Micro-sized polyethylene particles decrease cell viability and increase mitochondrional superoxide production in human colorectal adenocarcinoma Caco-2 cells

2021 ◽  
Vol 350 ◽  
pp. S186-S187
Author(s):  
M. Herrala ◽  
M. Huovinen ◽  
E. Järvelä ◽  
P. Tolonen ◽  
M. Lahtela-Kakkonen ◽  
...  
Keyword(s):  
Cell Viability ◽  
Colorectal Adenocarcinoma ◽  
Superoxide Production ◽  
Polyethylene Particles

scholarly journals FORMULATION AND CHARACTERIZATION OF PAPAIN LOADED SOLID LIPID NANOPARTICLES AGAINST HUMAN COLORECTAL ADENOCARCINOMA CELL LINE

2018 ◽  
Vol 11 (10) ◽  
pp. 393
Author(s):  
Suriyakala Perumal Chandran ◽  
Kannikaparameswari Nachimuthu
Keyword(s):  
Particle Size ◽  
Drug Release ◽  
Zeta Potential ◽  
Cell Viability ◽  
Cell Line ◽  
Solid Lipid Nanoparticles ◽  
Colorectal Adenocarcinoma ◽  
Lipid Nanoparticles ◽  
In Vitro Drug Release

Objective: Colorectal cancer is one of the most commonly diagnosed cancer and also most common gastrointestinal malignancy with high prevalence rate in the younger population. Usually, cancer cells are surrounded by a fibrin coat which is resistant to fibrinolytic degradation. This fibrin coat is act as self-protective against natural killing mechanism. The main objective was to prepare papain-loaded solid lipid nanoparticles (P-SLN) by melt dispersion-ultrasonication method and investigated the cytotoxic efficacy against colorectal adenocarcinoma (human colorectal adenocarcinoma [HCT 15]) cells.Methods: Optimized polymer ratio was characterized by differential scanning calorimetry, Fourier-transform infrared, X-ray diffraction, scanning electron microscopy, entrapment efficiency, particle size and zeta potential analysis, in vitro drug release, and in vitro cytotoxicity studies on HCT-15 colorectal adenocarcinoma cells.Results: The results showed that the particle size, morphological character and zeta potential value of optimized batch P-SLN were 265 nm, spherical and −26.5 Mv, respectively. The in vitro drug profile of P-SLN exhibited that it produced sustain drug release, and the cell viability of HCT-15 against P-SLN shown better efficacy than pure papain enzyme.Conclusion: P-SLNs were successfully prepared and investigated the in vitro drug release and in vitro cell viability against HCT-15 cell line.

scholarly journals Mitochondrial Respiratory Chain Inhibitors Involved in ROS Production Induced by Acute High Concentrations of Iodide and the Effects of SOD as a Protective Factor

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Lingyan Wang ◽  
Qi Duan ◽  
Tingting Wang ◽  
Mohamed Ahmed ◽  
Na Zhang ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Viability ◽  
Respiratory Chain ◽  
Complex I ◽  
Mitochondrial Respiratory Chain ◽  
Superoxide Production ◽  
Mitochondrial Superoxide ◽  
Ldh Release ◽  
Relative Cell Viability ◽  
Mitochondrial Respiratory

A major source of reactive oxygen species (ROS) generation is the mitochondria. By using flow cytometry of the mitochondrial fluorescent probe, MitoSOX Red, western blot of mitochondrial ROS scavenger Peroxiredoxin (Prx) 3 and fluorescence immunostaining, ELISA of cleaved caspases 3 and 9, and TUNEL staining, we demonstrated that exposure to 100 μM KI for 2 hours significantly increased mitochondrial superoxide production and Prx 3 protein expression with increased expressions of cleaved caspases 3 and 9. Besides, we indicated that superoxide dismutase (SOD) at 1000 unit/mL attenuated the increase in mitochondrial superoxide production, Prx 3 protein expression, and lactate dehydrogenase (LDH) release and improved the relative cell viability at 100 μM KI exposure. However, SOD inhibitor diethyldithiocarbamic acid (DETC) (2 mM), Rotenone (0.5 μM), a mitochondrial complex I inhibitor, and Antimycin A (10 μM), a complex III inhibitor, caused an increase in mitochondrial superoxide production, Prx 3 protein expression, and LDH release and decreased the relative cell viability. We conclude that the inhibitors of mitochondrial respiratory chain complex I or III may be involved in oxidative stress caused by elevated concentrations of iodide, and SOD demonstrates its protective effect on the Fischer rat thyroid cell line (FRTL) cells.

