scholarly journals In Vitro Assessment of the Impact of Nickel on the Viability and Steroidogenesis in the Human Adrenocortical Carcinoma (NCI-H295R) Cell Line

2020 ◽  
pp. 871-883
Author(s):  
Norbert LUKAC ◽  
Z FORGACS ◽  
H DURANOVA ◽  
T JAMBOR ◽  
J ZEMANOVA ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Line ◽  
Adrenocortical Carcinoma ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Cytotoxic Action ◽  
Disruptive Effect ◽  
17Β Estradiol ◽  
The Impact

Nickel is a ubiquitous environmental pollutant, which has various effects on reproductive endocrinology. In this study, human adrenocortical carcinoma (NCI-H295R) cell line was used as an in vitro biological model to study the effect of nickel chloride (NiCl2) on the viability and steroidogenesis. The cells were exposed to different concentrations (3.90; 7.80; 15.60; 31.20; 62.50; 125; 250 and 500 μM) of NiCl2 and compared with control group (culture medium without NiCl2). The cell viability was measured by the metabolic activity assay. Production of sexual steroid hormones was quantified by enzyme linked immunosorbent assay. Following 48 h culture of the cells in the presence of NiCl2 a dose-dependent depletion of progesterone release was observed even at the lower concentrations. In fact, lower levels of progesterone were detected in groups with higher doses (≥125 μM) of NiCl2 (P<0.01), which also elicited cytotoxic action. A more prominent decrease in testosterone production (P<0.01) was also noted in comparison to that of progesterone. On the other hand, the release of 17β-estradiol was substantially increased at low concentrations (3.90 to 62.50 μM) of NiCl2. The cell viability remained relatively unaltered up to 125 μM (P>0.05) and slightly decreased from 250 μM of NiCl2 (P<0.05). Our results indicate endocrine disruptive effect of NiCl2 on the release of progesterone and testosterone in the NCI-H295R cell line. Although no detrimental effect of NiCl2 (≤62.50 μM) could be found on 17β-estradiol production, its toxicity may reflect at other points of the steroidogenic pathway.

scholarly journals The Effects of Three Chlorhexidine-Based Mouthwashes on Human Osteoblast-Like SaOS-2 Cells. An In Vitro Study

2021 ◽  
Vol 22 (18) ◽  
pp. 9986
Author(s):  
Giulia Brunello ◽  
Kathrin Becker ◽  
Luisa Scotti ◽  
Dieter Drescher ◽  
Jürgen Becker ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cetylpyridinium Chloride ◽  
Control Cell ◽  
In Vitro Study ◽  
Control Group ◽  
Sterile Saline ◽  
Lack Of Information ◽  
And Control ◽  
The Impact

Several decontamination methods for removing biofilm from implant surfaces during surgical peri-implantitis treatment have been reported, including the intraoperative usage of chlorhexidine (CHX)-based antiseptics. There is a lack of information on possible adverse effects on bone healing. The study aimed to examine the impact of three CHX-based mouthwashes on osteoblast-like cells (SaOS-2) in vitro. Cells were cultured for three days in 96-well binding plates. Each well was randomly treated for either 30, 60 or 120 s with 0.05% CHX combined with 0.05% cetylpyridinium chloride (CPC), 0.1% CHX, 0.2% CHX or sterile saline (NaCl) as control. Cell viability, cytotoxicity and apoptosis were assessed at day 0, 3 and 6. Cell viability resulted in being higher in the control group at all time points. At day 0, the CHX 0.2 group showed significantly higher cytotoxicity values compared to CHX 0.1 (30 s), CHX + CPC (30 s, 60 s and 120 s) and control (60 s and 120 s), while no significant differences were identified between CHX + CPC and both CHX 0.1 and NaCl groups. All test mouthwashes were found to induce apoptosis to a lower extent compared to control. Results indicate that 0.2% CHX presented the highest cytotoxic effect. Therefore, its intraoperative use should be carefully considered.

scholarly journals Human Adenovirus Serotype 3 Infection Modulates the Biogenesis and Composition of Lung Cell-Derived Extracellular Vesicles

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Ayodeji O. Ipinmoroti ◽  
Brennetta J. Crenshaw ◽  
Rachana Pandit ◽  
Sanjay Kumar ◽  
Brian Sims ◽  
...  
Keyword(s):  
Cell Viability ◽  
Extracellular Vesicles ◽  
Hemorrhagic Cystitis ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
A549 Cells ◽  
Control Group ◽  
Epithelial Cell Line ◽  
The Impact

