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#81 RE: News aus der Forschung von wmuees 04.02.2019 20:56


LEF ist die Life Extension Foundation. Lesen würde ich dort:

Und dann lies mal:

#82 RE: News aus der Forschung von Dr.Faust 04.02.2019 22:11


Vielleicht ist das bei Parkinson von Interesse?

#83 RE: News aus der Forschung von Speedy 11.02.2019 03:32

Activation of SIRT1 by L-serine increases fatty acid oxidation and reverses insulin resistance in C2C12 myotubes (L-serine activates SIRT1 in C2C12 myotubes).

#84 RE: News aus der Forschung von Fichtennadel 19.02.2019 10:36

Hier kommt ein knaller, ist ganz neu:

Also: Mit den ganzen NAD+-Precursoren a la Nia-Riboside, Niacinamide und NMN ist es im Alter nicht getan. Im Plasma ist NAD+ dennoch beim Altern disreguliert.
Durch diese neue Feststellung wird für mich wieder Methylene blue interessanter, da es unabhängig von der Präkursor-Situation die NAD/NADH-Balance Richtung NAD+ verschiebt. Nicht zuletzt zeigte sich MB effecktiv bei der Behandlung von Progerie und der Hautalterung. Das deckt sich mit einer möglichen ganz realen Anti-Age Wirkung durch seine Einfluss auf die Zelltmung aber auch NAD+


Nicotinamide adenine dinucleotide (NAD+) is an essential pyridine nucleotide that serves as an electron carrier in cellular metabolism and plays a crucial role in the maintenance of balanced redox homeostasis. Quantification of NAD+:NADH and NADP+:NADPH ratios are pivotal to a wide variety of cellular processes, including intracellular secondary messenger signaling by CD38 glycohydrolases, DNA repair by poly(adenosine diphosphate ribose) polymerase (PARP), epigenetic regulation of gene expression by NAD-dependent histone deacetylase enzymes known as sirtuins, and regulation of the oxidative pentose phosphate pathway. We quantified changes in the NAD+ metabolome in plasma samples collected from consenting healthy human subjects across a wide age range (20–87 years) using liquid chromatography coupled to tandem mass spectrometry. Our data show a significant decline in the plasma levels of NAD+, NADP+, and other important metabolites such as nicotinic acid adenine dinucleotide (NAAD) with age. However, an age-related increase in the reduced form of NAD+ and NADP+—NADH and NADPH—and nicotinamide (NAM), N-methyl-nicotinamide (MeNAM), and the products of adenosine diphosphoribosylation, including adenosine diphosphate ribose (ADPR) was also reported. Whereas, plasma levels of nicotinic acid (NA), nicotinamide mononucleotide (NMN), and nicotinic acid mononucleotide (NAMN) showed no statistically significant changes across age groups. Taken together, our data cumulatively suggest that age-related impairments are associated with corresponding alterations in the extracellular plasma NAD+ metabolome. Our future research will seek to elucidate the role of modulating NAD+ metabolites in the treatment and prevention of age-related diseases.

In the last decade, there has been growing interest in the role of redox active nucleotides in the metabolism.1 The significance of pyridine nucleotide coenzymes, such as nicotinamide adenine dinucleotide (NAD+) and its phosphorylated form NADP+, as main electron transfer molecules and substrates for over 700 oxidoreductase enzymes is undebated.2 We and others have previously demonstrated that disturbances in the redox balance, for example, following exposure to chronic oxidative stress, often represents an important component of the pathobiology of cell loss in cardiovascular and neurodegenerative diseases.3,4 Exogenous stressors, such as overfeeding, starvation, alcohol ingestion, or drug treatment can alter the intracellular redox status of these coenzymes.5

NAD+ represents one of the most important coenzymes in the hydride transfer reactions.6 NAD+ is the precursor of the pyridine nucleotide family, including NADH, NADP+, and NADPH, and is the end product of tryptophan metabolism via the kynurenine pathway.7 It has been well established that NAD+ is a substrate for major dehydrogenase enzymes involved in nutrient catabolism, including alcohol and lactate dehydrogenase reactions.8 As well, NADH, which is the reduced form of NAD+, preferentially provides electrons to power mitochondrial oxidative phosphorylation. Apart from its roles in fuel utilization, NAD+ also serves as an exclusive substrate for the nuclear repair enzymes poly(adenosine diphosphate [ADP] ribose) polymerases (PARP). PARPs are a family of enzymes that are activated by double- or single-stranded DNA breaks in DNA, and are thought to promote DNA repair by the ADP-ribosylation of histones and other nuclear proteins.9 NAD+ is also a substrate for the enzyme NAD+ glycohydrolases (CD38) that leads to the production of cyclic ADP-ribose, a calcium efflux effector.10 NAD+ has also been shown to be the sole substrate for a new class of NAD-dependent histone deacetylase (“HDAC”) enzymes known as sirtuins.11 Increasing histone acetylation is associated with age-related pathologies, whereas gene silencing by upregulation of sirtuins has been shown to extend lifespan in yeast and small organisms.12 HDACs are also being found to interact with a variety of nonhistone proteins and to thereby change their function, activity, and stability by post-translational modifications.

