хорошая новость для любителей перекиси водорода :)
из конфы http://groups.yahoo.com/group/h-longevity/
от Игоря Артюхова материальчик...
мой инглиш не совершенен, но вроде бы разобрался.
именно то, что и предполагали: перекись повышает адаптационные способности клетки,
то есть тренирует клетку.
в тексте это названо - hormesis-эффект.
впервые о том, что некоторые не стабильные (метастабильные) своб. радикалы могут
тренировать антиоксидантную систему организма я узнал, когда изучал установки
"изумруд" - электро-химическая активация воды.
спецы из НГЦ писали, что после обработки воды на изумруде, в воде появляется
много радикалов, которые, однако, живут не долго, то есть, вреда, видимо, нанести
не успевают, а организм начинает в ответ вырабатывать антиоксиданты.
это, своего рода, прививка.
с люстрой Чижевского та же картина.
и перекись видимо как-то быстро обезвреживается в организме, не успевая нанести
урона клетке, но привику клетка получает, и дальше лучше борется уже с реальными
радикалами.
однако, вопрос о приёме перекиси внутрь остаётся открытым.
дозы, длительность курсов, побочные эффекты - есть ли ответы на эти вопросы?
у меня нет...
С уважением, Рязанов Дмитрий.
Продление жизни, научный иммортализм
www.bessmertie.ru Dmit***@b*****.ru
| | IA> Аскорбил-2-О-фосфат и Аскорбил-2-О-альфа-глюкоза увеличивают
IA> ПЖ клеток (но не аскорбиновая кислота). А также (неожиданно!) -
IA> перекись водорода.
IA> J Cell Biochem. 2004 Oct 15;93(3):588-97
IA> Slow-down of age-dependent telomere shortening is executed in
IA> human skin
IA> keratinocytes by hormesis-like-effects of trace hydrogen
IA> peroxide or by
IA> anti-oxidative effects of pro-vitamin C in common concurrently
IA> with
IA> reduction of intracellular oxidative stress.
IA> The cellular life-span of cultivated human skin epidermis
IA> keratinocytes
IA> NHEK-F was shown to be extended up to 150% of population
IA> doubling levels
IA> (PDLs) by repetitive addition with two autooxidation-resistant
IA> derivatives of ascorbic acid (Asc),
IA> Asc-2-O-phosphate (Asc2P),
IA> and
IA> Asc-2-O-alpha-glucoside (Asc2G), respectively, but to be not
IA> extended with
IA> Asc itself. In contrast, hydrogen peroxide (H(2)O(2)) as dilute
IA> as 20
IA> microM which was non-cytotoxic to the keratinocytes, or at 60
IA> microM
IA> being marginally cytotoxic achieved the cellular longevity,
IA> unexpectedly,
IA> up to 160 and 120% of PDLs, respectively, being regarded as a
IA> hormesis-like stimulatory effect. The lifespan-extended cells
IA> that were
IA> administered with Asc2P, Asc2G, or 20 microM H(2)O(2) were
IA> prevented from
IA> senescence-induced symptoms such as PDL-dependent enlargement of
IA> a cell
IA> size of 14.7 microm finally up to 17.4 microm upon Hayflick's
IA> limit-called
IA> loss of proliferation ability as estimated with a channelizer,
IA> and
IA> retained young cell morphological aspects such as thick and
IA> compact shape
IA> and intense attachment to the culture substratum even upon
IA> advanced PDLs,
IA> whereas other non-extended cells looked like thin or fibrous
IA> shape and
IA> large size upon lower PDLs. The PDL-dependent shortening of
IA> telomeric DNA
IA> of 11.5 kb finally down to 9.12-8.10 kb upon Hayflick's limit
IA> was
IA> observed in common for each additive-given cells, but was
IA> decelerated in
IA> the following order: 20 microM H(2)O(2) > Asc2P = Asc2G > 60
IA> microM |
H(2)O(2) >> Asc = no additive, being in
H(2)O(2) >> accord with the order of
| | IA> cell
IA> longevity. Intracellular reactive oxygen species (ROS) was
IA> diminished by
IA> Asc2P, Asc2G or 20 microM H(2)O(2), but not significantly by Asc
IA> or 60
IA> microM H(2)O(2) as estimated by fluorometry using the redox
IA> indicator dye
IA> CDCFH. There was no appreciable difference among NHEK
IA> keratinocytes that
IA> were administered with or without diverse additives in terms of
IA> telomerase activity per cell, which was 1.40 x 10(4)-4.48 x
IA> 10(4) times
IA> lower for the keratinocytes than for HeLa cells which were
IA> examined as
IA> the typical tumor cells. Thus longevity of the keratinocytes was
IA> suggested
IA> to be achieved by slowdown of age-dependent shortening of
IA> telomeric DNA
IA> rather than by telomerase; telomeres may suffer from less DNA
IA> lesions due
IA> to the continuous and thorough repression of intracellular ROS,
IA> which was
IA> realized either by pro-vitamin C such as Asc2P or Asc2G that
IA> exerted an
IA> antioxidant ability more persistent than Asc itself or by 20
IA> microM
IA> H(2)O(2) which diminished intracellular ROS assumedly through a
IA> hormesis-like effect. |
| | IA> In Vitro Cell Dev Biol Anim. 2004 Mar-Apr;40(3-4):71-3.