Adenovirus (Ad) is a major causal agent of acute respiratory infections. However, they are a powerful delivery system for gene therapy and vaccines. Some Ad serotypes antagonize the immune system leading to meningitis, conjunctivitis, gastroenteritis, and/or acute hemorrhagic cystitis. Studies have shown that the release of small, membrane-derived extracellular vesicles (EVs) may offer a mechanism by which viruses can enter cells via receptor-independent entry and how they influence disease pathogenesis and/or host protection considering their existence in almost all bodily fluids. We proposed that Ad3 could alter EV biogenesis, composition, and trafficking and may stimulate various immune responses in vitro. In the present study, we evaluated the impact of in vitro infection with Ad3 vector on EV biogenesis and composition in the human adenocarcinoma lung epithelial cell line A549. Cells were infected in an exosome-free media at different multiplicity of infections (MOIs) and time points. The cell viability was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and fluorometric calcein-AM. EVs were isolated via ultracentrifugation. Isolated EV proteins were quantified and evaluated via nanoparticle tracking, transmission electron microscopy, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and immunoblotting assays. The cell viability significantly decreased with an increase in MOI and incubation time. A significant increase in particle mean sizes, concentrations, and total EV protein content was detected at higher MOIs when compared to uninfected cells (control group). A549 cell-derived EVs revealed the presence of TSG101, tetraspanins CD9 and CD63, and heat shock proteins 70 and 100 with significantly elevated levels of Rab5, 7, and 35 at higher MOIs (300, 750, and 1500) when compared to the controls. Our findings suggested Ad3 could modulate EV biogenesis, composition, and trafficking which could impact infection pathogenesis and disease progression. This study might suggest EVs could be diagnostic and therapeutic advancement to Ad infections and other related viral infections. However, further investigation is warranted to explore the underlying mechanism(s).

scholarly journals Klotho Alleviates Lung Injury Caused by Paraquat via Suppressing ROS/P38 MAPK-Regulated Inflammatory Responses and Apoptosis

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Zhiqiang Zhang ◽  
Qing Nian ◽  
Gang Chen ◽  
Shuqing Cui ◽  
Yuzhen Han ◽  
...  
Keyword(s):  
Lung Injury ◽  
Cell Viability ◽  
P38 Mapk ◽  
Inflammatory Responses ◽  
A549 Cells ◽  
Control Group ◽  
Ros Production ◽  
The Impact

Acute lung injury (ALI) induced by paraquat (PQ) progresses rapidly with high mortality; however, there is no effective treatment, and the specific mechanism is not well understood. The antiaging protein klotho (KL) has multiple functions and exerts significant influences on various pathophysiological processes. This work evaluated the impact of KL on PQ-induced ALI and investigated its underlying mechanisms. As for in vivo research, C57BL/6 mice were treated with PQ (30 mg/kg) intraperitoneal (IP) injection to create a toxicity model of ALI (PQ group). The mice were divided into control group, KL group, PQ group, and PQ+KL group. For in vitro experiment, A549 cells were incubated with or without KL and then treated in the presence or absence of PQ for 24 h. In vivo result indicated that KL reduced the mortality, reduced IL-1β and IL-6 in the bronchoalveolar lavage fluid (BALF), attenuated ALI, and decreased apoptosis in situ. In vitro result revealed that KL significantly improved cell viability, reduced the levels of IL-1β and IL-6 in culture supernatants, suppressed cell apoptosis, inhibited caspase-3 activation, and enhanced mitochondrial membrane potential (ΔΨm) after PQ treatment. Besides, KL effectively abated reactive oxygen species (ROS) production, improved GSH content, and lowered lipid peroxidation in PQ-exposed A549 cells. Further experiments indicated that phosphorylated JNK and P38 MAPK was increased after PQ treatment; however, KL pretreatment could significantly lower the phosphorylation of P38 MAPK. Suppression of P38 MAPK improved cell viability, alleviated inflammatory response, and reduced apoptosis-related signals; however, it had no obvious effect on the production of ROS. Treatment with N-acetylcysteine (NAC), a classic ROS scavenger, could suppress ROS production and P38 MAPK activation. These findings suggested that KL could alleviate PQ-caused ALI via inhibiting ROS/P38 MAPK signaling-regulated inflammatory responses and mitochondria-dependent apoptosis.

scholarly journals Ellagitannins – Compounds From Pomegranate as Possible Effector in Steroidogenesis of Rabbit Ovaries