Accurate determination of the NAD+ metabolome is of major interest due to its potential association with cognitive decline, including AIDS dementia complex,13–15 cancer,16–18 aging, and a plethora of age-related disorders. Recently, nicotinic acid adenine dinucleotide (NAAD), an intermediate of NAD+ synthesis from nicotinic acid (NA) via the NAD+ salvage pathway, has been shown to increase following ingestion with niacin.19 This finding suggests that increased NAD+ anabolism by supplementation with NAD+ precursors not only increases the accumulation of by-products of NAD+ catabolism (such as ADP-ribose and N-methyl-nicotinamide [MeNAM]), but also stimulates retrograde synthesis of NAAD and nicotinic acid mononucleotide (NAMN). However, the mechanism responsible for this elusive biochemical reaction is yet to be identified.

Given the significance of the NAD+ metabolome in a multitude of biological processes, accurate quantification of its concentration and redox state in plasma and tissue is essential for better understanding of important biochemical processes, and determining the metabolic state of organisms in response to treatment with various compounds and disease states. We and others have shown that the NAD+:NADH ratio varies between 1 and 10 in catabolic tissue of “physiologically” aged female Wistar rats, and human subjects.3,4,20 As NAD+ also serves as an oxidative agent in some biochemical processes such as fatty acid oxidation, glycolysis, and citrate cycle, changes to the NAD+:NADH ratio may also represent an indicator of alterations in metabolic processes and several diseases including multiple sclerosis. In 2011, we were the first to prove that NAD+ is an essential factor in the aging process in major declining levels of catabolic tissue such as the brain, heart, lung, liver and kidney of rats, and in human pelvic tissue.3,4,20 Increased NAD+ anabolism has been shown to ameliorate mitochondrial dysfunction in a mechanism dependent on SIRT1, a nuclear sirtuin.

While it is thought that NAD+ is predominantly an intracellular nucleotide, emerging evidence suggests that extracellular NAD+ crosses the plasma membrane and replenishes intracellular NAD+.21 Intracellular NAD+ concentrations have been shown to range between 10 and 1000 μM, and are much higher than the levels reported in the extracellular space.22 This is because (1) NAD+ is released from cells at low amounts; (2) NAD+ catabolism is rapid leading to biologically active products; and (3) NAD+ directly interacts with cell surface receptors such as connexion 43 channels and several subtypes of purinergic P2 receptors.23

Therefore, accurate monitoring of the plasma NAD+ metabolome is necessary and may provide valuable information regarding the effect of various lifestyle and dietary factors, pharmacological and nutraceutical supplementation of NAD+ and/or its metabolites. Monitoring the plasma NAD+ metabolome levels will also allow drug candidates to be screened for a new type of potentially adverse effect—the depletion of NAD+ and/or other desirable metabolites. Moreover, the ratio (e.g. the NAD:NADH ratio) of oxidized and reduced forms of pyridine dinucleotides provides important information regarding redox metabolism disorders or alterations to cellular bioenergetics and may become important biomarkers for the early detection of pathological states.

#85 RE: News aus der Forschung von Fichtennadel 19.02.2019 10:52

Ich behaupte also im Lichte der obigen Studie, dass die teuren Supps wie Niagen und Nicotinmononukelotid gar keinen "Anti-age"-Effekt haben können, der über einfaches Niacinamide hinausgeht.

Sowohl Niacinamide-Riboside als auch Niaciamidmononukleotid sind Stoffe, die aus Niacin bzw. Niacinamide und Ribose synthetisiert werden. In Zellen. NR und NMN werden im Magen und Darm durch Enzyme aufgespalten, in die Blutbahn geraten dann also wieder Niacinamide und Ribose.

Für die angenommene NAD+-Altershemmung wäre also Niacinamide genauso effektiv wie die weitaus teureren Supps.

