Literature DB >> 27078710

Bevacizumab is superior to Temozolomide in causing mitochondrial dysfunction in human brain tumors.

Danop Nanegrungsunk1,2, Nattayaporn Apaijai2, Chontida Yarana2, Jirapas Sripetchwandee2, Kriengsak Limpastan3, Wanarak Watcharasaksilp3, Tanat Vaniyapong3, Nipon Chattipakorn2, Siriporn C Chattipakorn2,4.   

Abstract

OBJECTIVE: Current chemotherapy treatments available for treating high-grade brain tumors, Temozolomide (TMZ) or Bevacizumab (BEV), not only have specific anti-tumor mechanisms, but also have an effect on mitochondria. However, effects of both drugs on mitochondria isolated from human brain tumors have not been thoroughly investigated. This study determined the direct effects of TMZ and BEV as well as the neurotoxic condition (calcium overload), on the function of mitochondria and compared these effects on mitochondria isolated from low- and high-grade human brain tumors.
METHODS: Mitochondria were isolated from either low- or high-grade human primary brain tumors. Calcium overload conditions (100 or 200 μM), TMZ (300 μM), and BEV (2 mg/mL) were applied to isolated mitochondria from low- and high-grade brain tumors. Following the treatment, mitochondrial function, including reactive oxygen species production, membrane potential changes, and swelling, were determined. The mitochondrial morphology was also examined.
RESULTS: In calcium overload conditions, mitochondrial dysfunction was only found to have occurred in low-grade tumors. In TMZ and BEV treatment, BEV, rather than TMZ, caused greater membrane depolarization and mitochondrial swelling in both grades of brain tumors.
CONCLUSIONS: TMZ and BEV can directly cause the dysfunction of mitochondria isolated from human brain tumors. However, BEV has a greater ability to disturb mitochondrial function in mitochondria isolated from human brain tumors than either TMZ or calcium overload conditions.

Entities:  

Keywords:  Calcium overload; Human brain tumor; Mitochondria; Temozolomide and bevacizumab

Mesh:

Substances:

Year:  2016        PMID: 27078710     DOI: 10.1080/01616412.2015.1114233

Source DB:  PubMed          Journal:  Neurol Res        ISSN: 0161-6412            Impact factor:   2.448


  5 in total

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Authors:  Thomas N Seyfried; Laura Shelton; Gabriel Arismendi-Morillo; Miriam Kalamian; Ahmed Elsakka; Joseph Maroon; Purna Mukherjee
Journal:  Neurochem Res       Date:  2019-04-25       Impact factor: 3.996

2.  Bevacizumab induces oxidative cytotoxicity and apoptosis via TRPM2 channel activation in retinal pigment epithelial cells: Protective role of glutathione.

Authors:  Dilek Özkaya; Mustafa Nazıroğlu
Journal:  Graefes Arch Clin Exp Ophthalmol       Date:  2021-02-05       Impact factor: 3.117

3.  Autophagy modulates temozolomide-induced cell death in alveolar Rhabdomyosarcoma cells.

Authors:  Adel Rezaei Moghadam; Simone C da Silva Rosa; Ehsan Samiei; Javad Alizadeh; Jared Field; Philip Kawalec; James Thliveris; Mohsen Akbari; Saeid Ghavami; Joseph W Gordon
Journal:  Cell Death Discov       Date:  2018-10-25

4.  FOXO3a protects glioma cells against temozolomide-induced DNA double strand breaks via promotion of BNIP3-mediated mitophagy.

Authors:  Chuan He; Shan Lu; Xuan-Zhong Wang; Chong-Cheng Wang; Lei Wang; Shi-Peng Liang; Tian-Fei Luo; Zhen-Chuan Wang; Mei-Hua Piao; Guang-Fan Chi; Peng-Fei Ge
Journal:  Acta Pharmacol Sin       Date:  2021-04-20       Impact factor: 6.150

Review 5.  Metabolic management of microenvironment acidity in glioblastoma.

Authors:  Thomas N Seyfried; Gabriel Arismendi-Morillo; Giulio Zuccoli; Derek C Lee; Tomas Duraj; Ahmed M Elsakka; Joseph C Maroon; Purna Mukherjee; Linh Ta; Laura Shelton; Dominic D'Agostino; Michael Kiebish; Christos Chinopoulos
Journal:  Front Oncol       Date:  2022-08-17       Impact factor: 5.738

  5 in total

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