Lupeol protects against acetaminophen-induced oxidative stress and cell death in rat primary hepatocytes

2012 ◽  
Vol 50 (5) ◽  
pp. 1781-1789 ◽  
Author(s):  
Archana Kumari ◽  
Poonam Kakkar
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Primary Hepatocytes ◽  
Rat Primary Hepatocytes

scholarly journals Investigation of sphingosin-1-phosphate-triggered matriptase activation using a rat primary hepatocyte model

2019 ◽  
Vol 67 (4) ◽  
pp. 578-587
Author(s):  
Réka Fanni Barna ◽  
Judit Mercédesz Pomothy ◽  
Zsuzsanna Paréj ◽  
Erzsébet Pásztiné Gere
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cell Viability ◽  
Mechanism Of Action ◽  
Sandwich Elisa ◽  
Colorimetric Method ◽  
Redox Status ◽  
Primary Hepatocytes ◽  
Rat Primary Hepatocytes ◽  
Sphingosine 1 Phosphate

Sphingosine-1-phosphate (S1P) has been reported as a matriptase activator. The aim of this study was to reveal if S1P can influence hepcidin production. Furthermore, we investigated how S1P can affect the viability and the redox status of primary hepatocytes. Rat primary hepatocytes were cultivated for 72 h and were treated with 50, 200, 1000 ng/ml S1P. Cell-free supernatants were collected every 24 h. Cell viability was tested by a colorimetric method using tetrazolium compound (MTS). The hepcidin levels in the cell-free supernatants were examined with hepcidin sandwich ELISA to determine the effect of S1P on the hepcidin-modulating ability of matriptase. In order to estimate the extent of S1P-generated oxidative stress, extracellular H2O2 measurements were performed by the use of fluorescent dye. Based on the findings, S1P treatment did not cause cell death for 72 h at concentrations up to 1000 ng/ml. S1P did not influence the extracellular H2O2 production for 72 h. The hepcidin levels were significantly suppressed in hepatocytes exposed to S1P treatment. Further studies would be needed to explore the exact mechanism of action of S1P.

Protective effects of dried flower extracts of Hibiscus sabdariffa L. against oxidative stress in rat primary hepatocytes

1997 ◽  
Vol 35 (12) ◽  
pp. 1159-1164 ◽  
Author(s):  
T.-H. Tseng ◽  
E.-S. Kao ◽  
C.-Y. Chu ◽  
F.-P. Chou ◽  
H.-W. Lin Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hibiscus Sabdariffa ◽  
Protective Effects ◽  
Primary Hepatocytes ◽  
Rat Primary Hepatocytes

Deltamethrin induced RIPK3-mediated caspase-independent non-apoptotic cell death in rat primary hepatocytes

2016 ◽  
Vol 479 (2) ◽  
pp. 217-223 ◽  
Author(s):  
Deepika Arora ◽  
Mohammed Haris Siddiqui ◽  
Pradeep Kumar Sharma ◽  
Yogeshwer Shukla
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Primary Hepatocytes ◽  
Rat Primary Hepatocytes

Oxidative stress is involved in Dasatinib-induced apoptosis in rat primary hepatocytes

2012 ◽  
Vol 261 (3) ◽  
pp. 280-291 ◽  
Author(s):  
Tao Xue ◽  
Peihua Luo ◽  
Hong Zhu ◽  
Yuqin Zhao ◽  
Honghai Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Primary Hepatocytes ◽  
Rat Primary Hepatocytes ◽  
Induced Apoptosis

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

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