2015 ◽  
pp. 583-585 ◽  
Author(s):  
D. PACKOVA ◽  
A. A. CARBONELL-BARRACHINA ◽  
A. KOLESAROVA
Keyword(s):  
Steroid Hormones ◽  
Mature Female ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Progesterone Secretion ◽  
New Zealand White Rabbits ◽  
17Β Estradiol ◽  
Dose Dependent ◽  
Sexually Mature

This study has observed possible effect of ellagitannins – compounds from pomegranate on process of steroidogenesis in ovaries. The aim of the study was to investigate the possible effect of punicalagin on secretion of steroid hormones – progesterone, androstenedione, testosterone and 17β-estradiol by ovarian fragments of rabbits in vitro. Ovarian fragments from sexually mature female New Zealand white rabbits (n=20) were incubated without (control group) or with punicalagin at various doses 1, 10 and 100 μg.ml−1 for 24 h. Hormones were evaluated by ELISA (The Enzyme-Linked Immunosorbent Assay). Data showed that progesterone and 17β-estradiol (but not androstenedione and testosterone) release by rabbit ovarian fragments was significantly affected by punicalagin addition at various doses. Punicalagin (at 100 μg.ml−1) significantly (P<0.05) increased progesterone secretion. On the other hand, the release of 17β-estradiol was significantly (P<0.005) decreased by punicalagin addition (at 10 μg.ml−1). Our results suggest that punicalagin could have dose-dependent impact on secretion of steroid hormones progesterone and 17β-estradiol by rabbit ovarian fragments and it may be effector in process of ovarian steroidogenesis.

scholarly journals PENGARUH EKSTRAK METANOL DAUN SIRSAK (Annona muricata Linn.) TERHADAP VIABILITAS GALUR SEL KANKER PROSTAT

2015 ◽  
Vol 37 (3) ◽  
pp. 187
Author(s):  
Retno Yulianti ◽  
Ria Kodariah ◽  
Puspita Ekawuyung
Keyword(s):  
Prostate Cancer ◽  
Cell Viability ◽  
Cell Line ◽  
Cancer Cell ◽  
Cell Morphology ◽  
Methanol Extract ◽  
Prostate Cancer Cell ◽  
Control Group ◽  
Annonaceous Acetogenins

AbstrakDaun sirsak mengandung senyawa aktif annonaceous acetogenins yang memiliki efek sitotoksik pada sel kanker. Penelitian ini bertujuan untuk mengetahui pengaruh ekstrak daun sirsak terhadap viabilitas dan peningkatan daya hambat terhadap galur sel kanker prostat PC3. Desain penelitian adalah eksperimental in vitro. Subyek penelitian adalah cell line PC3 yang terbagi 5 kelompok yaitu kelompok kontrol sel, kelompok perlakuan dengan ekstrak metanol daun sirsak (EMDS) dengan konsentrasi 6,25; 12,5 dan 25 mg/mL dan kelompok doksorubisin. Kelompok perlakuan diuji viabilitas sel dengan MTT assay pada inkubasi 0 dan 24 jam dan dilakukan pengamatan morfologi sel. Data dianalisis dengan uji statistik ANOVA. Hasil penelitian menunjukkan penurunan nilai OD pada kelompok EMDS 6,25 dan 12,5 ug/mL, namun uji statistik tidak berbeda bermakna dan kemampuan menghambat viabilitas sel paling besar ada pada kelompok EMDS 12,5 ug/mL (nilai OD 0,94). Pengamatan morfologi sel menunjukkan efek sitotoksik. Kesimpulan: Ekstrak metanol daun sirsak memiliki peran potensial sebagai antikanker terhadap galur sel kanker prostat PC3 meskipun sangat kecil efek penghambatannya.AbstractSoursop leaves contain annonaceous acetogenins active compounds that have a cytotoxic effect on cancer cells. The aim of this study is to determine the effect of soursop leaf extract on the viability and inhibitory rate on the prostate cancer cell line PC3. The study was an experimental in vitro study. Subjects were 5 groups of PC3 cell line: cell control group, the group treated with methanol extract of soursop leaves (EMDS) with the concentrations of 6.25; 12.5 and 25 mg/mL and the doxorubicin group. The groups were tested using the MTT cell viability assay at 0 and 24 hours of incubation followed by PC3 cell morphology examination. Data were analyzed by ANOVA test. The results showed a decrease in the OD value of 6.25 and 12.5 ug/mL EMDS group, but statistical tests did not differ significantly and the EMDS 12.5 mg/mL group showed the highest ability in inhibiting cell viability (OD 0.94). Observation of cell morphology showed cytotoxic effects. Conclusion: The methanol extract of soursop leaf has a potential as an anticancer against prostate cancer cell lines despite the very small inhibitory effect.