IA> Suppressive effects of ascorbate derivatives on
IA> ultraviolet-B-induced
IA> injury in HaCaT human keratinocytes.
IA> The aging of skin, including sunburning, is caused by
IA> ultraviolet (UV)
IA> irradiation. Here, we examined the inhibitory effect of ascorbic
IA> acid
IA> (AsA) and its derivatives AsA 2-phosphate (AA-2P) and AsA
IA> 2-glucoside
IA> (AA-2G) on UV-B- induced cytotoxicity in HaCaT keratinocytes.
IA> Results
IA> show that cell viability significantly decreased when exposed to
IA> UV-B at
IA> 0.1-0.4 J/cm2 in a dose-dependent manner. In this study, AsA
IA> could not
IA> inhibit cytotoxicity, but AA-2P and AA-2G was able to cancel the
IA> harmful
IA> effect of UV-B when treated at high levels of 0.5-5 mM. These
IA> results
IA> indicate that the masking of the C-2 OH group may be an
IA> effective
IA> modification for AsA to inhibit UV-B-induced cytotoxicity in
IA> human
IA> keratinocytes. |
| | IA> J Cell Biochem. 2004 Sep 9;93(4):653-663 [Epub ahead of print]
IA> Cytoprotection of vascular endotheliocytes by phosphorylated
IA> ascorbate
IA> through suppression of oxidative stress that is generated
IA> immediately
IA> after post-anoxic reoxygenation or with alkylhydroperoxides.
IA> Vascular endotheliocytes BAE-2 underwent the gradually
IA> proceeding cell
IA> death until 48 h after reoxygenation (Reox) following 3 h anoxia
IA> (Anox),
IA> but protected by pre-Anox administration with L-ascorbic acid
IA> (Asc)-2-O-phosphate (Asc2P), an
IA> autooxidation-resistant Asc
IA> derivative,
IA> but not by Asc itself. This cytoprotection with Asc2P was
IA> achieved in a
IA> glucose (Glc)-lacking buffer more advantageously than in a
IA> Glc-containing
IA> buffer where less efficiency had been
IA> demonstrated for Asc entry
IA> into
IA> BAE-2 cells than in a Glc-lacking buffer. Superoxide anion
IA> radicals were
IA> detected explosively in the extracellular space at 2-5 min after
IA> Reox
IA> following the Anox treatment of HUVE
IA> endotheliocytes, and were
IA> thereafter
IA> retained at levels as high as approximately one-half of the
IA> maximum level
IA> until 60 min after Reox, as shown by cytochrome c reduction
IA> assay.
IA> Superoxide anions at 3 and 60 min after Reox were suppressed by
IA> pre-Anox
IA> administration with Asc2P, but not with Asc or dehydro-Asc, and
IA> were not
IA> suppressed by post-Anox administration with Asc2P; the
IA> cytoprotection may
IA> need the intracellular accumulation of the ROS-scavenging
IA> effector Asc
IA> that is converted from Asc2P until 3 min after Reox. The
IA> ROS-generator
IA> tert-butylhydroperoxide (t-BuOOH) also induced both the
IA> diminished cell
IA> viability and nuclear DNA strand cleavages of BAE-2
IA> endotheliocytes,
IA> which were also protected dose-dependently with Asc2P. The
IA> cytoprotection
IA> was attributed to reduction of intracellular ROS including
IA> hydroperoxide and hydrogen peroxide with Asc2P as shown by
IA> fluorometry
IA> with the redox indicator CDCFH-DA. Thus Anox/Reox-induced cell
IA> death can
IA> be prevented by Asc2P that suppresses
IA> ROS-generation immediately
IA> after
IA> Reox following Anox more efficiently in the intracellular sphere
IA> rather
IA> than in the extracellular space. |
| | IA> Cell Biol Int. 1999;23(4):287-98
IA> Reduced viability of vascular endothelial cells by high
IA> concentration of
IA> ascorbic acid in vitreous humor.
IA> Normal mammalian vitreous humor maintains its avascularity
IA> after
IA> regression of hyaloid vessels. Neovascularization in adults is
IA> only
IA> detected under pathological conditions which suggests that
IA> antiangiogenic
IA> factors are present in the vitreous humor. To elucidate the
IA> mechanism of
IA> vitreal angiogenic inhibition, we investigated the effect of
IA> vitreous
IA> humor on cultured vascular endothelial cells. When bovine aortic
IA> endothelial cells were cultured in the presence of bovine
IA> vitreous humor
IA> in medium, a decrease in cell viability was observed within 24
IA> h.
IA> Ascorbic acid from vitreous humor has been identified as a cell
IA> death
IA> inducing factor with high performance liquid chromatography
IA> (HPLC) and
IA> molecular mass analysis. Ascorbic acid reduced endothelial cell
IA> viability
IA> at concentrations normally present in vitreous humor. This
IA> effect was
IA> completely inhibited by antioxidants, N-acetylcysteine and
IA> catalase.
IA> Amongst the ascorbic acid derivatives tested, ascorbic acid
IA> 2-phosphate
IA> did not induce cell death, suggesting that the production of
IA> ascorbyl
IA> radical is required for induction of cell death. Furthermore,
IA> capillary
IA> formation in three-dimensional collagen gel cultures
IA> characteristic of
IA> vascular endothelial cells were disrupted in the presence of
IA> ascorbic
IA> acid. Since ascorbic acid is highly concentrated in ocular
IA> tissues,
IA> especially in vitreous humor, it may function as a
IA> neovascularization
IA> inhibitor. |
| | IA> Life Sci. 1998;63(11):935-48
IA> Age-dependent telomere shortening is slowed down by enrichment
IA> of
IA> intracellular vitamin C via suppression of oxidative stress.
IA> Telomeres in eukaryotic somatic cells are destined to the
IA> age-dependent
IA> shortening, which has not been demonstrated to correlate to
IA> direct lesion
IA> of telomeric DNA by reactive oxygen intermediates (ROI); still
IA> less
IA> explicable is the inhibitory effect of ROI-scavenging on
IA> telomere
IA> shortening. Here, we succeeded in artificial slowdown of
IA> age-dependent
IA> telomere shortening to 52-62% of the untreated control, in human
IA> vascular
IA> endothelial cells, by addition of the oxidation-resistant type
IA> of
IA> ascorbic acid (Asc), Asc-2-O-phosphate (Asc2P), which
IA> concurrently
IA> achieved both extension of cellular life-span and prevention of
IA> cell size
IA> enlargement indicative of cellular senescence. The results are
IA> attributable to a 3.9-fold more marked enrichment of
IA> intracellular Asc
IA> (Asc(in)) by addition of Asc2P, subsequently dephosphorylated
IA> before or
IA> during transmembrane influx, than by addition of Asc itself, and
IA> also
IA> attributed to diminution of intracellular ROI to 53% of the
IA> control level
IA> by Asc2P; telomerase activity was at a trace level and underwent
IA> an
IA> age-dependent decline, which was significantly decelerated by
IA> Asc2P.
IA> Thus, age-dependent telomere-shortening can be decelerated by
IA> suppression of intracellular oxidative stress and/or by
IA> telomerase
IA> retention, both of which are achieved by enriched Asc(in) but
IA> not by
IA> extracellular Asc overwhelmingly more abundant than Asc(in). |
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клетки,
могут
Они живут не долго, потому, что сразу с чем-то реагируют, на то они и радикалы.
то есть, вреда, видимо, нанести
Анолит содержит целый спектр в том числе самые известные, опасные радикалы, они
не могут не нанести вреда.
Нет, совсем иная картина - там аэроионы проявляют антиоксидантную активность.
Клетку может ин витро при определённых условиях, а вот попасть в кровь, через
печень, а потом к клеткам, сомниваюсь.
Инъекции - точно будет вред, окисление составляющих крови, эндотелия и образование
вторичных перекисных соединений (МДА...)
Наверное очень узки рамки условий, что бы польза СР перевешивала вред.
--
С уважением, Станислав .
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