Nun sehen wir aber leider, dass auch das nicht reicht um im Alter die NAD+/NADH-Balance im Sinne eines Anti-Age aufrecht zu erhalten. Prometheus hatte es schon geschrieben, CD-38 scheint dabei eine Rolle zu spielen, wahrscheinlich noch wie so oft ander verzahnte Feedback-Mechanismen usw.

Ein paar weitere Gedanken.
Niacin bzw. Niacinamide scheinen in der gängigen westlichen Ernährung nicht eben knapp zu sein, insbesonder bei Fleischessern. Ich dachte daher länger an D-Ribose als Rate-Limiting für eine endogene NAD+-Synthese. Aber auch Ribose ist letzlich ein Metablit von Glucose und sollte daher nicht knapp sein. Ausserdem fördert es als superphysiologisches Supplement vlt. erhablich die AGEs:

Überhaupt weiß man aus mittlerweile mehreren umfangreichen Publikationen über NAD+/NADH über Niacinamide, dass es im Übermaß gehörige Auswirkungen auf das Immunsystem haben kann, eher nachteilige (Allergien uvm.) Offenbar sind wir evolutiv nicht gut an ein Dauer- und Überangebot von Niacinamide angepasst. Feast and Fast scheint insbesondere hinsichtlich Niacinamide der Anpassungszustand zu sein und erklärt u.a. vlt. auch die positiven longevity-Effekte von imtermittend fasting/Calorie-Restriction mit

Meat Intake and the Dose of Vitamin B3 – Nicotinamide: Cause of the Causes of Disease Transitions, Health Divides, and Health Futures?

Meat and vitamin B3 – nicotinamide – intake was high during hunter-gatherer times. Intake then fell and variances increased during and after the Neolithic agricultural revolution. Health, height, and IQ deteriorated. Low dietary doses are buffered by ‘welcoming’ gut symbionts and tuberculosis that can supply nicotinamide, but this co-evolved homeostatic metagenomic strategy risks dysbioses and impaired resistance to pathogens. Vitamin B3 deficiency may now be common among the poor billions on a low-meat diet. Disease transitions to non-communicable inflammatory disorders (but longer lives) may be driven by positive ‘meat transitions’. High doses of nicotinamide lead to reduced regulatory T cells and immune intolerance. Loss of no longer needed symbiotic ‘old friends’ compounds immunological over-reactivity to cause allergic and auto-immune diseases. Inhibition of nicotinamide adenine dinucleotide consumers and loss of methyl groups or production of toxins may cause cancers, metabolic toxicity, or neurodegeneration. An optimal dosage of vitamin B3 could lead to better health, but such a preventive approach needs more equitable meat distribution. Some people may require personalised doses depending on genetic make-up or, temporarily, when under stress.

#86 RE: News aus der Forschung von Fichtennadel 19.02.2019 11:04

Zu guter Letzt, da Niacinamide immer mal wieder als Sirt1-Inhibitor genannt wird (und für Studien auch verwendet), muss man wohl auch hier umdenken.
NA ist durchaus ein Sirt1-Aktivator, die Sirt1-Inhibition scheint immer nur ein kurzfristg auftretender "transient" Effekt zu sein. Bestätigt zum einen meine obige These, dass die teuren Supps gänzlich ohne Mehrwert sind, Niacinamide alleine aber eben auch nicht ausreicht um NAD/NADH im "jungen" Maße zu gewährleisten.

Nicotinamide is an inhibitor of SIRT1 in vitro, but can be a stimulator in cells.

Nicotinamide (NAM), a form of vitamin B3, plays essential roles in cell physiology through facilitating NAD+ redox homeostasis and providing NAD+ as a substrate to a class of enzymes that catalyze non-redox reactions. These non-redox enzymes include the sirtuin family proteins which deacetylate target proteins while cleaving NAD+ to yield NAM. Since the finding that NAM exerts feedback inhibition to the sirtuin reactions, NAM has been widely used as an inhibitor in the studies where SIRT1, a key member of sirtuins, may have a role in certain cell physiology. However, once administered to cells, NAM is rapidly converted to NAD+ and, therefore, the cellular concentration of NAM decreases rapidly while that of NAD+ increases. The result would be an inhibition of SIRT1 for a limited duration, followed by an increase in the activity. This possibility raises a concern on the validity of the interpretation of the results in the studies that use NAM as a SIRT1 inhibitor. To understand better the effects of cellular administration of NAM, we reviewed published literature in which treatment with NAM was used to inhibit SIRT1 and found that the expected inhibitory effect of NAM was either unreliable or muted in many cases. In addition, studies demonstrated NAM administration stimulates SIRT1 activity and improves the functions of cells and organs. To determine if NAM administration can generate conditions in cells and tissues that are stimulatory to SIRT1, the changes in the cellular levels of NAM and NAD+ reported in the literature were examined and the factors that are involved in the availability of NAD+ to SIRT1 were evaluated. We conclude that NAM treatment can hypothetically be stimulatory to SIRT1.

