Yerba mate (Ilex paraguariensis) inhibits lymphocyte activation in vitro

2016 ◽  
Vol 7 (11) ◽  
pp. 4556-4563 ◽  
Author(s):  
Maider Muñoz-Culla ◽  
Matías Sáenz-Cuesta ◽  
Maier J. Guereca-Barandiaran ◽  
Marcelo L. Ribeiro ◽  
David Otaegui
Keyword(s):  
Cell Viability ◽  
Lymphocyte Activation ◽  
Ilex Paraguariensis ◽  
Yerba Mate ◽  
Dependent Manner ◽  
Dose Dependent

In the presence of yerba mate lymphocyte activation is reduced without affecting cell viability in a dose-dependent manner.

scholarly journals Effects of ambient particulate matter on a reconstructed human corneal epithelium model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ryota Ko ◽  
Masahiko Hayashi ◽  
Miho Tanaka ◽  
Tomoaki Okuda ◽  
Chiharu Nishita-Hara ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Cell Viability ◽  
Corneal Epithelium ◽  
Dependent Manner ◽  
Ambient Particulate Matter ◽  
Tissue Sections ◽  
Human Corneal Epithelium ◽  
Vitro Model ◽  
Dose Dependent

AbstractWe evaluated the effects of ambient particulate matter (PM) on the corneal epithelium using a reconstructed human corneal epithelium (HCE) model. We collected two PM size fractions [aerodynamic diameter smaller than 2.4 µm: PM0.3–2.4 and larger than 2.4 µm: PM>2.4] and exposed these tissues to PM concentrations of 1, 10, and 100 µg/mL for 24 h. After exposure, cell viability and interleukin (IL) IL-6 and IL-8 levels were determined, and haematoxylin and eosin and immunofluorescence staining of the zonula occludens-1 (ZO-1) were performed on tissue sections. In addition, the effects of a certified reference material of urban aerosols (UA; 100 µg/mL) were also examined as a reference. The viability of cells exposed to 100 μg/mL UA and PM>2.4 decreased to 76.2% ± 7.4 and 75.4% ± 16.1, respectively, whereas PM0.3–2.4 exposure had a limited effect on cell viability. These particles did not increase IL-6 and IL-8 levels significantly even though cell viability was decreased in 100 μg/mL UA and PM>2.4. ZO-1 expression was reduced in a dose-dependent manner in all groups. Reconstructed HCE could be used as an in vitro model to study the effects of environmental PM exposure on ocular surface cell viability and inflammation.

scholarly journals The Olive Leaves Extract Has Anti-Tumor Effects against Neuroblastoma through Inhibition of Cell Proliferation and Induction of Apoptosis

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2178
Author(s):  
Fabio Morandi ◽  
Veronica Bensa ◽  
Enzo Calarco ◽  
Fabio Pastorino ◽  
Patrizia Perri ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Cell Cycle Progression ◽  
Treatment Strategies ◽  
Annexin V ◽  
Dependent Manner ◽  
Induction Of Apoptosis ◽  
Dose Dependent

Neuroblastoma (NB) is the most common extra-cranial solid tumor of pediatric age. The prognosis for high-risk NB patients remains poor, and new treatment strategies are desirable. The olive leaf extract (OLE) is constituted by phenolic compounds, whose health beneficial effects were reported. Here, the anti-tumor effects of OLE were investigated in vitro on a panel of NB cell lines in terms of (i) reduction of cell viability; (ii) inhibition of cell proliferation through cell cycle arrest; (iii) induction of apoptosis; and (iv) inhibition of cell migration. Furthermore, cytotoxicity experiments, by combining OLE with the chemotherapeutic topotecan, were also performed. OLE reduced the cell viability of NB cells in a time- and dose-dependent manner in 2D and 3D models. NB cells exposed to OLE underwent inhibition of cell proliferation, which was characterized by an arrest of the cell cycle progression in G0/G1 phase and by the accumulation of cells in the sub-G0 phase, which is peculiar of apoptotic death. This was confirmed by a dose-dependent increase of Annexin V+ cells (peculiar of apoptosis) and upregulation of caspases 3 and 7 protein levels. Moreover, OLE inhibited the migration of NB cells. Finally, the anti-tumor efficacy of the chemotherapeutic topotecan, in terms of cell viability reduction, was greatly enhanced by its combination with OLE. In conclusion, OLE has anti-tumor activity against NB by inhibiting cell proliferation and migration and by inducing apoptosis.

