally, seventy-six differential metabolites and the steroid biosynthesis pathway of BEAS-2B cells were observed after treatment of TiO2 NPs. Lipid and lipid-like metabolites were the most significant classes among the metabolite products induced by TiO2 NPs. TiO2 NPs resulted in a dose-dependent increase in intracellular ROS levels, and correlated with most of the differential metabolites. In conclusion, TiO2 NPs increased the level of the oxidative stress, which could contribute to the altered signature represented by lipid metabolism in BEAS-2B cells.

Toxicology and Applied Pharmacology published new progress about Bronchial epithelium. 434-16-2 belongs to class alcohols-buliding-blocks, and the molecular formula is C27H44O, Name: (3S,9S,10R,13R,14R,17R)-10,13-Dimethyl-17-((R)-6-methylheptan-2-yl)-2,3,4,9,10,11,12,13,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Shin, Mi Hee; Lee, Yuri; Kim, Min-Kyoung; Lee, Dong Hun; Chung, Jin Ho published the artcile< UV increases skin-derived 1α,25-dihydroxyvitamin D3 production, leading to MMP-1 expression by altering the balance of vitamin D and cholesterol synthesis from 7-dehydrocholesterol>, Recommanded Product: (3S,9S,10R,13R,14R,17R)-10,13-Dimethyl-17-((R)-6-methylheptan-2-yl)-2,3,4,9,10,11,12,13,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol, the main research area is UV radiation dihydroxyvitamin D3 MMP1 vitamin D cholesterol dehydrocholesterol; 1α,25-dihydroxyvitamin D(3); 7-dehydrocholesterol; 7-dehydrocholesterol reductase; CYP27B1; Cholesterol; MMP-1; UV.

Here, we investigated the effect of skin-derived 1α,25(OH)2D3, synthesized purely within the keratinocytes, on MMP-1 expression. Treatment of human epidermal keratinocytes with 1α,25(OH)2D3, but not 7DHC or 25OHD3, significantly increased MMP-1 expression. UV irradiation increases 1α,25(OH)2D3 levels, and ketoconazole inhibits UV-induced production of 1α,25(OH)2D3. Upregulation of MMP-1 by UV was reversed by inhibition of 1α,25(OH)2D3 synthesis using ketoconazole or CYP27B1 siRNA. In keratinocytes, 7DHC is a substrate for both cholesterol and 1α,25(OH)2D3 synthesis. We demonstrated that UV irradiation leads to decreased expression of DHCR7 (7-dehydrocholesterol reductase), the enzyme that converts 7DHC to cholesterol. Inhibition of DHCR7 with its inhibitor BM15766 decreased cholesterol synthesis and increased UV-induced MMP-1 expression, which was attenuated by ketoconazole. These findings suggest that UV-induced reduction of DHCR7 leads to a decrease in cholesterol synthesis, thereby increasing 7DHC availability for 1α,25(OH)2D3 production, which enhances MMP-1 expression. Finally, UV irradiation in human skin in vivo significantly increased CYP27B1 mRNA and decreased DHCR7 mRNA expression.

Journal of Steroid Biochemistry and Molecular Biology published new progress about Homo sapiens. 434-16-2 belongs to class alcohols-buliding-blocks, and the molecular formula is C27H44O, Recommanded Product: (3S,9S,10R,13R,14R,17R)-10,13-Dimethyl-17-((R)-6-methylheptan-2-yl)-2,3,4,9,10,11,12,13,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Shin, Mi Hee; Lee, Yuri; Kim, Min-Kyoung; Lee, Dong Hun; Chung, Jin Ho published the artcile< UV increases skin-derived 1α,25-dihydroxyvitamin D3 production, leading to MMP-1 expression by altering the balance of vitamin D and cholesterol synthesis from 7-dehydrocholesterol>, Recommanded Product: (3S,9S,10R,13R,14R,17R)-10,13-Dimethyl-17-((R)-6-methylheptan-2-yl)-2,3,4,9,10,11,12,13,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol, the main research area is UV radiation dihydroxyvitamin D3 MMP1 vitamin D cholesterol dehydrocholesterol; 1α,25-dihydroxyvitamin D(3); 7-dehydrocholesterol; 7-dehydrocholesterol reductase; CYP27B1; Cholesterol; MMP-1; UV.

