Genotoxic and cytotoxic effects of storax in vitro

2011 ◽  
Vol 29 (2) ◽  
pp. 181-186 ◽  
Author(s):  
Bulent Karadeniz ◽  
Zeynep Ulker ◽  
Lokman Alpsoy
Keyword(s):  
Cell Proliferation ◽  
Lactate Dehydrogenase ◽  
Cell Number ◽  
Test System ◽  
Inhibitory Effects ◽  
Genotoxic Effects ◽  
Cytotoxic Effects ◽  
Ldh Assay ◽  
Sce Test

The aim of this study is to investigate the effects of the storax balsam, which is a kind of sweet gum obtained from the Liquidambar orientalis Mill trees, on cell viability, cytotoxicity and genotoxicity in human lymphocyte in vitro. We studied the genotoxic effects of the extract of storax balsam (SE) using sister chromatid exchange (SCE) test system. Also the cytotoxic and inhibitory effects on cell proliferation of SE were evaluated using lactate dehydrogenase (LDH) assay and cell proliferation (WST-1) assay. The SCE frequency was increased when the cells were treated with 1.6 and 4.0 µg/mL SE concentrations ( p < 0.05). Moreover, treatment of the cells with the same concentrations significantly depleted the cell number at 24th and 48th hours and elevated the LDH levels ( p < 0.05) at 48th hour. These results suggest that SE can be used as an alternative antibacterial and antipathogenic agent due to its cytotoxic and genotoxic effects.

scholarly journals Alantolactone: A Natural Plant Extract as a Potential Therapeutic Agent for Cancer

2021 ◽  
Vol 12 ◽  
Author(s):  
Yuan Cai ◽  
Kewa Gao ◽  
Bi Peng ◽  
Zhijie Xu ◽  
Jinwu Peng ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Cancer Colorectal ◽  
Therapeutic Potential ◽  
Inhibitory Effects ◽  
Cytotoxic Effects ◽  
Cancer Breast ◽  
Anticancer Effects ◽  
Inula Helenium

Alantolactone (ALT) is a natural compound extracted from Chinese traditional medicine Inula helenium L. with therapeutic potential in the treatment of various diseases. Recently, in vitro and in vivo studies have indicated cytotoxic effects of ALT on various cancers, including liver cancer, colorectal cancer, breast cancer, etc. The inhibitory effects of ALT depend on several cancer-associated signaling pathways and abnormal regulatory factors in cancer cells. Moreover, emerging studies have reported several promising strategies to enhance the oral bioavailability of ALT, such as combining ALT with other herbs and using ALT-entrapped nanostructured carriers. In this review, studies on the anti-tumor roles of ALT are mainly summarized, and the underlying molecular mechanisms of ALT exerting anticancer effects on cells investigated in animal-based studies are also discussed.

Dechroming: An Alternative Treatment for Leather Shavings, to Obtain a Biocompatible Collagen without Environmental Impacts

2018 ◽  
Vol 930 ◽  
pp. 535-540
Author(s):  
Nelissa Garcia Balarim ◽  
Dalita Gomes Silva Morais Cavalcante ◽  
Andressa Silva Gomes ◽  
Flavio Camargo Cabrera ◽  
Aldo Eloizo Job
Keyword(s):  
Solid Waste ◽  
Hazardous Waste ◽  
Alternative Treatment ◽  
Scientific Literature ◽  
Test System ◽  
Leather Industry ◽  
Genotoxic Effects ◽  
Toxic Materials ◽  
Valuable Product

One of the biggest problems facing the leather industry is the production of solid waste with chromium. Dechroming process remove chrome from leather waste and it is designed to recover the value of collagen in the waste. Thus, the aim of this study was try to improve a methodology of dechroming process already described in the scientific literature, seeking to increase the percentage of dechroming ratio, as well as to evaluate the cytotoxic and genotoxic effects of the dechromed samples obtained from the leather residue for possible applications that require non-toxic materials based on collagens. As results, the dechroming process has been shown to be effective, with 99.29% of chromium removed from the shavings. In addition, it is possible to infer that the process of dechroming performed in this study was efficient in the neutralization step of hexavalent chromium and that the collagen from the leather residue did not shows cytotoxic and genotoxic effects for the evaluatedin vitrotest system. Therefore, this treatment allows to obtain a valuable product extracted from what was previously a hazardous waste.