scholarly journals MYD88 L265P Mutations Influence Clinical Outcome and Identify a Pathway for Targeted Inhibition in Chronic Lymphocytic Leukemia

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 491-491
Author(s):  
Bethany Tesar ◽  
Reina Improgo ◽  
Josephine L. Klitgaard ◽  
Reuma Magori-Cohen ◽  
Lijian Yu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Clinical Outcome ◽  
Cell Viability ◽  
Clinical Characteristics ◽  
Dependent Manner ◽  
Myd88 Signaling ◽  
Dose Dependent ◽  
Myd88 Pathway ◽  
Myd88 L265p

Abstract The L265P somatic mutation in the Myeloid Differentiation Primary Response 88 (MYD88) gene is recurrently observed in CLL; although this mutation has been demonstrated to have functional effects in multiple hematologic malignancies, its role in CLL is largely unknown. To address this gap in knowledge, we examined the clinical and biological impact of MYD88 L265P mutations in CLL by analysis of gene expression, cell viability and Toll-like Receptor 9 (TLR9)-induced signaling and cytokine production. Out of 160 CLL patient samples subjected to whole-exome sequencing and previously reported by our group, 10 were found to harbor MYD88 L265P mutations, all of which possessed mutated immunoglobulin heavy chain variable (IGHV) regions (p = 0.006). While IGHV mutated patients are generally known to exhibit better prognosis compared to IGHV unmutated patients, the presence of MYD88 L265P within the IGHV mutated subset was associated with earlier age of disease onset (p = 0.04) and worse overall survival (OS; p = 0.00017), comparable to IGHV unmutated samples with wild-type (WT) MYD88. No association with the presence of chromosome 13q deletions (p = 0.26) or prior treatment at the time of sampling (p = 0.10) was observed. Gene expression microarray analysis restricted to the IGHV mutated subset (MYD88 WT: n = 76; MYD88 L265P: n=10) and conducted using a PAM-based approach demonstrated that MYD88 L265P mutation was associated with differential expression of 28 genes, whose expression was then examined across all CLL samples with available gene expression data (n = 150). Using Cox modeling, a composite gene signature score was determined for each patient, who were subsequently dichotomized based on median signature. This method was able to predict both OS and event free survival (EFS) in a univariable analysis (OS: p = 1.2E-06; EFS: p = 7.6E-13). Statistical significance was maintained when a multivariable analysis was conducted, adjusting for known CLL risk factors including age, IGHV status, ZAP70 expression, cytogenetics and prior treatment (p < 0.0001 for OS and EFS). The univariable (OS: p = 1.6E-05; EFS: p = 5.7E-10) and multivariable findings (p < 0.003 for OS and EFS) were further confirmed in an independent validation cohort (n = 87). To identify a more parsimonious gene set, we applied a L1 penalized proportional hazards model to the discovery and validation cohorts, separately. This approach identified 5 overlapping genes (BCAT1, BMP6, CHAD, IKZF2, and TRIO) between the two cohorts that appear to be the main drivers of the predictive signature. To inhibit MYD88 signaling in CLL cells, we treated MYD88 L265P and WT cells (n = 6/group, matched for clinical characteristics: IGHV, ZAP70, cytogenetic, and treatment status) in vitro with a highly-selective small molecule IRAK4 inhibitor, ND-2158 (Nimbus Therapeutics). ND-2158 significantly reduced cell viability in a dose dependent manner in both MYD88 WT and L265P primary CLL cells, either alone or in combination with a fixed concentration of the B-cell receptor (BCR) pathway inhibitor, ibrutinib. The TLR9 agonist CpG was used to stimulate signaling through the MYD88 pathway in vitro. ND-2158 inhibition of CpG-induced IRAK4 activation in CLL cells (n = 3/group, matched for clinical characteristics) blocked IRAK1 and IκBα degradation and led to a dose-dependent decrease in the ratio of phospho/total proteins. No significant differences were noted between MYD88 WT and L265P samples, consistent with our cell viability results. CLL-secreted levels of IL-6, IL-10 and CCL3 were measured in culture supernatants treated with ND-2158+/- CpG stimulation (n = 4/group, matched for clinical characteristics). CpG stimulated cytokine levels (p < 0.0001 for all cytokines+/- CpG) were significantly inhibited in a dose-dependent manner by ND-2158. Again, no significant differences were observed between MYD88 WT and L265P CLL with respect to cytokine production, either at baseline or in CpG-stimulated DMSO treated control cells. In conclusion, the differences in clinical outcome and gene expression observed between MYD88 WT and L265P IGHV mutated CLLs indicate a functional role for MYD88 L265P in CLL. The inferior clinical outcome in IGHV mutated CLL with L265P mutation suggests that MYD88 signaling may be a relevant target in CLL. ND-2158 inhibits signaling in the MYD88 pathway, suggesting potential therapeutic utility of IRAK4 inhibitors in CLL. Disclosures Chaudhary: Nimbus Therapeutics: Equity Ownership. Miao:Nimbus Therapeutics: Employment. Westlin:Nimbus Therapeutics: Employment.