scholarly journals Potential Anticarcinogenic Effects From Plasma of Elderly After Exercise Training: A Pilot Study

2021 ◽  
Author(s):  
Alessandra Peres ◽  
Gilson Dorneles ◽  
Gisele Branchini ◽  
Fernanda Nunes ◽  
Pedro Romão ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Exercise Training ◽  
Cell Viability ◽  
Cell Line ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Institutionalized Elderly ◽  
Pc3 Cells ◽  
The Impact

Abstract This study aimed to evaluate the impact of exercise training plasma on in vitro prostate cancer cell viability and proliferation. PC3 prostate cancer cells were incubated with plasma obtained from young women with high and low physical fitness (PF) and with the plasma collected from institutionalized elderly before and after multimodal exercise training. Plasma from High PF women induced the lowest cell viability and proliferation after incubation time. PC3 cells presented lower cell viability and diminished rates of cell proliferation after the incubation with post-training plasma samples of elderly. The incubation of PC3 cells with post-training plasma of elderly decreased the mitochondrial membrane polarization and increased mitochondrial reactive oxygen species (ROS) production without changes in cytosolic ROS. Post-training plasma did not change apoptosis or necrosis rates in the PC-3 cell line. Multimodal exercise training increased the plasma levels of IL-2, IL-10, IFN-α, and FGF-1, and decreased TNF-α concentrations in institutionalized elderly. In conclusion, we showed that systemic adaptations in plasma mediators of institutionalized elderly may alter cell viability and proliferation by targeting mitochondrial ROS in a prostate cancer cell line.

The Impact of Antioxidants from the Diet on Breast Cancer Cells Monitored by Raman Microspectroscopy

2018 ◽  
Vol 16 (2) ◽  
pp. 127-137
Author(s):  
Paula Sofia Coutinho Medeiros ◽  
Ana Lúcia Marques Batista de Carvalho ◽  
Cristina Ruano ◽  
Juan Carlos Otero ◽  
Maria Paula Matos Marques
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Breast Adenocarcinoma ◽  
Coumaric Acid ◽  
Human Breast ◽  
The Impact

Background: The impact of the ubiquitous dietary phenolic compound p-coumaric acid on human breast cancer cells was assessed, through a multidisciplinary approach: Combined biological assays for cytotoxicity evaluation and biochemical profiling by Raman microspectroscopic analysis in cells. </P><P> Methods: Para-coumaric acid was shown to exert in vitro chemoprotective and antitumor activities, depending on the concentration and cell line probed: a significant anti-invasive ability was detected for the triple-negative MDA-MB-231 cells, while a high pro-oxidant effect was found for the estrogen- dependent MCF-7 cells. A striking cell selectivity was obtained, with a more noticeable outcome on the triple-negative MDA-MB-231 cell line. Results: The main impact on the cellular biochemical profile was verified to be on proteins and lipids, thus justifying the compound´s anti-invasive effect and chemoprotective ability. Conclusion: p-Coumaric acid was thus shown to be a promising chemoprotective/chemotherapeutic agent, particularly against the low prognosis triple-negative human breast adenocarcinoma.

VDAC1 Mediated Anticancer Activity of Gallic Acid in Human Lung Adenocarcinoma A549 Cells

2018 ◽  
Vol 18 (2) ◽  
pp. 255-262 ◽  
Author(s):  
Aikebaier Maimaiti ◽  
Amier Aili ◽  
Hureshitanmu Kuerban ◽  
Xuejun Li
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Gallic Acid ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Dependent Manner ◽  
Lung Carcinoma Cells ◽  
Induced Apoptosis ◽  
The Impact

Aims: Gallic acid (GA) is generally distributed in a variety of plants and foods, and possesses cell growth-inhibiting activities in cancer cell lines. In the present study, the impact of GA on cell viability, apoptosis induction and possible molecular mechanisms in cultured A549 lung carcinoma cells was investigated. Methods: In vitro experiments showed that treating A549 cells with various concentrations of GA inhibited cell viability and induced apoptosis in a dose-dependent manner. In order to understand the mechanism by which GA inhibits cell viability, comparative proteomic analysis was applied. The changed proteins were identified by Western blot and siRNA methods. Results: Two-dimensional electrophoresis revealed changes that occurred to the cells when treated with or without GA. Four up-regulated protein spots were clearly identified as malate dehydrogenase (MDH), voltagedependent, anion-selective channel protein 1(VDAC1), calreticulin (CRT) and brain acid soluble protein 1(BASP1). VDAC1 in A549 cells was reconfirmed by western blot. Transfection with VDAC1 siRNA significantly increased cell viability after the treatment of GA. Further investigation showed that GA down regulated PI3K/Akt signaling pathways. These data strongly suggest that up-regulation of VDAC1 by GA may play an important role in GA-induced, inhibitory effects on A549 cell viability.

