Nuclear DNA strand breaks during ethanol‐induced oxidative stress in rat brain

Renis, Marcella; Calabrese, Vittorio; Russo, Alessandra; Calderone, Agata; Barcellona, Maria Luisa; Rizza, V.

doi:10.1016/0014-5793(96)00647-3

Cited by 86 publications

(44 citation statements)

References 18 publications

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“…The prodeath role of Hsp60 seemed to involve caspase-3 maturation but when Hsp60 played a pro-survival role, it did not associate with active caspase-3 (Chandra et al, 2007). The aim of the present work was to explore whether Hsp60 interacts with p-C3 and p53 in a cancer model system submitted to OS, a type of stress known to occur in many tumors, causing not only nuclear but also mitochondrial and cytosolic damage (Renis et al, 1996;Grasso et al, 2003). For this purpose, the tumor cell line NCI-H292 was chosen as a model system and studied before and after OS induction with H2O2.…”

Section: Discussionmentioning

confidence: 99%

Upon oxidative stress, the antiapoptotic Hsp60/procaspase-3 complex persists in mucoepidermoid carcinoma cells

Campanella¹,

Bucchieri²,

Ardizzone³

et al. 2009

Eur J Histochem

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Hsp60, a mitochondrial chaperonin highly conserved during evolution, has been found elevated in the cytosol of cancer cells, both in vivo and in vitro, but its role in determining apoptosis during oxidative stress (OS) has not yet been fully elucidated. The aim of the present work was to study the effects of OS on Hsp60 levels and its interactions with procaspase- 3 (p-C3) and p53 in tumor cells. NCI-H292 (mucoepidermoid carcinoma) cells were exposed to various concentrations of hydrogen peroxide (H2O2) for 24 hours. Cell viability was determined by Trypan blue and MTT assays. DNA damage was assessed by the Comet assay, and apoptosis was measured by the AnnexinV cytofluorimetric test. Exposure to increasing concentrations of H2O2 resulted in a reduction of cell viability, DNA damage, and early apoptotic phenomena. Hsp60, p-C3, p53, and p21 were assessed by Western blotting and immunocytochemistry before and after OS. Hsp60 and p-C3 were present before and after OS induction. Immunoprecipitation experiments showed an Hsp60/p-C3 complex before OS that persisted after it, while an Hsp60/p53 complex was not detected in either condition. The presence of wild type (wt) p53 was confirmed by RT-PCR, and p21 detection suggested p53 activation after OS. We postulate that, although OS may induce early apoptosis in NCI-H292 cells, Hsp60 exerts an anti-apoptotic effect in these cells and, by extension, it may do so in other cancer cells

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Section: Discussionmentioning

confidence: 99%

Upon oxidative stress, the antiapoptotic Hsp60/procaspase-3 complex persists in mucoepidermoid carcinoma cells

Campanella¹,

Bucchieri²,

Ardizzone³

et al. 2009

Eur J Histochem

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“…It has been shown, in different experimental systems, that signals transduced through TNFR1 (p55) can induce an activation of proteases, including caspases. Caspases mediate apoptosis by proteolytic cleavage of the death substrates (26,(33)(34)(35)(36)(37)(38). TNF-␣ also increases synthesis of NO in different cells, and this molecule has been extensively associated with induction of DNA damage and apoptosis (39 -42).…”

Section: Discussionmentioning

confidence: 99%

ChlamydiapneumoniaeInhibits Apoptosis in Human Peripheral Blood Mononuclear Cells Through Induction of IL-10

Geng¹,

Shane²,

Berencsi

et al. 2000

The Journal of Immunology

124

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Chlamydia pneumoniae is a common cause of pulmonary infection, with serum positivity in at least 50% of the general population. In this study, we report that human PBMCs exposed to C. pneumoniae are resistant to apoptosis induced by the potent photoactivated chemotherapeutic agents 8-methoxypsoralen and hypericin. In contrast, PBMCs treated with a heat-inactivated inoculum exhibit normal susceptibility to apoptosis. We also observed that human PBMCs are responsive to C. pneumoniae infection by secretion of key immune regulatory cytokines, including IL-12 and IL-10. While IL-12 may play an important role in limiting C. pneumoniae proliferation within cells, IL-10 serves an anti-inflammatory function by down-regulating proinflammatory cytokines such as IL-12 and TNF-α. Depletion of endogenous IL-10, but not of IL-12, abolished the apoptosis resistance of C. pneumoniae-infected PBMCs. Furthermore, addition of exogenous IL-10, but not IL-12, significantly increased the resistance of control inoculum-treated PBMCs to photoactivated 8-methoxypsoralen- and hypericin-induced apoptosis. Therefore, we conclude that C. pneumoniae possesses an antiapoptotic mechanism. The resistance to apoptosis observed in PBMCs exposed to C. pneumoniae is due, at least partially, to the IL-10 induced during C. pneumoniae infection.