scholarly journals Nicotinamide N-methyltransferase catalyses the N-methylation of the endogenous β-carboline norharman: evidence for a novel detoxification pathway

2016 ◽  
Vol 473 (19) ◽  
pp. 3253-3267 ◽  
Author(s):  
Martin G. Thomas ◽  
Davide Sartini ◽  
Monica Emanuelli ◽  
Matthijs J. van Haren ◽  
Nathaniel I. Martin ◽  
...  
Keyword(s):  
Cell Viability ◽  
Dependent Manner ◽  
Methyltransferase Activity ◽  
Cellular Processes ◽  
Specificity Constant ◽  
Expression Model ◽  
Dose Dependent ◽  
Detoxification Pathway ◽  
Time Point

Nicotinamide N-methyltransferase (NNMT) is responsible for the N-methylation of nicotinamide to 1-methylnicotinamide. Our recent studies have demonstrated that NNMT regulates cellular processes fundamental to the correct functioning and survival of the cell. It has been proposed that NNMT may possess β-carboline (BC) N-methyltransferase activity, endogenously and exogenously produced pyridine-containing compounds which, when N-methylated, are potent inhibitors of Complex I and have been proposed to have a role in the pathogenesis of Parkinson's disease. We have investigated the ability of recombinant NNMT to N-methylate norharman (NH) to 2-N-methylnorharman (MeNH). In addition, we have investigated the toxicity of the BC NH, its precursor 1,2,3,4-tetrahydronorharman (THNH) and its N-methylated metabolite MeNH, using our in vitro SH-SY5Y NNMT expression model. Recombinant NNMT demonstrated NH 2N-methyltransferase activity, with a Km of 90 ± 20 µM, a kcat of 3 × 10−4 ± 2 × 10−5 s−1 and a specificity constant (kcat/Km) of 3 ± 1 s−1 M−1. THNH was the least toxic of all three compounds investigated, whereas NH demonstrated the greatest, with no difference observed in terms of cell viability and cell death between NNMT-expressing and non-expressing cells. In NNMT-expressing cells, MeNH increased cell viability and cellular ATP concentration in a dose-dependent manner after 72 and 120 h incubation, an effect that was not observed after 24 h incubation or in non-NNNT-expressing cells at any time point. Taken together, these results suggest that NNMT may be a detoxification pathway for BCs such as NH.

scholarly journals Modulation of Synthetic Tracheal Grafts with Extracellular Matrix Coatings

2021 ◽  
Vol 8 (8) ◽  
pp. 116
Author(s):  
Lumei Liu ◽  
Sayali Dharmadhikari ◽  
Robert A. Pouliot ◽  
Michael M. Li ◽  
Peter M. Minneci ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Extracellular Matrix ◽  
Cell Viability ◽  
Dependent Manner ◽  
Orthotopic Implantation ◽  
Synthetic Scaffolds ◽  
Cell Biocompatibility ◽  
Dose Dependent