scholarly journals Cyclic stretch attenuates effects of hyperoxia on cell proliferation and viability in human alveolar epithelial cells

2006 ◽  
Vol 291 (2) ◽  
pp. L166-L174 ◽  
Author(s):  
Ryan M. McAdams ◽  
Shamimunisa B. Mustafa ◽  
Jeffrey S. Shenberger ◽  
Patricia S. Dixon ◽  
Barbara M. Henson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Cell Injury ◽  
A549 Cells ◽  
Cell Number ◽  
Alveolar Epithelial Cells ◽  
Cyclic Stretch ◽  
Pulmonary Epithelium ◽  
Alveolar Epithelial

The treatment of severe lung disease often requires the use of high concentrations of oxygen coupled with the need for assisted ventilation, potentially exposing the pulmonary epithelium to both reactive oxygen species and nonphysiological cyclic stretch. Whereas prolonged hyperoxia is known to cause increased cell injury, cyclic stretch may result in either cell proliferation or injury depending on the pattern and degree of exposure to mechanical deformation. How hyperoxia and cyclic stretch interact to affect the pulmonary epithelium in vitro has not been previously investigated. This study was performed using human alveolar epithelial A549 cells to explore the combined effects of cyclic stretch and hyperoxia on cell proliferation and viability. Under room air conditions, cyclic stretch did not alter cell viability at any time point and increased cell number after 48 h compared with unstretched controls. After exposure to prolonged hyperoxia, cell number and [3H]thymidine incorporation markedly decreased, whereas evidence of oxidative stress and nonapoptotic cell death increased. The combination of cyclic stretch with hyperoxia significantly mitigated the negative effects of prolonged hyperoxia alone on measures of cell proliferation and viability. In addition, cyclic stretch resulted in decreased levels of oxidative stress over time in hyperoxia-exposed cells. Our results suggest that cyclic stretch, as applied in this study, can minimize the detrimental effects of hyperoxia on alveolar epithelial A549 cells.

scholarly journals Cytotoxic and genotoxic effects of the ent-kaurenoic acid and ent-kaurenoic acid enriched Mikania glomerata extract in V79

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Natália Ferreira ◽  
Arthur Ribeiro ◽  
Mariângela Morais ◽  
Aline Peixoto ◽  
Marcela Bernardino ◽  
...  
Keyword(s):  
Test System ◽  
Control Group ◽  
In Vitro Test ◽  
Genotoxic Effects ◽  
V79 Cells ◽  
Kaurenoic Acid ◽  
Biological Potential ◽  
Vitro Test ◽  
Mikania Glomerata

Abstract. Ferreira NH, Ribeiro AB, Morais MD, Peixoto AM, Bernardino MA, Moreira MR, Soares ACF, Heleno VCG, Veneziani RCS, Tavares DC. 2018. Cytotoxic and genotoxic effects of the ent-kaurenoic acid and ent-kaurenoic acid-enriched Mikania glomerata extract in V79. Biofarmasi J Nat Prod Biochem 17: xxxx. The ent-kaurenoic acid-rich extract from Mikania glomerata Sprengel was effective to inhibit the formation of Streptococcus mutans biofilm. In view of the biological potential of this extract and its major component, the present study was carried out to evaluate the safety of the ent-kaurenoic acid-rich extract from Mikania glomerata Sprengel and ent-kaurenoic acid alone in an in vitro test system. The results showed that the ent-kaurenoic acid-rich extract from Mikania glomerata Sprengel was cytotoxic at concentrations up to 40.0 μg/mL. Genotoxic effects were observed in cell cultures treated with the highest concentrations tested of ent-kaurenoic acid-rich extract from Mikania glomerata Sprengel (10.0 and 15.0 µg/mL) and ent-kaurenoic acid alone (2.5, 5.0 and 7.5 µg/mL) when compared to the control group. Therefore, the ent-kaurenoic acid-rich extract from Mikania glomerata Sprengel demonstrated cytotoxicity and genotoxicity effects at the highest concentrations tested, while ent-kaurenoic acid showed to be genotoxic at the same concentrations present in ent-kaurenoic acid-rich extract from Mikania glomerata Sprengel in V79 cells. These results demonstrate that the ent-kaurenoic acid should be responsible, at least in part, of the genotoxicity of ent-kaurenoic acid-rich extract from Mikania glomerata Sprengel.

