Oxidative stress-induced apoptosis is associated with alterations in mitochondrial caspase activity and Bcl-2-dependent alterations in mitochondrial pH (pHm)

Takahashi, Akiyuki; Masuda, Akira; Sun, Mao; Centonze, Victoria E.; Herman, Brian

doi:10.1016/j.brainresbull.2003.07.009

Cited by 193 publications

(132 citation statements)

References 34 publications

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“…Many studies highlight the role of oxidative damage in the pathogenesis of degenerative POAG 1,[55][56][57] and its capacity of damaging not only HTM but also the optic nerve head. 58 HTMs of glaucoma-bearing patients display increased level of oxidative damage as compared to those of unaffected subjects, 17 resulting in the occurrence of histological and functional alterations, 59 including cell shrinkage, chromatin condensation, internucleosomal DNA fragmentation, and cell death.…”

Section: Discussionmentioning

confidence: 99%

Antioxidant activity of timolol on endothelial cells and its relevance for glaucoma course

Izzotti

Saccà²,

Marco

et al. 2007

Eye

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Purpose A growing evidence in the scientific literature suggests that oxidative damage plays a pathogenic role in primary open-angle glaucoma. Therefore, it is of interest to test whether drugs effective against glaucoma display antioxidant activity. We test the hypothesis that the classic b-blocker therapy for glaucoma with timolol involves the activation of antioxidant protective mechanisms towards endothelial cells. Methods Oxidative stress was induced in cultured human endothelial cells by iron/ ascorbate with or without timolol pretreatment. Analysed parameters included cell viability (neutral red uptake and tetrazolium salt tests), lipid peroxidation (thiobarbituric reactive substances), and occurrence of molecular oxidative damage to DNA (8-hydroxy-2 0 -deoxyguanosine).Results Oxidative stress decreased 1.8-fold cell viability, increased 3.0-fold lipid peroxidation and 64-fold oxidative damage to DNA. In the presence of timolol, oxidative stress did not modify cell viability, whereas lipid peroxidation was increased 1.3-fold, and DNA oxidative damage 3.6-fold only.Conclusions The obtained results indicate that timolol exerts a direct antioxidant activity protecting human endothelial cells from oxidative stress. These cells employ mechanisms similar to those observed in the vascular endothelium. It is hypothesized that this antioxidant activity is involved in the therapeutic effect of this drug against glaucoma.

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Section: Discussionmentioning

confidence: 99%

Antioxidant activity of timolol on endothelial cells and its relevance for glaucoma course

Izzotti

Saccà²,

Marco

et al. 2007

Eye

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“…In addition to the CsA-sensitive and Ca 2+ -dependent mPT pore, there exists a CsA-insensitive mPT pore (He and Lemasters, 2002), although its mechanism is totally unknown. Mitochondria are the major sources of ROS, which can do some oxidative damage to themselves (Takahashi et al, 2004). It has been recently suggested that mPT pore opening is the result of coactions of Ca 2+ overload and ROS generation (Mather and Hagai Rottenberg, 2000), and Ca 2+ overload can also enhance ROS generation in mitochondria (Grijalba et al, 1999).…”

Section: Mitochondria and Apoptosis In Oocytesmentioning

confidence: 99%

Mitochondrial functions on oocytes and preimplantation embryos

Wang

Zou

et al. 2009

J. Zhejiang Univ. Sci. B

138

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Oocyte quality has long been considered as a main limiting factor for in vitro fertilization (IVF). In the past decade, extensive observations demonstrated that the mitochondrion plays a vital role in the oocyte cytoplasm, for it can provide adenosine triphosphate (ATP) for fertilization and preimplantation embryo development and also act as stores of intracellular calcium and proapoptotic factors. During the oocyte maturation, mitochondria are characterized by distinct changes of their distribution pattern from being homogeneous to heterogeneous, which is correlated with the cumulus apoptosis. Oocyte quality decreases with the increasing maternal age. Recent studies have shown that low quality oocytes have some age-related dysfunctions, which include the decrease in mitochondrial membrane potential, increase of mitochondrial DNA (mtDNA) damages, chromosomal aneuploidies, the incidence of apoptosis, and changes in mitochondrial gene expression. All these dysfunctions may cause a high level of developmental retardation and arrest of preimplantation embryos. It has been suggested that these mitochondrial changes may arise from excessive reactive oxygen species (ROS) that is closely associated with the oxidative energy production or calcium overload, which may trigger permeability transition pore opening and subsequent apoptosis. Therefore, mitochondria can be seen as signs for oocyte quality evaluation, and it is possible that the oocyte quality can be improved by enhancing the physical function of mitochondria. Here we reviewed recent advances in mitochondrial functions on oocytes.

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“…This change in Bcl-2 and Bax expression may be enough to facilitate pore opening. Disruption of MMP is an early event in mitochondrial mediated apoptosis (Takahashi et al, 2004). After the reduction of membrane potential, a critical step is the formation of apoptosomes, which ultimately cleave procaspase-3 to form active caspase-3.…”

Section: Discussionmentioning

confidence: 99%

Resibufogenin inhibits the growth of human osteosarcoma MG-63 cells via mitochondrial pathway

Zhang

Quan

Cheng

et al. 2014

Bangladesh J Pharmacol

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Oxidative stress-induced apoptosis is associated with alterations in mitochondrial caspase activity and Bcl-2-dependent alterations in mitochondrial pH (pHm)

Cited by 193 publications

References 34 publications

Antioxidant activity of timolol on endothelial cells and its relevance for glaucoma course

Antioxidant activity of timolol on endothelial cells and its relevance for glaucoma course

Mitochondrial functions on oocytes and preimplantation embryos

Resibufogenin inhibits the growth of human osteosarcoma MG-63 cells via mitochondrial pathway

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