Synthetic scaffolds for the repair of long-segment tracheal defects are hindered by insufficient biocompatibility and poor graft epithelialization. In this study, we determined if extracellular matrix (ECM) coatings improved the biocompatibility and epithelialization of synthetic tracheal grafts (syn-TG). Porcine and human ECM substrates (pECM and hECM) were created through the decellularization and lyophilization of lung tissue. Four concentrations of pECM and hECM coatings on syn-TG were characterized for their effects on scaffold morphologies and on in vitro cell viability and growth. Uncoated and ECM-coated syn-TG were subsequently evaluated in vivo through the orthotopic implantation of segmental grafts or patches. These studies demonstrated that ECM coatings were not cytotoxic and, enhanced the in vitro cell viability and growth on syn-TG in a dose-dependent manner. Mass spectrometry demonstrated that fibrillin, collagen, laminin, and nephronectin were the predominant ECM components transferred onto scaffolds. The in vivo results exhibited similar robust epithelialization of uncoated and coated syn-TG patches; however, the epithelialization remained poor with either uncoated or coated scaffolds in the segmental replacement models. Overall, these findings demonstrated that ECM coatings improve the seeded cell biocompatibility of synthetic scaffolds in vitro; however, they do not improve graft epithelialization in vivo.

scholarly journals RETRACTED ARTICLE: Titanium particles damage osteocytes and inhibit osteoblast differentiation

2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Li Chen ◽  
Ziyue Wang ◽  
Wei Xu ◽  
Qirong Dong
Keyword(s):  
Cell Viability ◽  
Osteoblast Differentiation ◽  
Cell Counting ◽  
Cell Contact ◽  
Dependent Manner ◽  
Retracted Article ◽  
Ti Particles ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Abstract Purposes to study the effect of titanium particles on MLO-Y4 and the effects of osteocytes alterations on osteoblasts. Methods cultured MLO-Y4 osteocytes were exposed to different concentrations of titanium (Ti) particles, cell viability was measured using the Cell Counting Kit-8 (CCK-8) assay, apoptosis of MLO-Y4 cells was evaluated by flow cytometry, Real-time PCR quantification of mRNA expression of SOST, at the same time with Western Blot detection sclerosteosis protein expression levels.MC3T3-E1 cells culture with MLO-Y4 cells exposed to different concentrations of titanium (Ti) particles in vitro, in order to detection of osteoblast osteogenetic activity. Results Our results showed that Ti particles inhibited cell viability of MLO-Y4 osteocytes in a dose-dependent manner. Incubation with Ti particles caused apoptosis of MLO-Y4cells.Treatment with Ti particles significantly increased expression of the osteocytic marker SOST/sclerostin. Furthermore, treatment of MLO-Y4 cells with Ti particles produced a dose-dependent decrease in ALP activity and decreased mineralization of MC3T3-E1 cells through direct cell-cell contact. Conclusions Titanium particles damage osteocytes and inhibit osteoblast differentiation.

scholarly journals In Vitro Analysis of Antioxidant, Anticancer, and Bioactive Components of Apocynum venetum Tea Extracts

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Chong Li ◽  
Guangbin Huang ◽  
Fang Tan ◽  
Xianrong Zhou ◽  
Jianfei Mu ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Viability ◽  
Hepg2 Cells ◽  
Dependent Manner ◽  
Human Hepatoma ◽  
Bioactive Components ◽  
Human Embryonic Kidney ◽  
Apocynum Venetum ◽  
Dose Dependent