scholarly journals ICT1 Knockdown inhibits osteosarcoma cell proliferation by regulating cell apoptosis through targeting BCL-2

2020 ◽  
Author(s):  
Xiaohui Pan ◽  
Jingxue Tan ◽  
Rui Du ◽  
Yuqing Jiang ◽  
Yiping Weng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Immunohistochemical Analysis ◽  
Osteosarcoma Cell ◽  
Inhibitory Effects ◽  
Mitochondrial Translation ◽  
Functional Studies ◽  
Translation Methods

Abstract Background Osteosarcoma (OS) which occurs mainly in the young people is a common malignant bone tumor. Apoptosis is a form of programmed and controlled cell death and promoting apoptosis of OS cells is an important treatment for OS. However, the pathways of controlling apoptosis in OS remain unclear. Immature colon carcinoma transcript-1 (ICT1) which is previously named DS-1 belongs to a family of four putative mitochondrial translation release factors. It controls the termination stage of translation. Methods In this study, the function of ICT1 was elucidated by a series of in vivo and in vitro assays. The potential downstream targets of ICT1 in the OS was identified by qRT-PCR and western blotting, while immunohistochemical analysis and rescue experiment were performed to confirm this result. Results ICT1 was upregulated in OS, and higher expression of ICT1 was associated with worse overall survival rate. Functional studies suggested that knockdown of ICT1 could inhibit OS cell proliferation in vitro or in vivo. In addition, suppression of ICT1 could promote apoptosis of OS cells. Furthermore, we demonstrated that BCL-2, apoptotic related-genes, is a potential target of ICT1 and BCL-2 overexpression partly reversed the inhibitory effects of ICT1 knockdown on the pro-tumorigenic properties of OS cells in vitro. Conclusion The ICT1 protein was overexpressed in the OS and has identified a novel mechanism by which ICT1 inhibits osteosarcoma cell proliferation by regulating cell apoptosis through targeting BCL-2.

Targeting CCR1 for the Treatment of Osteolytic Bone Disease in Multiple Myeloma.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2503-2503
Author(s):  
Sonia Vallet ◽  
Noopur Raje ◽  
MariaTeresa Fulciniti ◽  
Kenji Ishitsuka ◽  
Teru Hideshima ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Proliferation ◽  
Clinical Trials ◽  
Bone Disease ◽  
Cell Number ◽  
In Vivo Studies ◽  
Protective Effects ◽  
Osteolytic Bone Disease