scholarly journals The impact of FGF19/FGFR4 signaling inhibition in antitumor activity of multi-kinase inhibitors in hepatocellular carcinoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hiroaki Kanzaki ◽  
Tetsuhiro Chiba ◽  
Junjie Ao ◽  
Keisuke Koroki ◽  
Kengo Kanayama ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Molecular Mechanisms ◽  
Kinase Inhibitors ◽  
Progression Free Survival ◽  
Erk Signaling ◽  
Enzyme Linked Immunosorbent Assay ◽  
Antitumor Effects ◽  
The Impact

AbstractFGF19/FGFR4 autocrine signaling is one of the main targets for multi-kinase inhibitors (MKIs). However, the molecular mechanisms underlying FGF19/FGFR4 signaling in the antitumor effects to MKIs in hepatocellular carcinoma (HCC) remain unclear. In this study, the impact of FGFR4/ERK signaling inhibition on HCC following MKI treatment was analyzed in vitro and in vivo assays. Serum FGF19 in HCC patients treated using MKIs, such as sorafenib (n = 173) and lenvatinib (n = 40), was measured by enzyme-linked immunosorbent assay. Lenvatinib strongly inhibited the phosphorylation of FRS2 and ERK, the downstream signaling molecules of FGFR4, compared with sorafenib and regorafenib. Additional use of a selective FGFR4 inhibitor with sorafenib further suppressed FGFR4/ERK signaling and synergistically inhibited HCC cell growth in culture and xenograft subcutaneous tumors. Although serum FGF19high (n = 68) patients treated using sorafenib exhibited a significantly shorter progression-free survival and overall survival than FGF19low (n = 105) patients, there were no significant differences between FGF19high (n = 21) and FGF19low (n = 19) patients treated using lenvatinib. In conclusion, robust inhibition of FGF19/FGFR4 is of importance for the exertion of antitumor effects of MKIs. Serum FGF19 levels may function as a predictive marker for drug response and survival in HCC patients treated using sorafenib.

scholarly journals Impact of RARα and miR-138 on retinoblastoma etoposide resistance

Tumor Biology ◽  
2021 ◽  
Vol 43 (1) ◽  
pp. 11-26
Author(s):  
Maike Busch ◽  
Natalia Miroschnikov ◽  
Jaroslaw Thomas Dankert ◽  
Marc Wiesehöfer ◽  
Klaus Metz ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Lines ◽  
Cancer Progression ◽  
Treated Patient ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Gene Assay ◽  
The Impact

BACKGROUND: Retinoblastoma (RB) is the most common childhood eye cancer. Chemotherapeutic drugs such as etoposide used in RB treatment often cause massive side effects and acquired drug resistances. Dysregulated genes and miRNAs have a large impact on cancer progression and development of chemotherapy resistances. OBJECTIVE: This study was designed to investigate the involvement of retinoic acid receptor alpha (RARα) in RB progression and chemoresistance as well as the impact of miR-138, a potential RARα regulating miRNA. METHODS: RARα and miR-138 expression in etoposide resistant RB cell lines and chemotherapy treated patient tumors compared to non-treated tumors was revealed by Real-Time PCR. Overexpression approaches were performed to analyze the effects of RARα on RB cell viability, apoptosis, proliferation and tumorigenesis. Besides, we addressed the effect of miR-138 overexpression on RB cell chemotherapy resistance. RESULTS: A binding between miR-138 and RARα was shown by dual luciferase reporter gene assay. The study presented revealed that RARα is downregulated in etoposide resistant RB cells, while miR-138 is endogenously upregulated. Opposing RARα and miR-138 expression levels were detectable in chemotherapy pre-treated compared to non-treated RB tumor specimen. Overexpression of RARα increases apoptosis levels and reduces tumor cell growth of aggressive etoposide resistant RB cells in vitro and in vivo. Overexpression of miR-138 in chemo-sensitive RB cell lines partly enhances cell viability after etoposide treatment. CONCLUSIONS: Our findings show that RARα acts as a tumor suppressor in retinoblastoma and is downregulated upon etoposide resistance in RB cells. Thus, RARα may contribute to the development and progression of RB chemo-resistance.

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