scholarly journals A high mannose concentration is well tolerated by colorectal adenocarcinoma and melanoma cells but toxic to normal human gingival fibroblast: an in vitro investigation

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Muhammad Alif Mazlan ◽  
Muhammad Lokman Md. Isa ◽  
Moustafa Ibrahim
Keyword(s):  
Cell Viability ◽  
Cell Lines ◽  
Colorectal Adenocarcinoma ◽  
Ht29 Cell ◽  
Rapid Decline ◽  
Human Gingival Fibroblast ◽  
Gingival Fibroblast ◽  
In Vitro Investigation ◽  
High Mannose ◽  
Risk Of Cancer

Abstract Background The primary cause of cancer is gene mutation which allows the growth of abnormal and damaged cells. Nutrition is one of the key factors that either increases or decreases the risk of cancer. Mannose has been found in many fruits such as oranges, apples and berries. Mannose has been linked to increase the risk factors or potential therapeutic for cancers. However, insufficient information is available on the effects of high mannose concentration on the normal and cancer cell lines. This study aimed to evaluate the viability patterns of human cancer and normal cell lines treated with mannose. Human gingival fibroblast (HGF), skin malignant melanoma (A375) and colorectal adenocarcinoma (HT29) cell lines were cultured and treated with additional mannose in three respective concentrations: 1 mg/ml, 5 mg/ml and 10 mg/ml. Then, cell viability was measured using an MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide)-assay. Results The HGF cells’ percentage pattern of viability showed a rapid decline of nearly 95% on the third day of treatment. A375 cells were able to survive in high mannose condition as the cell viability percentage was at the highest value on Day 5. Meanwhile, HT29 cells showed declining cell viability pattern when treated with mannose. The data exhibited significance; the p value was less than 0.001. Conclusions High mannose concentration can be toxic to HGF. In addition, A375 is adaptive to mannose at all concentrations in which it shares the same pattern with the untreated group. However, the cell viability pattern for HT29 cell is declining.

scholarly journals The effect of cadmium-nickel interactions on superoxide production, cell viability and membrane potential (EM) in roots of two maize cultivars

2015 ◽  
Vol 66 (2) ◽  
pp. 192-204 ◽  
Author(s):  
Roderik Fiala ◽  
Vladimír Repka ◽  
Milada Čiamporová ◽  
Michal Martinka ◽  
Ján Pavlovkin
Keyword(s):  
Membrane Potential ◽  
Cell Viability ◽  
Superoxide Production ◽  
Maize Cultivars ◽  
Production Cell

scholarly journals Tanshinone IIA and Cryptotanshinone Prevent Mitochondrial Dysfunction in Hypoxia-Induced H9c2 Cells: Association to Mitochondrial ROS, Intracellular Nitric Oxide, and Calcium Levels

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Hyou-Ju Jin ◽  
Chun-Guang Li
Keyword(s):  
Nitric Oxide ◽  
Cell Viability ◽  
Cell Injury ◽  
Superoxide Production ◽  
Tanshinone Iia ◽  
H9c2 Cells ◽  
Sod Activity ◽  
Mitochondrial Superoxide ◽  
Atp Levels ◽  
Mitochondrial Ros

The protective actions of tanshinones on hypoxia-induced cell damages have been reported, although the mechanisms have not been fully elucidated. Given the importance of nitric oxide (NO) and reactive oxygen species (ROS) in regulation of cell functions, the present study investigated the effects of two major tanshinones, Tanshinone IIA (TIIA) and cryptotanshinone (CT), on hypoxia-induced myocardial cell injury and its relationships with intracellular NO and ROS, calcium, and ATP levels in H9c2 cells. Chronic hypoxia significantly reduced cell viability which accompanied with LDH release, increase in mitochondrial ROS, intracellular NO and calcium levels, decrease in superoxide dismutase (SOD) activity, and cellular ATP contents. TIIA and CT significantly prevented cell injury by increasing cell viability and decreasing LDH release. The protective effects of tanshinones were associated with reduced mitochondrial superoxide production and enhanced mitochondrial SOD activity. Tanshinones significantly reduced intracellular NO and Ca2+levels. ATP levels were also restored by TIIA. These findings suggest that the cytoprotective actions of tanshinones may involve regulation of intracellular NO, Ca2+, ATP productions, mitochondrial superoxide production, and SOD activity, which contribute to their actions against hypoxia injuries.