Abstract Osteolytic bone disease (OBD) is a frequent complication of multiple myeloma (MM), affecting 70 to 80% of the patients. OBD is characterized by imbalanced bone remodeling, due to decreased osteoblast (OB) number and increased osteoclast (OC) formation and activity. MM cells secrete osteoclastogenic factors, such as receptor activator of nuclear factor kappa B ligand (RANKL) and CCL3. In turn, OC support MM cell proliferation and survival, thus promoting a positive feedback that exacerbates bone resorption. Chemokines modulate osteoclastogenesis and promote MM cell proliferation, in particular CCL3 and its receptor CCR1 play an important role in mediating OBD in MM. MLN3897 (Millennium Pharmaceuticals, Cambridge) is a novel small molecule specific antagonist of human CCR1 (IC50 0.8 nM). It has a favorable toxicity profile in healthy volunteers and is currently undergoing phase II clinical trials in rheumatoid arthritis and multiple sclerosis. Here we evaluate the effects of MLN3897 on OC function and activity, as well as OC-MM cell interactions. Our in vitro data demonstrates a dual mechanism of action for MLN3897: it inhibits osteoclastogenesis and also overcomes the protective effects conferred by OC on MM cells. Our data further shows inhibition of OC formation and function by 40 and 70%, respectively, following MLN3897 treatment. This is mediated via inhibition of the fusion process and is accompanied by downregulation of pERK and c-fos signaling. To analyze its effect on MM cells, we verified CCR1 and CCR5 expression levels on MM1.S (15% and 3.6%) and OPM1 (3.8 and 0.7%). Our data show that OC secrete high levels of CCL3 which triggers MM cell migration; and that MLN3897 abrogates these effects by inhibiting the PI3K/Akt pathway. Moreover, MLN3897 overcomes the proliferative advantage conferred by OC on MM cells, as demonstrated in INA6, MM1.S and MM patient derived primary cells. OC induced MM cell proliferation is mediated by adhesion and cytokine secretion, and MLN3897 abrogates both MM cell-to-OC adhesion and interleukin-6 (IL6) secretion by OC in a co-culture system, thereby resulting in decreased MM cell survival and proliferation. To confirm these in vitro results, in vivo studies in a SCID-hu mouse model are underway. Implanted SCID-Hu INA-6 bearing mice are treated with twice daily oral MLN3897 for 3 weeks. The evaluation of osteolytic lesions and OC, OB and endothelial cell number; and tumor burden will be presented. Our in vitro results therefore show novel biologic sequelae of CCL3 and its inhibition on both osteoclastogenesis and MM cell growth. Our in vivo experiments will further validate the role of CCR1 in a human BM microenvironment-MM model, providing the framework for clinical trials of MLN3897 for the treatment of OBD in MM.

scholarly journals The role of IGF1 on the differentiation of prolactin secreting cells in the mouse anterior pituitary

2009 ◽  
Vol 203 (2) ◽  
pp. 231-240 ◽  
Author(s):  
Tamiki Hikake ◽  
Shinji Hayashi ◽  
Taisen Iguchi ◽  
Tomomi Sato
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cells ◽  
Anterior Pituitary ◽  
Cell Number ◽  
Postnatal Period ◽  
Gh Cells ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

IGF1 knockout (IGF1KO) mice show a reduced number of prolactin (PRL) producing cells (PRL cells); however, the role of IGF1 in PRL cell proliferation and differentiation in immature mice is unclear. In this study, ontogenic changes in the percentages of PRL cells, GH producing cells (GH cells), and 5-bromo-2′-deoxyuridine (BrdU)-labeled cells in the anterior pituitary of male IGF1KO mice during the postnatal period were investigated. The percentage of PRL cells in IGF1KO mice was significantly lower at day 20 compared with that in wild-type (WT) mice, while GH cells in IGF1KO mice were significantly increased from day 10. From days 5 to 20, the percentage of BrdU-labeled cells in WT and IGF1KO mice was similar. PRL cells and GH cells are thought to originate from the same progenitor cells, therefore, PRL cells in IGF1KO mice are not able to differentiate because progenitor cells have already committed to be GH cells. However, IGF1, 17β-estradiol (E2), epidermal growth factor (EGF), or IGF1 plus E2 treatments increased the PRL cell number in the pituitaries in vitro of 10-day-old WT and IGF1KO mice. This fact suggests that these factors are involved in PRL cell proliferation and differentiation. In addition, the increase of PRL cells in IGF1KO mice stimulated by E2 or EGF was less than that of WT mice. Thus, IGF1 plays a crucial role in PRL cell proliferation and differentiation in mouse pituitaries by regulating the differentiation of progenitor cells and mediating the actions of E2 and EGF.