Here, we investigated the effect of skin-derived 1α,25(OH)2D3, synthesized purely within the keratinocytes, on MMP-1 expression. Treatment of human epidermal keratinocytes with 1α,25(OH)2D3, but not 7DHC or 25OHD3, significantly increased MMP-1 expression. UV irradiation increases 1α,25(OH)2D3 levels, and ketoconazole inhibits UV-induced production of 1α,25(OH)2D3. Upregulation of MMP-1 by UV was reversed by inhibition of 1α,25(OH)2D3 synthesis using ketoconazole or CYP27B1 siRNA. In keratinocytes, 7DHC is a substrate for both cholesterol and 1α,25(OH)2D3 synthesis. We demonstrated that UV irradiation leads to decreased expression of DHCR7 (7-dehydrocholesterol reductase), the enzyme that converts 7DHC to cholesterol. Inhibition of DHCR7 with its inhibitor BM15766 decreased cholesterol synthesis and increased UV-induced MMP-1 expression, which was attenuated by ketoconazole. These findings suggest that UV-induced reduction of DHCR7 leads to a decrease in cholesterol synthesis, thereby increasing 7DHC availability for 1α,25(OH)2D3 production, which enhances MMP-1 expression. Finally, UV irradiation in human skin in vivo significantly increased CYP27B1 mRNA and decreased DHCR7 mRNA expression.

Journal of Steroid Biochemistry and Molecular Biology published new progress about Homo sapiens. 434-16-2 belongs to class alcohols-buliding-blocks, and the molecular formula is C27H44O, Recommanded Product: (3S,9S,10R,13R,14R,17R)-10,13-Dimethyl-17-((R)-6-methylheptan-2-yl)-2,3,4,9,10,11,12,13,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Bampidis, Vasileios; Bastos, Maria de Lourdes; Christensen, Henrik; Dusemund, Birgit; Kouba, Maryline; Kos Durjava, Mojca; Lopez-Alonso, Marta; Lopez Puente, Secundino; Marcon, Francesca; Mayo, Baltasar; Pechova, Alena; Petkova, Mariana; Ramos, Fernando; Sanz, Yolanda; Villa, Roberto Edoardo; Woutersen, Ruud; Tarres-Call, Jordi; Azimonti, Giovanna; EFSA Panel on Additives and Products or Substances used in Animal Feed published the artcile< Safety for the environment of vitamin D3 for salmonids>, Related Products of 434-16-2, the main research area is environmental safety vitamin D3 salmonid; cholecalciferol; fish; nutritional additive; safety; vitamin D3; vitamins and provitamins.

The Panel on Additives and Products or Substances used in Animal Feed (FEEDAP Panel) of EFSA assessed the safety for the target species and the consumer of the use of a maximum total level of 1.5 mg vitamin D3/kg feed in fish nutrition (2017). The assessment was based on data that had been provided by the Norwegian Food Safety Authority (NFSA). Since the data set provided by the NFSA did not include any new information concerning the safety for the user and the environment, the 2017 opinion did not address the potential effects of the proposed increase in the maximum authorised levels of vitamin D3 on the safety for the user and the environment. The NFSA has submitted addnl. data and the European Commission has requested EFSA to deliver a new opinion on the safety for the environment of vitamin D3 as a nutritional additive for salmonids. Planktonic microalgae, inhabiting the sea, are a large group of photosynthetic organisms that contain both vitamin D3 and provitamin D3. Marine phytoplankton is distributed throughout the sea serving as the basis for all marine food webs. Therefore, since it is produced by phytoplankton, vitamin D3 may also be considered as being ubiquitous in the aquatic environment. Considering the different sources of vitamin D3 already present in the marine environment, the FEEDAP Panel considers that an increase in concentration of vitamin D3 when used as a feed additive in compound feed for salmonids up to a maximum of 1.5 mg/kg is not expected to pose a risk for the environment.

EFSA Journal published new progress about Aquatic environment. 434-16-2 belongs to class alcohols-buliding-blocks, and the molecular formula is C27H44O, Related Products of 434-16-2.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Rybchyn, Mark S.; Abboud, Myriam; Puglisi, David A.; Gordon-Thomson, Clare; Brennan-Speranza, Tara C.; Mason, Rebecca S.; Fraser, David R. published the artcile< Skeletal muscle and the maintenance of vitamin D status>, HPLC of Formula: 434-16-2, the main research area is review vitamin D skeletal muscle; muscle; parathyroid hormone; vitamin D; vitamin D-binding protein.

