Apoptosis and dna fragmentation as induced by tertiary butylhydroperoxide in the brain

Mukherjee, Suman; Yasharel, Ramona; Klaidman, Lori K.; Hutchin, Tim; Adams, James D.

doi:10.1016/0361-9230(96)80157-2

Cited by 22 publications

(4 citation statements)

References 21 publications

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“…A DNA fragmentation assay was carried out as described previously (Mukherjee et al, 1995). A volume of ice-cold lysis buffer (10 mM Tris-HCl, pH 7.5, 1 mM EDTA, and 0.2% Triton X-100) was added to fetal brain tissue, and the lysate was centrifuged at 12,000 ϫ g for 25 min to separate the intact DNA from the fragmented DNA.…”

Section: Measurement Of Dna Fragmentationmentioning

confidence: 99%

In Utero Ethanol Exposure Causes Mitochondrial Dysfunction, Which Can Result in Apoptotic Cell Death in Fetal Brain: A Potential Role for 4‐Hydroxynonenal

Vinitha

Pérez

Chen

et al. 2001

Alcoholism Clin & Exp Res

147

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These studies illustrate that in utero ethanol exposure can elicit a cascade of events in the fetal brain that are consistent with mitochondrially mediated apoptotic cell death. Additionally, the increase in mitochondrial content of HNE after ethanol intake and the ability of HNE added to fetal brain mitochondria to mimic these effects of in vivo ethanol exposure support a potential role for HNE in the proapoptotic responses to ethanol.

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Section: Measurement Of Dna Fragmentationmentioning

confidence: 99%

In Utero Ethanol Exposure Causes Mitochondrial Dysfunction, Which Can Result in Apoptotic Cell Death in Fetal Brain: A Potential Role for 4‐Hydroxynonenal

Vinitha

Pérez

Chen

et al. 2001

Alcoholism Clin & Exp Res

147

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“…Oxidative stress has been implicated as an important element in neuronal dysfunction that leads to aging and various disease conditions [1,2,3]. Studies suggest the involvement of multiple processes in the pathogenesis of cell injury during oxidative stress.…”

mentioning

confidence: 99%

“…Since it was observed that nicotinamide is able to prevent apoptosis in the mouse brain [1], it is important to determine the effects of nicotinamide on different pro-and anti-apoptotic proteins. Apoptosis can be induced via caspase-dependent extrinsic and intrinsic pathways and via a caspase-independent pathway involving apoptosis inducing factor (AIF).…”

mentioning

confidence: 99%

A Review of the Regulatory Role of Nicotinamide on Pro- and Anti-apoptotic Proteins in Neuronal Cells

Mukherjee¹,

Sonee²,

Adams³

2005

LDDD

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Numerous studies have shown that nicotinamide can prevent cell death via both necrosis and apoptosis. DNA fragmentation, NAD, poly(ADP-ribose) polymerase, apoptosis inducing factors, tumor necrosis factors, p53, caspases, inhibitor of apoptosis proteins and other factors are important in the action of nicotinamide. In this review, the regulatory effect of nicotinamide on individual pro-and anti-apoptotic proteins in neuronal cells have been delineated with a view to present a central molecular mechanism by which nicotinamide prevents apoptosis in the brain.

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“…For this reason, tBHP has been extensively used as an oxidative stress-inducing agent to study the effect of free radicals in different cell types and regions of the brain [20][21][22][23]. Low doses of tBHP cause mostly apoptosis, while higher concentrations lead to both necrosis and apoptosis in the brain [24,25]. In fact, French and collaborators reported an arrest of oligodendrocyte maturation at the low doses of tBHP [26].…”

Section: Introductionmentioning

confidence: 99%

ffect of Etazolate on ROS Production after tBHP-Induced Oxidative Stress in Oligodendroglial 158N Cell Line

Chierto

Cristinziano

Sapone

et al. 2020

ROS

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Oligodendrocytes are the key cells for the myelin synthesis in the central nervous system (CNS). They are sensitive to oxidative stress because of their lipid-rich membranes and their limited antioxidant defense against an excessive production of reactive oxygen species (ROS). Hence, antioxidant strategies are required for myelin protection. We have previously shown that etazolate has neuroprotective and remyelinating activities, and we hypothesized that part of etazolate effect is due to its antioxidant activity. The aim of our study was to test the antioxidant potential of etazolate, in 158N oligodendroglial cell line subjected to tert-butyl hydroperoxide (tBHP) in vitro. We developed a model of tBHP-induced oxidative stress in 158N oligodendroglial cell line and used WST-1 assay and FACS analysis to evaluate cell viability and ROS production. tBHP caused cell death and ROS production in 158N oligodendroglial cells, and etazolate did not protect cells at the concentration range of 0.02 to 200 µM. At the neuroprotective and remyelinating concentration of 2 µM, etazolate did not reduce ROS production, while N-acetylcysteine (NAC), a potent antioxidant compound, counteracted tBHP effects. In conclusion, etazolate does not exert an antioxidant activity in vitro, and the previously reported antioxidant activity of etazolate in vivo might be related to an indirect effect.

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Apoptosis and dna fragmentation as induced by tertiary butylhydroperoxide in the brain

Cited by 22 publications

References 21 publications

In Utero Ethanol Exposure Causes Mitochondrial Dysfunction, Which Can Result in Apoptotic Cell Death in Fetal Brain: A Potential Role for 4‐Hydroxynonenal

In Utero Ethanol Exposure Causes Mitochondrial Dysfunction, Which Can Result in Apoptotic Cell Death in Fetal Brain: A Potential Role for 4‐Hydroxynonenal

A Review of the Regulatory Role of Nicotinamide on Pro- and Anti-apoptotic Proteins in Neuronal Cells

ffect of Etazolate on ROS Production after tBHP-Induced Oxidative Stress in Oligodendroglial 158N Cell Line

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