Effects of periodontal dressings on fibroblasts and gingival wound healing in dogs

2004 ◽  
Vol 52 (1) ◽  
pp. 33-46 ◽  
Author(s):  
M. Petelin ◽  
Z. Pavlica ◽  
Urška Batista ◽  
Draga Štiblar-Martinčič ◽  
U. Skalerič
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Inflammatory Reaction ◽  
Inhibitory Effect ◽  
The Other ◽  
Gingival Tissue ◽  
Histological Evaluation ◽  
Beagle Dogs ◽  
Inhibitory Effects

In the present study the effects of different commercially available periodontal dressings (Peripac, Barricaid, Fittydent, Reso-Pack and Myzotect-tincture) on fibroblast (V-79-379A) proliferation and survival were tested in vitro. Barricaid, Fittydent and Reso-Pack periodontal dressings have only small inhibitory effects on cell proliferation (83.3 ± 9%, 71.6 ± 8.7% and 87.3 ± 4.5% of control after 48 h, respectively) in comparison with the great inhibitory effect of Myzotect-tincture (2.9 ± 0.1%) and Peripac (33.7 ± 11.4%) (p < 0.001). Barricaid was the only dressing where 41% of cells survived after exposure, while the other four dressings killed all the cells in 6 days. In addition, the healing of artificially created gingival wounds covered by Barricaid and Reso-Pack was followed for 7 days in 12 Beagle dogs. Histological evaluation of gingival tissue demonstrated that wounds covered by Reso-Pack showed the best epithelisation and vascularity and the least inflammatory reaction in first 4days. Later the observed parameters were similar with those of wounds covered by Barricaid or without pack. The present results indicate that Peripac periodontal dressing and Myzotect-tincture showed the highest cytotoxicity to fibroblasts in vitro. From the histological observations in Beagle dogs Reso-Pack has been found to be the most suitable dressing, followed by Barricaid.

scholarly journals In vitro bioassessment of novel δ- carboline derivatives as an antiproliferative agent

2020 ◽  
Vol 11 (3) ◽  
pp. 3563-3568
Author(s):  
Chandrasekar MJN ◽  
Raman Rajeshkumar ◽  
Arivukkarasi Varadharajan
Keyword(s):  
Anticancer Agents ◽  
Preliminary Analysis ◽  
Cell Number ◽  
Damage Analysis ◽  
Srb Assay ◽  
Cytotoxic Effects ◽  
Antiproliferative Agent ◽  
Noticeable Reduction ◽  
Hct116 Cells

Several carboline derivatives are anticancer agents and studied for antiproliferative action against various cancer cells. Based on the preliminary analysis using insilico strategies, we have selected eight compounds for the study. All compounds have been synthesised and characterised for their purity and chemical composition. Antiproliferative activity was assessed by insilico Carcinogenicity assay, Cytotoxicity analysis by sulphorhodamine B, Antiproliferation assay and DNA damage analysis. The cytotoxic effects of the CH5, CH17, CH29, CH34, CH37, CH39, CH42 and CH47 on Vero, HeLa, A549, BRL3A, HCT116, and MCF7 were determined using the SRB assay. CH5, CH34, CH37 and CH42 was the most potent cytotoxic towards HCT116 cells with CTC50 value of 62.1±0.19, 47.1±0.41, 78.5±1.26 and 32.1±1.11 µg/ml respectively. The assay revealed a noticeable reduction in cell number for CH5 and CH37 tested except CH34 and CH42. CH5 and CH37 observed cytotoxic effects were found to destroy the cells according to time, and cell viability decreased with that time length. To learn their role in cell death, CH5 and CH37 were therefore taken up for a further screening. This study suggested that CH5 and CH37 had a separate mechanism of action to kill and that in the cell line. Such results will provide enrichment of scientific knowledge on the molecular mechanism and target therapies of CH5 and CH37, thereby potentially helpful for patients with Colon cancer.

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