#87 RE: News aus der Forschung von Dr.Faust 19.02.2019 11:34


Danke für die Erörterung von NAD/NADH, kommt mir gerade recht, da ich meine B-Vitamine mal
wieder hinterfrage.

Eine m.E. gute Darstellung findet man bei Giuliano, ist irgendwann schon mal genannt worden.
Aber er hat auch eine neue ppt-Präsentation.

Was sind denn nun die Schlussfolgerungen? Was soll ich nehmen, ohne zu messen? Ich bin
moderater Fleischesser, Käse (keine Milch), Eier one/d. Und Niacin 15 mg/d.

Ich war ui.a. auf das Thema durch eine mail von sunday naturals darauf gekommen.
Sie bieten 500mg Nicotinamid Kapseln (flushfrie!) an:

PS: Hier eine ganze Konferenz über NAD:

Wohl die führenden Fachleute. Bin gespannt, ob am Ende was brauchbares herauskommt.
Hab mir die Beiträge bisher nicht angesehen.

#88 RE: News aus der Forschung von Fichtennadel 19.02.2019 12:02

Giulianos Ausführungen sind veraltet, sowohl was Sirt-Inhibiton durch Niacinamide und was die NAD/NADH-Ratio im Alter angeht bzw. unsere Möglichkeiten zur Beeinflussung.

B3 und andere Supps wie NR und NMD überhaupt nicht supplementieren ist mein Standpunkt. Und auch hohe NAD+ - Spiegel werden letztlich Nebenwirkungen haben. Das finden gerade auch die experimentierfreudigen Nutzer auf Longecity heraus.

#89 RE: News aus der Forschung von Fichtennadel 19.02.2019 12:17

Die Blogs von Giuliani die du verlinkt hast sind allerdings ziemlich gut trotzdem. Überfliege gerade ganz gierig.

#90 RE: News aus der Forschung von Dr.Faust 19.02.2019 13:16


Hab grad mal die ppt-Präs. abgespielt. ich bon kein Biochemiker, sondern wie Giuliano aus dem Computer-Bereich
(komisch, de Grey auch und Kurzweil). ich kann die Richtigkeit nicht beurteilen. Immerhin auf einer NAD-Konferenz
2018 gehalten. Da kann er es sich nicht leisten große Fehler zu machen.

Also ich bleibe bei meinen 15 mg Niacin, ich kann sie eh nicht aus Vit B-Komplex herausnehmen. Aber 500 mg von sunday,
das ist reichlich. Und Guiliano sagt ja auch nicht, dass man Niacin nehmen soll, sondern es geht ihm wohl darum,
den Abbau von NAD zu verhindern.

#91 RE: News aus der Forschung von Julie 19.02.2019 14:25


Ich nehme ca. 100 mg Niacin. Mehr vertrage ich nicht, bekomme dann Flush von Kopf bis Fuß.

#92 RE: News aus der Forschung von Speedy 22.02.2019 01:06

New Insight Into the Balance Between the Tumor-suppressive and Tumor-promoting Effects of Cellular Senescence

#93 RE: News aus der Forschung von Prometheus 22.02.2019 07:12


Danke @Speedy!

Zusammenfassend steht in dem Artikel, dass NAD+ die sensezenten Zellen zu einer gesteigerten Entzündungsreaktion anregt, so dass sich die Wahrscheinlichkeit einer malignen Entartung von Zellen erhöht.

Ich halte die Ergebnisse für stimmig, da NAD+ natürlich auch in sensezenten Zellen für mehr Energie sorgt.

Hier mal ein paar Überlegungen:

-Wirkt eine NAD+ Steigerung im alten Organismus anders als bei jugendlichen?

- Sollte man NAD+ steigende Maßnahmen mit entzündungshemmenden Maßnahmen kombinieren?

-Ist eine zyklische NAD+ Steigerung geeignet, die unerwünschte dauerhafte Steigerung des SASP zu umgehen?