A review. Vitamin D, unlike the micronutrients, vitamins A, E, and K, is largely obtained not from food, but by the action of solar UV light on its precursor, 7-dehydrocholesterol, in skin. With the decline in UV light intensity in winter, most skin production of vitamin D occurs in summer. Since no defined storage organ or tissue has been found for vitamin D, it has been assumed that an adequate vitamin D status in winter can only be maintained by oral supplementation. Skeletal muscle cells have now been shown to incorporate the vitamin D-binding protein (DBP) from blood into the cell cytoplasm where it binds to cytoplasmic actin. This intracellular DBP provides an array of specific binding sites for 25-hydroxyvitamin D (25(OH)D), which diffuses into the cell from the extracellular fluid. When intracellular DBP undergoes proteolytic breakdown, the bound 25(OH)D is then released and diffuses back into the blood. This uptake and release of 25(OH)D by muscle accounts for the very long half-life of this metabolite in the circulation. Since 25(OH)D concentration in the blood declines in winter, its cycling in and out of muscle cells appears to be upregulated. Parathyroid hormone is the most likely factor enhancing the repeated cycling of 25(OH)D between skeletal muscle and blood. This mechanism appears to have evolved to maintain an adequate vitamin D status in winter.

Nutrients published new progress about Cytoplasm. 434-16-2 belongs to class alcohols-buliding-blocks, and the molecular formula is C27H44O, HPLC of Formula: 434-16-2.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Chen, Liang; Ma, Mei-Yan; Sun, Ming; Jiang, Lu-Yi; Zhao, Xue-Tong; Fang, Xian-Xiu; Lam, Sin Man; Shui, Guang-Hou; Luo, Jie; Shi, Xiong-Jie; Song, Bao-Liang published the artcile< Endogenous sterol intermediates of the mevalonate pathway regulate HMGCR degradation and SREBP-2 processing>, Safety of (3S,9S,10R,13R,14R,17R)-10,13-Dimethyl-17-((R)-6-methylheptan-2-yl)-2,3,4,9,10,11,12,13,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol, the main research area is sterol HMGCR SREBP2 CYP51A1 signaling cervical cancer; 3-hydroxy-3-methylglutaryl-coenzyme A reductase degradation; clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR associated protein 9 (Cas9); lanosterol; mevalonate; sterol intermediates; sterol regulatory element-binding protein-2; sterol regulatory element-binding protein-2 cleavage.

Sterol-regulated HMG-CoA reductase (HMGCR) degradation and SREBP-2 cleavage are two major feedback regulatory mechanisms governing cholesterol biosynthesis. Reportedly, lanosterol selectively stimulates HMGCR degradation, and cholesterol is a specific regulator of SREBP-2 cleavage. However, it is unclear whether other endogenously generated sterols regulate these events. Here, we investigated the sterol intermediates from the mevalonate pathway of cholesterol biosynthesis using a CRISPR/Cas9-mediated genetic engineering approach. With a constructed HeLa cell line expressing the mevalonate transporter, we individually deleted genes encoding major enzymes in the mevalonate pathway, used lipidomics to measure sterol intermediates, and examined HMGCR and SREBP-2 statuses. We found that the C4-dimethylated sterol intermediates, including lanosterol, 24,25-dihydrolanosterol, follicular fluid meiosis activating sterol, testis meiosis activating sterol, and dihydro-testis meiosis activating sterol, were significantly upregulated upon mevalonate loading. These intermediates augmented both degradation of HMGCR and inhibition of SREBP-2 cleavage. The accumulated lanosterol induced rapid degradation of HMGCR, but did not inhibit SREBP-2 cleavage. The newly synthesized cholesterol from the mevalonate pathway is dispensable for inhibiting SREBP-2 cleavage. Together, these results suggest that lanosterol is a bona fide endogenous regulator that specifically promotes HMGCR degradation, and that other C4-dimethylated sterol intermediates may regulate both HMGCR degradation and SREBP-2 cleavage.