The dry leaf of Apocynum venetum tea extracts (AVTEs) belonging to the Apocynaceae family is a traditional Chinese medicine. The aim of this study is to identify the bioactive components of AVTE and analyse its antioxidant and anticancer activity in vitro. Method. Flavones and polyphenols in AVTE were determined by high-performance liquid chromatography (HPLC) assay. The scavenging capacity of tea extracts to 1,1-diphenyl-2-picrylhydrazyl (DPPH); 2,2′-azino-bis-(3-ethylbenzthiazoline-6-sulfonic acid) diammonium salt (ABTS); hydroxyl (OH); and superoxide anion-free radicals were investigated by spectrophotometry. We also detailed the cytotoxicity assay of AVTE (50, 100, and 200 μg/mL) to human embryonic kidney 293T cells, the protective effect of AVTE on 293T cells induced by hydrogen peroxide (0.3 mmol/L), and the anticancer effect against the human hepatoma HepG2 cells via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. We investigated the antioxidative effects of AVTE in human embryonic kidney 293T cells and the anticancer mechanism in HepG2 human hepatoma cells via quantitative real-time reverse transcription-polymerase chain reaction (RT-qPCR) assay. Results. HPLC analysis showed that AVTEs contain neochlorogenic acid, chlorogenic acid, rutin, isoquercetin, isochlorogenic acid B, astragalin, isochlorogenic acid C, rosmarinic acid, quercetin, and trans-cinnamic acid. These extracts have high antioxidant activity and dose-dependent relation through free radical scavenging experiments. The cell viability of 293T cells treated with hydrogen peroxide (0.3 mmol/L) was significantly lower than that of normal cells, and the cell viability of oxidatively stressed 293T cells after AVTE (50, 100, and 200 μg/mL) treatment was significantly improved (P<0.05). Moreover, cytotoxicity experiments showed that the survival rate of 293T cells was over 90%, but the proliferation of HepG2 cells was significantly inhibited in a dose-dependent manner by AVTE. Furthermore, cytoprotective effects in 293T cells were induced via upregulation of glutathione peroxidase (GSH-Px), GSH, superoxide dismutase (SOD), and catalase (CAT) antioxidant-related factors, as well as apoptosis in HepG2 cells was induced via upregulation of caspase-3, caspase-9, p21, and p53 apoptosis-associated factors, as assessed via mRNA expression levels after treatment with AVTE, which were consistent with the results of antioxidant gene detections. As a conclusion, AVTE appears to be an effectively functional drink, due to its rich functional components and antioxidant and anticancer activities.

scholarly journals INVESTIGATION ON PHARMACOGNOSY OF KATHA POWDER AS WELL AS IT’S IN VITRO CYTOTOXIC ACTIVITY

2021 ◽  
pp. 133-140
Author(s):  
PANKAJ SHARMA
Keyword(s):  
Cell Viability ◽  
Cytotoxic Activity ◽  
Cell Lines ◽  
Hepg2 Cells ◽  
Trypan Blue ◽  
Dependent Manner ◽  
Colorimetric Assays ◽  
Dose Dependent ◽  
Mcf 7

Objective: The present study delves into the investigation of quantitative phytochemical in Katha powder, and it is in vitro cytotoxic activity. Methods: Coarsely dried chips of Acacia catechu heartwood were treated with a 10% hydro-alcoholic solution to obtain Katha as the final product. The powdered Katha was standardized through pharmacognostic parameters. Phytochemical investigations were carried out to screen polyphenols (tannins and flavonoids) of interest which later were confirmed by thin-layer chromatography. The cytotoxicity effect of Katha powder on MCF-7, A431, and HepG2 cells was characterized by the trypan blue dye exclusion and MTT colorimetric assays technique. Control assay was carried out for samples containing only the appropriate volumes of blank solutions and showed no effect on cell growth. Different cells were exposed to Katha powder for about 48 h and performed cytotoxicity assays. The effect of Katha powder against these cell lines concentration range 10–100 μg/ml showed a decrease in percent cell viability in a dose-dependent manner, as compared with that of the control when examined by the trypan blue exclusion assay technique and MTT colorimetric assays technique. Results: Quantitative phytochemical investigations were showed that Katha is rich in the content of polyphenols (tannins and flavonoids) and having good pharmacological potential. The effect of Katha powder against these cell lines concentration range 10–100 μg/ml showed a decrease in percent cell viability in a dose-dependent manner. Conclusion: So from this investigation it is to be suggested that the Katha powder is rich in the phenolic compound and shows a good anticancer effect against MCF-7, A431, and HepG2 cells.

scholarly journals Probucol enhances the therapeutic efficiency of mesenchymal stem cells in the treatment of erectile dysfunction in diabetic rats by prolonging their survival time via Nrf2 pathway