scholarly journals Two Antibiotics, Ampicillin and Tetracycline, Exert Different Effects in HT-29 Colorectal Adenocarcinoma Cells in Terms of Cell Viability and Migration Capacity

2021 ◽  
Vol 28 (4) ◽  
pp. 2466-2480
Author(s):  
Emil-Florin Hut ◽  
Matilda Radulescu ◽  
Nicolae Pilut ◽  
Ioana Macasoi ◽  
Delia Berceanu ◽  
...  
Keyword(s):  
Cell Viability ◽  
Molecular Mechanisms ◽  
Colorectal Adenocarcinoma ◽  
Chorioallantoic Membrane ◽  
Modern Medicine ◽  
Cellular Migration ◽  
Starting Point ◽  
The Impact ◽  
Ht 29

Antibiotics are considered the cornerstone of modern medicine; however, currently, antibiotic resistance has become a global health issue. Antibiotics also find new uses in the treatment of other pathologies as well as cancer. The present study aimed to verify the impact of tetracycline and ampicillin in a colorectal adenocarcinoma cell line, HT-29. The effects of the two antibiotics on cell viability and nucleus were evaluated by the means of MTT assay and the Hoechst staining method, respectively. The irritant potential at vascular level of the chorioallantoic membrane was tested by the HET-CAM assay. Treatment of HT-29 cells with the two antibiotics determined different effects: (i) tetracycline induced a dose- and time-dependent cytotoxic effect characterized by decreased cell viability, changes in cells morphology, apoptotic features (nuclear fragmentation), and inhibition of cellular migration, whereas (ii) ampicillin exerted a biphasic response—cytotoxic at low doses and proliferative at high concentrations. In terms of effect on blood vessels, both antibiotics exerted a mild irritant effect. These results are promising and could be considered as starting point for further in vitro studies to define the molecular mechanisms involved in the cytotoxic/proliferative effects.

Cytoprotective Effect of Tocotrienol-Rich Fraction and α-Tocopherol Vitamin E Isoforms Against Glutamate-Induced Cell Death in Neuronal Cells

2014 ◽  
Vol 84 (3-4) ◽  
pp. 0140-0151 ◽  
Author(s):  
Thilaga Rati Selvaraju ◽  
Huzwah Khaza’ai ◽  
Sharmili Vidyadaran ◽  
Mohd Sokhini Abd Mutalib ◽  
Vasudevan Ramachandran ◽  
...  
Keyword(s):  
Vitamin E ◽  
Cell Viability ◽  
Neuronal Cells ◽  
Positive Control ◽  
Post Treatment ◽  
Mitochondrial Activity ◽  
Before And After ◽  
Pre Treatment ◽  
Tocotrienol Rich Fraction ◽  
Major Mediator

Glutamate is the major mediator of excitatory signals in the mammalian central nervous system. Extreme amounts of glutamate in the extracellular spaces can lead to numerous neurodegenerative diseases. We aimed to clarify the potential of the following vitamin E isomers, tocotrienol-rich fraction (TRF) and α-tocopherol (α-TCP), as potent neuroprotective agents against glutamate-induced injury in neuronal SK-N-SH cells. Cells were treated before and after glutamate injury (pre- and post-treatment, respectively) with 100 - 300 ng/ml TRF/α-TCP. Exposure to 120 mM glutamate significantly reduced cell viability to 76 % and 79 % in the pre- and post-treatment studies, respectively; however, pre- and post-treatment with TRF/α-TCP attenuated the cytotoxic effect of glutamate. Compared to the positive control (glutamate-injured cells not treated with TRF/α-TCP), pre-treatment with 100, 200, and 300 ng/ml TRF significantly improved cell viability following glutamate injury to 95.2 %, 95.0 %, and 95.6 %, respectively (p < 0.05).The isomers not only conferred neuroprotection by enhancing mitochondrial activity and depleting free radical production, but also increased cell viability and recovery upon glutamate insult. Our results suggest that vitamin E has potent antioxidant potential for protecting against glutamate injury and recovering glutamate-injured neuronal cells. Our findings also indicate that both TRF and α-TCP could play key roles as anti-apoptotic agents with neuroprotective properties.

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