15-Deoxy-Δ12,14-prostaglandin J2 induces apoptosis of a thyroid papillary cancer cell line (CG3 cells) through increasing intracellular iron and oxidative stress

2002 ◽  
Vol 13 (7) ◽  
pp. 759-765 ◽  
Author(s):  
Shu-Yi Chen ◽  
Fung-Jou Lu ◽  
Rung-Jiun Gau ◽  
Mei-Ling Yang ◽  
Tien-Shang Huang
2017 ◽  
Vol 41 ◽  
pp. 141-147 ◽  
Author(s):  
Petar ČANOVIĆ ◽  
Jovana BOGOJESKI ◽  
Jelena V. KOŠARIĆ ◽  
Snežana D. MARKOVIĆ ◽  
Marko N. ŽIVANOVIĆ

2021 ◽  
Vol 82 (1) ◽  
Author(s):  
Alaaeldin Ahmed Hamza ◽  
Soha Osama Hassanin ◽  
Salsabil Hamza ◽  
Ali Abdalla ◽  
Amr Amin

Abstract Background The therapeutic value of doxorubicin as an effective anti-neoplastic agent is limited by its cardiotoxic side effects. We investigated the effects of ethanolic leaf extracts of olive leaf OL on cardiotoxicity as well as oxidative stress which was induced by doxorubicin (DOX) in Wistar rats. The cardiotoxicity was induced by intraperitoneally injecting a single dose of doxorubicin (10 mg kg−1) after 7 days of OL administration. OL was given by gastric gavage in 250 mg/kg, 500 mg/kg and 1000 mg/kg doses of extract for 10 days. Results Cardiac toxicity of DOX was evidenced by histopathological changes in cardiac tissues and an increase in the activities of serum markers of heart damage (AST and CK). DOX caused oxidative stress as evidenced by the elevation of malondialdehyde, protein carbonyl content levels, and catalase activity. That stress was also accompanied by a concurrent depletion of the activity of superoxide dismutase within cardiac tissues. The cardiotoxicity and oxidative stress damages caused by DOX also coincided with an increase of myeloperoxidase activity and iNOS expression. Most of these doxorubicin-induced biochemical and histological alterations were effectively attenuated by prior administration of OL. OL combination with DOX significantly increased its cytotoxicity in HepG2 liver cancer cell line and IC50 dropped from 259.35 to 158.12 μg/ml. Conclusion OL potentiated the cytotoxicity of DOX in liver cancer cell line and may play a role in the protection against its cardiotoxicity and thus can be a useful adjuvant therapy where doxorubicin is the common liver cancer-treating drug.


2014 ◽  
Vol 926-930 ◽  
pp. 1061-1064
Author(s):  
Yan Li Xi ◽  
Xiang Qun Wu ◽  
Jie Yu ◽  
Wei Guo Xu ◽  
Tong Zhao ◽  
...  

It is a good therapeutic method that add exogenous ROS to trigger oxidative stress causing death of cancer cells. In the present study, we investigated the inhibitory effects of 3,4,5-trihydroxybenzoic acid (TBA), a polyhydroxyphenolic compound, on high metastatic human lung cancer cell line (95-D) based on inducing reactive oxygen species (ROS). The experiments in vitro showed that 95-D cell viability was inhibited by various amounts of TBA and death was induced in a dose-dependent manner. The possible mechanism was that TBA can induce cell death by decreasing mitochondrial membrane potential (MMP; ΔΨm) and increasing hydrogen peroxide (H2O2) level. These results imply that TBA efficiently induces death in 95-D lung cancer cells and that TBA exerts cytotoxicity on cancer cells by its pro-oxidative activity.


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