2020 ◽  
Author(s):  
Haoran Wang ◽  
Keqin Zhang ◽  
Zheng Ruan ◽  
Dingqi Sun ◽  
Hui Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Cell Viability ◽  
Survival Time ◽  
Western Blotting ◽  
Dependent Manner ◽  
Nrf2 Pathway ◽  
Therapeutic Efficiency ◽  
Dose Dependent

Abstract Background: Intracavernous injection of mesenchymal stem cells (MSCs) is a promising method for Diabetic mellitus-induced erectile dysfunction (DMED), but short survival time of MSCs in cavernous is fatal defect for therapy. This study investigated therapeutic efficiency and potential mechanism of probucol combined with MSCs. Methods: In vivo study, total forty-eight 10-week-old male Sprague-Dawley (SD) rats were used in this study. Twelve rats received intraperitoneal injection of PBS as Sham Group; the rest received intraperitoneal injection of 60mg/kg streptozotocin to establish DM models. DM rats were randomly divided into three groups: received intracavernosal (IC) injection of either PBS (DM Group), MSCs (M Group), and administrated probucol after intracavernosal injection of MSCs (P+M Group). Erectile function was assessed by electrical stimulation of the cavernous nerves with real-time intracavernous pressure measurement. After euthanasia, penile tissue was investigated for histologic examination and Western blotting. In vitro experiment, H2O2 was used to create oxidative stress environment to detect changes in cell viability. CCK8 was used to measure cell viability of MSCs treated with or without probucol. Intracellular ROS changes were detected by flow cytometry. Autophagy and apoptosis were detected by Western blotting and confocal microscopy.Results: Recovery of erectile function was observed in the P+M Group. The combination therapy decreased fibrosis and increased endothelial function compared with MSCs therapy alone. Western blotting results confirmed the increased expression of Nrf2 and HO-1 in cavernous body. H2O2 induced high oxidative stress and reduced cell viability in vitro, which was gradually reversed with increased concentration of probucol. H2O2 reduced Nrf2 expression, which was reversed by probucol's intervention. Furthermore, the expression of Bax, Caspase3 and Cleaved-Caspase3 decreased, and the expression of Bcl-2 increased in a dose-dependent manner because of probucol's intervention. In addition, Beclin1 and LC3II both increased in a dose-dependent manner. Meanwhile, the expression of P62 decreased. In study of autophagy flux, we found probucol didn’t block it. Conclusion: Probucol enhanced therapeutic efficiency of MSCs in DMED by prolonging their survival time, which mediated through improving the transplanted microenvironment of MSCs, increasing self-antioxidant ability of MSCs, strengthening protective autophagy and inhibiting apoptosis of MSCs via Nrf2 pathway.

Oxygenation of 18-hydroxycorticosterone as the final reaction for aldosterone biosynthesis

1984 ◽  
Vol 107 (3) ◽  
pp. 395-400 ◽  
Author(s):  
Itaru Kojima ◽  
Etsuro Ogata ◽  
Hiroshi Inano ◽  
Bun-ichi Tamaoki
Keyword(s):  
Carbon Monoxide ◽  
Hydroxysteroid Dehydrogenase ◽  
Dependent Manner ◽  
In Vitro Production ◽  
Mitochondrial Preparation ◽  
Final Reaction ◽  
Vitro Production ◽  
Dose Dependent ◽  
Cytochrome P 450

Abstract. Incubation of 18-hydroxycorticosterone with the sonicated mitochondrial preparation of bovine adrenal glomerulosa tissue leads to the production of aldosterone, as measured by radioimmunoassay. The in vitro production of aldosterone from 18-hydroxycorticosterone requires both molecular oxygen and NADPH, and is inhibited by carbon monoxide. Cytochrome P-450 inhibitors such as metyrapone, SU 8000. SU 10603, SKF 525A, amphenone B and spironolactone decrease the biosynthesis of aldosterone from 18-hydroxycorticosterone. These results support the conclusion that the final reaction in aldosterone synthesis from 18-hydroxycorticosterone is catalyzed by an oxygenase, but not by 18-hydroxysteroid dehydrogenase. By the same preparation, the production of [3H]aldosterone but not [3H]18-hydroxycorticosterone from [1,2-3H ]corticosterone is decreased in a dose-dependent manner by addition of non-radioactive 18-hydroxycorticosterone.

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