Journal of Lipid Research published new progress about Homo sapiens Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 434-16-2 belongs to class alcohols-buliding-blocks, and the molecular formula is C27H44O, Safety of (3S,9S,10R,13R,14R,17R)-10,13-Dimethyl-17-((R)-6-methylheptan-2-yl)-2,3,4,9,10,11,12,13,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Liu, Shengzhi; Wu, Di; Sun, Xun; Fan, Yao; Zha, Rongrong; Jalali, Aydin; Teli, Meghana; Sano, Tomohiko; Siegel, Amanda; Sudo, Akihiro; Agarwal, Mangilal; Robling, Alexander; Li, Bai-Yan; Yokota, Hiroki published the artcile< Mechanical stimulations can inhibit local and remote tumor progression by downregulating WISP1>, Quality Control of 434-16-2, the main research area is WISP mech stimulation inhibit local remote tumor progression; TGFβ calcitriol; WISP1; bone metastasis; breast cancer; cholesterol; urine; vitamin D3.

Mech. stimulations can prevent bone loss, but their effects on the tumor-invaded bone or solid tumors are elusive. Here, we evaluated the effect of knee loading, dynamic loads applied to the knee, on metastasized bone and mammary tumors. In a mouse model, tumor cells were inoculated to the mammary fat pad or the proximal tibia. Daily knee loading was then applied and metabolic changes were monitored mainly through urine. Urine samples were also collected from human subjects before and after step aerobics. The result showed that knee loading inhibited tumor progression in the loaded tibia. Notably, it also reduced remotely the growth of mammary tumors. In the urine, an altered level of cholesterol was observed with an increase in calcitriol, which is synthesized from a cholesterol derivative In urinary proteins, knee loading in mice and step aerobics in humans markedly reduced WNT1-inducible signaling pathway protein 1, WISP1, which leads to poor survival among patients with breast cancer. In the ex vivo breast cancer tissue assay, WISP1 promoted the growth of cancer fragments and upregulated tumor-promoting genes, such as Runx2, MMP9, and Snail. Collectively, the present preclin. and human study demonstrated that mech. stimulations, such as knee loading and step aerobics, altered urinary metabolism and downregulated WISP1. The study supports the benefit of mech. stimulations for locally and remotely suppressing tumor progression. It also indicated the role of WISP1 downregulation as a potential mechanism of loading-driven tumor suppression.

FASEB Journal published new progress about Aerobic exercise. 434-16-2 belongs to class alcohols-buliding-blocks, and the molecular formula is C27H44O, Quality Control of 434-16-2.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Allen, Luke B.; Genaro-Mattos, Thiago C.; Anderson, Allison; Porter, Ned A.; Mirnics, Karoly; Korade, Zeljka published the artcile< Amiodarone Alters Cholesterol Biosynthesis through Tissue-Dependent Inhibition of Emopamil Binding Protein and Dehydrocholesterol Reductase 24>, COA of Formula: C27H44O, the main research area is amiodarone cholesterol toxicity; 8-dehydrocholesterol; cholesterol; desmosterol; emopamil binding protein; zymostenol; zymosterol.

Amiodarone is prescribed for the treatment and prevention of irregular heartbeats. Although effective in clin. practice, the long-term use of amiodarone has many unwanted side effects, including cardiac, pulmonary, hepatic, and neurol. toxicities. Our objective was to elucidate effects of amiodarone exposure on the cholesterol metabolism in cultured neuronal and non-neuronal cells and in individuals taking amiodarone. We observed that amiodarone increases distinct cholesterol precursors in different cell types in a dose-dependent manner. In liver and kidney cell lines, amiodarone causes increase in desmosterol levels, and in primary cortical neurons and astrocytes, amiodarone increases zymosterol, zymostenol, and 8-dehydrocholesterol (8-DHC). We conclude that amiodarone inhibits two enzymes in the pathway, emopamil binding protein (EBP) and dehydrocholesterol reductase 24 (DHCR24). Cortical neurons and astrocytes are more sensitive to amiodarone than liver and kidney cell lines. We confirmed the inhibition of EBP enzyme by analyzing the sterol intermediates in EBP-deficient Neuro2a cells vs. amiodarone-treated control Neuro2a cells. To determine if the cell culture experiments have clin. relevance, we analyzed serum samples from amiodarone users. We found that in patient serum samples containing detectable amount of amiodarone there are elevated levels of the sterol precursors zymosterol, 8-DHC, and desmosterol. This study illustrates the need for close monitoring of blood biochem. during prolonged amiodarone use to minimize the risk of side effects.