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“…With the use of new technology, including the transneuronal tracing of herpes simplex virus type 1, information is now available indicating that there exists an intricate cerebro-cerebellar system with both feed-forward and feedback connections (Middleton and Strick, 1997;Schmahmann and Pandya, 1997). These findings point to the importance of studying the cerebellum as a possible link to the understanding of FAS.The hippocampus and cerebellum are vulnerable to ethanol intoxication-induced redox changes (Renis et al, 1996). Changes in the cerebellum brought about by free radicals are particularly interesting since many neurodegenerative conditions can be induced by this mechanism.…”

mentioning

confidence: 98%

“…Changes in the cerebellum brought about by free radicals are particularly interesting since many neurodegenerative conditions can be induced by this mechanism. DNA strand breaks in the cerebellum and hippocampus after chronic (but not acute) ethanol administration correlate with significant increases in lipid peroxidation (Renis et al, 1996). Among the various possible sources of free radicals, cytochrome P450 IIEI (CYP2E1), NADPH oxidase, and NADPH cytochrome P450 reductase are particularly important due to their inducibility by ethanol.…”

mentioning

confidence: 99%

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In Utero Ethanol Suppresses Cerebellar Activator Protein-1 and Nuclear Factor-κB Transcriptional Activation in a Rat Fetal Alcohol Syndrome Model

Acquaah‐Mensah

Kehrer

Leslie³

2002

J Pharmacol Exp Ther

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A model of fetal alcohol syndrome was used to investigate prenatal ethanol effects on cerebellar transcription factors. Pregnant Sprague-Dawley rats were divided into three treatment groups: ethanol-exposed (E), calorically matched pair-fed (PF), and freely fed ad libitum (AL) groups. Ethanol exposure was stopped 2 days before parturition. The DNA binding in neonatal cerebella of the redox-sensitive transcription factors nuclear factor-B (NF-B) and activator protein-1 (AP-1) were determined by electrophoretic mobility shift assays. On the first postnatal day (PD1), there was decreased activation of these transcription factors in the E group relative to the control groups. The PD1 transcriptional effects were reversed as the neonate underwent development without further ethanol exposure. Western blot studies showed no corresponding decreases in protein amounts of both AP-1 and NF-B components on PD1. Postnatal glutathione levels and catalase activity, as measures of oxidative stress hypothesized to be a probable cause of the transcriptional effects, showed no statistically significant effects attributable to ethanol. Examination of prenatal cerebella on embryonic day 20 (EM20), a time during ethanol exposure, showed DNA-binding trends similar to those of PD1. EM20 Western blot studies showed decreases in the levels of the active form of glycogen synthase kinase-3 (GSK-3). GSK-3 inhibition was reversed by PD1. Blocking of GSK-3 activity with gestational dietary lithium diminished both AP-1 and NF-B DNA binding. Thus, prenatal ethanol exposure has the effect of diminishing pro-survival transcriptional activation, an effect possibly mediated by changes in GSK-3 activity.Victims of fetal alcohol syndrome (FAS) have severe learning, emotional, motor, and other impairments that adversely influence behavior (Conry, 1990). The cerebellum is emerging as being more crucial for cognition than previously thought. With the use of new technology, including the transneuronal tracing of herpes simplex virus type 1, information is now available indicating that there exists an intricate cerebro-cerebellar system with both feed-forward and feedback connections (Middleton and Strick, 1997;Schmahmann and Pandya, 1997). These findings point to the importance of studying the cerebellum as a possible link to the understanding of FAS.The hippocampus and cerebellum are vulnerable to ethanol intoxication-induced redox changes (Renis et al., 1996). Changes in the cerebellum brought about by free radicals are particularly interesting since many neurodegenerative conditions can be induced by this mechanism. DNA strand breaks in the cerebellum and hippocampus after chronic (but not acute) ethanol administration correlate with significant increases in lipid peroxidation (Renis et al., 1996). Among the various possible sources of free radicals, cytochrome P450 IIEI (CYP2E1), NADPH oxidase, and NADPH cytochrome P450 reductase are particularly important due to their inducibility by ethanol. CYP2E1 is widely expressed in the rat brain inclu...

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Nuclear DNA strand breaks during ethanol‐induced oxidative stress in rat brain

Cited by 86 publications

References 18 publications

Upon oxidative stress, the antiapoptotic Hsp60/procaspase-3 complex persists in mucoepidermoid carcinoma cells

Upon oxidative stress, the antiapoptotic Hsp60/procaspase-3 complex persists in mucoepidermoid carcinoma cells

ChlamydiapneumoniaeInhibits Apoptosis in Human Peripheral Blood Mononuclear Cells Through Induction of IL-10

In Utero Ethanol Suppresses Cerebellar Activator Protein-1 and Nuclear Factor-κB Transcriptional Activation in a Rat Fetal Alcohol Syndrome Model

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