-Ist es eine Option, vor der NAD+ Steigerung eine Senolyse durchzuführen?

#94 RE: News aus der Forschung von Udelle 22.02.2019 09:55

@Prometheus Danke, die Fragestellungen helfen mir bei der Reflexion über meine NAD+-Precursor-Supplementierung weiter.
Betr. zyklische Erhöhung: Ich frage mich, wie lange die NAD+-Konzentration bzw. das NAD+/NADH-Verhältnis nach Einnahme von Precursorn Intrazellulär/extrazellulär erhöht bleibt. Meine Idee dahinter ist, dass eine täglich einmalige Zufuhr vielleicht schon zu einer Zyklisierung führt.

#95 RE: News aus der Forschung von Dr.Faust 22.02.2019 10:37


Hier ein Paper von 2018 zu NAD. Auf den ersten Blick stimmt es mit dem ppt von Giuliano im Wesentlichen überein.

Grundsätzlich sollte alles was den Energielevel steigert, also auch andere "Mitoceuticals" wie Q10 z.B.
auch den Status senescenter Zellen "verbessern".

Ist die Wirkung bei Jüngeren anders als bei Älteren? Ja sicher, der Status der Zellen ist bei Älteren bekanntlich
ziemlich anders. Genau deshalb versucht man ja, die energetische Basis zu verbessern. Leiden die Zellen Mangel,
insbesondere die Mitos, dann gehts allen schlecht, den senescenten Zellen besonders. Es sei denn sie stellen ihren
Stoffwechsel um (Stichwort WARBURG) und brauchen keine "Mitoceuticals" mehr ...

Entzündungshemmende Maßnahmen halte ich entsprechend dem hormesischen Prinzip immer für gut. Man sollte
einerseits nicht krank werden, andererseits aber auch keine Allergien entwickeln. So diese Balance.

Zyklisch ist immer von Vorteil. Aber die SASP sind ja immer da, bei mehr Energie sicher mehr. Deswegen
würde ich keine Hochdosis NAD zuführen, aber B3 ist ja in fast jedem Supplement enthalten. Wenn man jetzt nicht fühlbaren
Energiemangel oder CFS etc. behandeln will, würde ich nichts weiter ergänzen, zumal der Körper NAD ja selber herstellen
kann und B3 kein echtes Vitamin ist.

Sicher ist es gut nicht so viele senescente Zellen zu haben. Ich bin aber bisher von der Selektivität von
Senolyse nicht überzeugt. Ich bringe die senscenten Zellen zur Apopotose und gleichzeitig bisher gesunde
Zellen an den Rand der Senescenz ??? Ich möchte meinen Stammzellpool nicht überlasten.

#96 RE: News aus der Forschung von Fichtennadel 28.02.2019 09:14

Wofür steht SASP hier?

Edit: Habs. Senescence-associated secretory phenotype (SASP)

#97 RE: News aus der Forschung von Fichtennadel 11.03.2019 17:06

ß-Lapachon steigert NQO1-Enzymaktivität sehr effektiv. Das wiederum steigert die intrazelluläre NAD/NADH-Ratio. Aber auch in Krebszellen.

1, NQO1 regulates the intracellular redox state of the cell and thus, the ratio of NAD/NADH in the cell.

This is the main reason why I now think that NQO1 is so important. Mice that are homozygous negative (both genes knocked out) for NQO1 have an increase in the NADH/NAD ratio (and an increase in the NADPH/NADP ratio). NQO1 knockout mice strangely enough have lower blood glucose levels, less abdominal fat. However, they have higher levels of triglycerides, beta-hydroxybutyrate, pyruvate, and lactate. They also have higher levels of glucagon. More importantly, the NQO1 “knock out” mice have lowered rates of pyridine nucleotide synthesis, reduced glucose metabolism, and reduced fatty acid metabolism. This is not surprising since NQO1 is the controller of the 20S PC mediated degradation of PGC-1alpha.

Unfortunately, cancer cells have also discovered this wonderful property of NQO1. Many cancers unregulate NQO1 either via Nrf2 pathways or by other methods, such as the loss of miR suppression of mRNA for NQO1. A recent study shows that higher levels of the NQO1 protein predict poor prognosis in non-small cell lung cancer. This is a sobering thought – cancer cells up-regulate antioxidant genes! This does not mean that we should avoid phytosubstances that up-regulate NQO1, it just means that “cancer cells are smart”.