ACS Chemical Neuroscience published new progress about Astrocyte. 434-16-2 belongs to class alcohols-buliding-blocks, and the molecular formula is C27H44O, COA of Formula: C27H44O.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Slominski, R. M.; Raman, C.; Elmets, C.; Jetten, A. M.; Slominski, A. T.; Tuckey, R. C. published the artcile< The significance of CYP11A1 expression in skin physiology and pathology>, SDS of cas: 434-16-2, the main research area is review CYP11A1 IL1 IL6 TNF alpha skin physiol pathol; CYP11A1; Corticosteroid biosynthesis; Hypothalamo-pituitaryadrenal axis; Lumisterol; Neuroendocrine functions of the skin; Secosteroids; Skin; Skin barrier function; Skin immune activity; Steroids.

A review. CYP11A1, a member of the cytochrome P 450 family, plays several key roles in the human body. It catalyzes the first and rate-limiting step in steroidogenesis, converting cholesterol to pregnenolone. Aside from the classical steroidogenic tissues such as the adrenals, gonads and placenta, CYP11A1 has also been found in the brain, gastrointestinal tract, immune systems, and finally the skin. CYP11A1 activity in the skin is regulated predominately by StAR protein and hence cholesterol levels in the mitochondria. However, UVB, UVC, CRH, ACTH, cAMP, and cytokines IL-1, IL-6 and TNFα can also regulate its expression and activity. Indeed, CYP11A1 plays several critical roles in the skin through its initiation of local steroidogenesis and specific metabolism of vitamin D, lumisterol, and 7-dehydrocholesterol. Products of these pathways regulate the protective barrier and skin immune functions in a context-dependent fashion through interactions with a number of receptors. Disturbances in CYP11A1 activity can lead to skin pathol.

Molecular and Cellular Endocrinology published new progress about Animal gene, CYP11A1 Role: BSU (Biological Study, Unclassified), PRP (Properties), BIOL (Biological Study). 434-16-2 belongs to class alcohols-buliding-blocks, and the molecular formula is C27H44O, SDS of cas: 434-16-2.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Kwon, Yu-Jin; Jang, Su-Nyeong; Liu, Kwang-Hyeon; Jung, Dong-Hyuk published the artcile< Effect of Korean red ginseng on cholesterol metabolites in postmenopausal women with hypercholesterolemia: a pilot randomized controlled trial>, SDS of cas: 434-16-2, the main research area is Korean red ginseng cholesterol postmenopause hypercholesterolemia; Korean red ginseng; cholesterol metabolism; menopause; sterols; women.

Korean red ginseng (KRG) is known to exert beneficial effects on cardiovascular health. Meanwhile, reduced estrogen at menopause has been shown to have various adverse impacts on cardiovascular risk factors, including blood lipids. The aim of this pilot study was to investigate the effect of KRG on cholesterol metabolites, which are surrogate markers of cholesterol absorption and biosynthesis, in postmenopausal women with hypercholesterolemia. The present study is an exploratory study which used data from a 4-wk, double-blinded, placebo-controlled clin. pilot study in 68 postmenopausal women with hypercholesterolemia. Patients received KRG (2 g) or placebo (2 g) once daily. The primary endpoints were changes in the levels of nine sterols. Serum sterols were analyzed using liquid chromatog.-mass spectrometry (LC-MS)/MS anal. Among the sterols, reduction in cholesterol level were significantly larger in the KRG group than in the placebo group (the changes: -148.3 ± 261.1 nmol/mL in the ginseng group vs. -23.0 ± 220.5 nmol/mL in the placebo group, p = 0.039). Addnl., changes in 7-hydroxycholesterol (7-OHC) were significantly larger in the KRG group than in the placebo group (the changes: -0.05 ± 0.09 nmol/mL in the ginseng group vs. -0.002 ± 0.1 nmol/mL in the placebo group, p = 0.047). Oxysterols, cholesterol derivates, have been known to play a role in chronic inflammation diseases such as cardiovascular diseases. KRG improves sterol metabolism by decreasing cholesterol and 7-OHC levels in postmenopausal women with hypercholesterolemia.

Nutrients published new progress about Bicycling. 434-16-2 belongs to class alcohols-buliding-blocks, and the molecular formula is C27H44O, SDS of cas: 434-16-2.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts