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We began analyzing https://link.springer.com/article/10.1007/s11064-011-0412-7, but it redirected us to https://link.springer.com/article/10.1007/s11064-011-0412-7. The analysis below is for the second page.

Title[redir]:
Lipoxygenases and Poly(ADP-Ribose) Polymerase in Amyloid Beta Cytotoxicity | Neurochemical Research
Description:
The 12/15-lipoxygenase(s) (LOX), poly(ADP-ribose) polymerase (PARP-1) activity and mitochondrial apoptosis inducing factor (AIF) protein in the amyloid β (Aβ) toxicity were investigated in PC12 cells that express either wild-type (APPwt) or double Swedish mutation (APPsw) forms of human Aβ precursor protein. Different levels of Aβ secretion and free radicals formation characterize these cells. The results demonstrated a relationship between the Aβ levels and LOX protein expression and activity. High Aβ concentration in APPsw cells correlated with a significant increase in free radicals and LOX activation, which leads to translocation of p65/NF-κB into the nucleus. An increase in AIF expression in mitochondria was observed concurrently with inhibition of PARP-1 activity in the nuclear fraction of APPsw cells. We suggested that AIF accumulation in mitochondria may be involved in adaptive/protective processes. However, inhibition of PARP-1 may be responsible for the disturbances in transcription and DNA repair as well as the degeneration of APP cells. Under conditions of increased nitrosative stress, evoked by the nitric oxide donor, sodium nitroprusside (SNP, 0.5 mM), 70–80% of all cells types died after 24 h, significantly more in APPsw cells. There was no further significant change in mitochondrial AIF level and PARP-1 activity compared to corresponding non-treated cells. Only one exception was observed in PC12 control, where SNP significantly inhibits PARP-1 activity. Moreover, SNP significantly activated gene expression for 12/15-LOX in all types of investigated cells. Inhibitors of all LOX isoforms and specific inhibitor of 12-LOX enhanced the survival of cells that were subjected to SNP. We conclude that the LOX pathways may play a role in Aβ toxicity and in nitrosative-stress-induced cell death and that inhibition of these pathways offers novel protective strategies.

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Keywords {🔍}

cells, lox, article, google, scholar, pubmed, cas, cell, appsw, activity, parp, aif, stress, level, death, mitochondrial, snp, strosznajder, amyloid, appwt, protein, free, expression, app, gene, nuclear, role, data, fig, activation, significantly, control, lipoxygenase, transfected, oxidative, polymerase, poly, adpribose, levels, radicals, significant, fraction, acid, factor, alzheimers, usa, experiments, beta, observed, inhibitors,

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bonferroni post-hoc test glucose-deprivation/reload-treated neuron human wild-type app nitrosative-stress-induced cell death aβ-induced oxidative/nitrosative stress ion channel-coupled receptors amyloid beta cytotoxicity apoptosis-inducing factor substitutes amyloid beta-peptide generation 14c-labeled β-nad+ article download pdf α-synuclein enhances secretion scientific network 28/e-32/bwsn-0053/2008 mitochondrial apoptosis-inducing factor initial β-secretase degradation lipid hydroperoxide-mediated oxidation polymer-induced cell death amyloid beta-induced apoptosis-inducing factor leads adaptive/protective processes developed γ-secretase cleavage double swedish mutation app human gene polyethyleneimine-coated 10-cm dishes amyloid beta peptides nf-kappab-dependent transcription nf-κb transcription factor transcription factor nf-κb anti-rabbit igg 000 anti-rabbit igg free radical cascade anti-β-actin igg appsw-expressing cell line blanks contained enzyme apoptosis-inducing factor 100 mm tris/hcl buffer 50 mm tris–hcl buffer β-amyloid peptide cytosolic phospholipase a2 free radicals cascade open access 12/15-lipoxygenase gene disruption amyloid precursor proteins free radical formation app-transfected pc12 cells programmed cell death apolipoprotein e-deficient mice aβ-induced toxicity aβ peptide toxicity full access

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Leuner K, Hauptmann S, Abdel-Kader R, Scherping I, Keil U, Strosznajder JB, Eckert A, Muller WE (2007) Mitochondrial dysfunction: the first domino in brain aging and Alzheimer’s disease?

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         headline:Lipoxygenases and Poly(ADP-Ribose) Polymerase in Amyloid Beta Cytotoxicity
         description:The 12/15-lipoxygenase(s) (LOX), poly(ADP-ribose) polymerase (PARP-1) activity and mitochondrial apoptosis inducing factor (AIF) protein in the amyloid β (Aβ) toxicity were investigated in PC12 cells that express either wild-type (APPwt) or double Swedish mutation (APPsw) forms of human Aβ precursor protein. Different levels of Aβ secretion and free radicals formation characterize these cells. The results demonstrated a relationship between the Aβ levels and LOX protein expression and activity. High Aβ concentration in APPsw cells correlated with a significant increase in free radicals and LOX activation, which leads to translocation of p65/NF-κB into the nucleus. An increase in AIF expression in mitochondria was observed concurrently with inhibition of PARP-1 activity in the nuclear fraction of APPsw cells. We suggested that AIF accumulation in mitochondria may be involved in adaptive/protective processes. However, inhibition of PARP-1 may be responsible for the disturbances in transcription and DNA repair as well as the degeneration of APP cells. Under conditions of increased nitrosative stress, evoked by the nitric oxide donor, sodium nitroprusside (SNP, 0.5 mM), 70–80% of all cells types died after 24 h, significantly more in APPsw cells. There was no further significant change in mitochondrial AIF level and PARP-1 activity compared to corresponding non-treated cells. Only one exception was observed in PC12 control, where SNP significantly inhibits PARP-1 activity. Moreover, SNP significantly activated gene expression for 12/15-LOX in all types of investigated cells. Inhibitors of all LOX isoforms and specific inhibitor of 12-LOX enhanced the survival of cells that were subjected to SNP. We conclude that the LOX pathways may play a role in Aβ toxicity and in nitrosative-stress-induced cell death and that inhibition of these pathways offers novel protective strategies.
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      headline:Lipoxygenases and Poly(ADP-Ribose) Polymerase in Amyloid Beta Cytotoxicity
      description:The 12/15-lipoxygenase(s) (LOX), poly(ADP-ribose) polymerase (PARP-1) activity and mitochondrial apoptosis inducing factor (AIF) protein in the amyloid β (Aβ) toxicity were investigated in PC12 cells that express either wild-type (APPwt) or double Swedish mutation (APPsw) forms of human Aβ precursor protein. Different levels of Aβ secretion and free radicals formation characterize these cells. The results demonstrated a relationship between the Aβ levels and LOX protein expression and activity. High Aβ concentration in APPsw cells correlated with a significant increase in free radicals and LOX activation, which leads to translocation of p65/NF-κB into the nucleus. An increase in AIF expression in mitochondria was observed concurrently with inhibition of PARP-1 activity in the nuclear fraction of APPsw cells. We suggested that AIF accumulation in mitochondria may be involved in adaptive/protective processes. However, inhibition of PARP-1 may be responsible for the disturbances in transcription and DNA repair as well as the degeneration of APP cells. Under conditions of increased nitrosative stress, evoked by the nitric oxide donor, sodium nitroprusside (SNP, 0.5 mM), 70–80% of all cells types died after 24 h, significantly more in APPsw cells. There was no further significant change in mitochondrial AIF level and PARP-1 activity compared to corresponding non-treated cells. Only one exception was observed in PC12 control, where SNP significantly inhibits PARP-1 activity. Moreover, SNP significantly activated gene expression for 12/15-LOX in all types of investigated cells. Inhibitors of all LOX isoforms and specific inhibitor of 12-LOX enhanced the survival of cells that were subjected to SNP. We conclude that the LOX pathways may play a role in Aβ toxicity and in nitrosative-stress-induced cell death and that inhibition of these pathways offers novel protective strategies.
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      name:Neurobiology Research Laboratory, Psychiatric University Clinic, Basel, Switzerland
      name:Department of Neurosurgery, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

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