Introducing: BET proteins

The opposite problem occurs in aging cells. Aging cells have lower levels of expression of the gene NQO1. This is not just due to a “lack of broccoli” or a “lack of exercise”. Instead, the gene NQO1 is down-regulated by proteins called “epigenetic readers”. The two “epigenetic readers” that suppress the Nrf2-induction of the NQO1 gene are called “Bromodomain and Extraterminal Proteins” (or BET proteins). Specifically, Brd2 and Brd4 proteins “sit on top” of the histone protein acetylated lysines at the promoters of the Nrf2-dependent genes. As a consequence, Nrf2 and the other transcription factors that “turn on” NQO1 gene cannot turn the gene on. (This is why BET inhibitors like JQ1 are so exciting).

Summary: NQO1 regulates the ratio of NAD/NADH and the ratio of NADP/NADPH by oxidizing NADH to NAD+. Warburg-type metabolism ensures that most of the NAD(H) within the cell is in the reduced form (NADH). NQO1 is one of the few genes that oxidizes NADH to NAD+. When both genes for NQO1 are “knocked out”, there is even more NADH in the reduced state. This results in a lower NAD/NADH ratio (or higher NADH/NAD ratio). Thus, NQO1 is the “anti-Warburg gene”. This is why NQO1 is so important.

Im gleichen Blog werden dann aber die Anti-Krebs-Eigenschaften von ß-Lapachon aufgeführt:

0. Beta-lapachone, a compound found in the bark of the South American Lapacho tree, is a potent activator of the NQO1 protein and produces ROS in cancer cells, but reduces ROS in non-cancer cells. It also inhibits pathological retinal neovascularization, but does not inhibit physiological neovascularization.

The most exciting thing about NQO1 is that there is a natural, cheap, compound found in the tree bark of a South American tree. The compound is called beta-Lapachone and is a NQO1 activator. Specifically, NQO1 is a “two-electron transfer” enzyme that can extinguish free radicals in normal cells, but produces free radicals in cancer cells. It has been shown to be a very effective compound for treating lung cancer. Here is how it works:

Beta-lapachone undergoes a redox cycle by NQO1, which reduces beta-lapachone to an unstable semiquinone. The semiquinone then rapidly undergoes a two-step oxidation back to the parent stable compound, beta-lapachone. This produces what is called a “perpetuating futile redox cycle”. This results in an unbalance of intracellular reactive oxygen species in cancer cells, resulting in the cell death of the cancer cells. This “perpetual futile redox cycle” is totally dependent on the concentration of NQO1 within cells. Here is a diagram of the reaction:


Illustration reference: 2014 The Chemotherapeutic Effects of Lapacho Tree Extract: β-Lapachone

The downstream effects of perpetual futile redox cycling include 4 apoptotic pathways and one necroptotic pathway:

Mitochondrial-induced apoptosis – The induction of ROS in mitochondria opens the MPTP pores and results in PARP activation and caspace activation. This induces apoptosis.
ER-induced apoptosis – The induction of ER stress induces sarcoplasmic release of calcium which induces high levels of cytoplasmic Ca++. This also induces apoptosis via the ER.
DNA-damage mediated apoptosis – beta-lapachone also induces Topoisomerase I and II. The activation of topoisomerases induces DNA breaks, which induces PARPs. This PARP hyper-activation induces apoptosis independently from mitochondrial ROS or ER stress.
Cell cycle arrest-induced apoptosis – The futile redox cycling of beta-lapachone also induces cycle cycle arrest via the activation of p21, p27, and the phosphorylation of JNK, PI3K, and Akt. This induces cancer cell apoptosis as well.
Calpain-induced cell necrosis – Unlike the 4 pathways above, futile redox cycling also induces calcium influx into the cells independently of ER stress. This calcium influx into the cell activates Calpain, which induces cell death by the necrosis pathway, not the apoptosis pathway.

Conclusion: beta-lapachone induces cancer cell death by five different pathways, all dependent on perpetual futile redox cycling which is dependent on NQO1

#98 RE: News aus der Forschung von Speedy 13.06.2019 01:49

NAD+ and Cellular Senescence Pathways Interact

#99 RE: News aus der Forschung von Speedy 23.07.2019 01:25

Clinicial Trial of Nicotinamide Riboside Completed

#100 RE: News aus der Forschung von Speedy 06.10.2019 16:55

A Reduced Form of Nicotinamide Riboside Defines a New Path for NAD+ Biosynthesis and Acts as an Orally Bioavailable NAD+ Precursor

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