Carnosine protects cells from oxidative stress induced by hyperhomocysteinemia

Makhro, Asya; Mashkina, Anna P.; Solenaya, O. A.; Трунова, О. А.; Tyulina, O. V.; Bulygina, E. R.; Boldyrev, Alexander A.

doi:10.1134/s1819712408030112

Cited by 8 publications

(5 citation statements)

References 14 publications

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“…Protective effect of carnosine can be realized via at least two directions. First, it is able to prevent accumulation of free radicals caused by the activation of NMDARs (Boldyrev et al 1999;Makhro et al 2008). This effect reflects the well-known property of carnosine to act as a direct antioxidant (Boldyrev et al 1987;Aruoma Fig.…”

Section: Discussionmentioning

confidence: 91%

“…To activate signaling pathways, cells were incubated for 2.5-40 min with 500 lM of HC in the presence of co-activator of NMDARs, glycine (in the presence or absence of the dipeptides tested). The HC concentration used in these experiments was found in previous experiments as sufficient for realization of exitotoxic action (Makhro et al 2008). After subsequent incubation, the cells were analyzed by western blotting.…”

Section: Methodsmentioning

confidence: 99%

“…The cells were incubated with homocysteine (in the presence or absence of the dipeptides), and analyzed using BD FACS Calibur flow cytometer (Becton-Dickinson, USA), gating the population corresponding to neuronal cells by size (about 10 lM) and expression of NMDARs (Boldyrev et al 1999;Makhro et al 2008). The mean fluorescence of DCF was used as an indicator of free radical levels within the cells.…”

Section: Methodsmentioning

confidence: 99%

“…Previously, we demonstrated that carnosine effectively protects animals from HC toxicity in vivo (Makhro et al 2008;Boldyrev 2009), but mechanism of its action remained unclear. In this study, we investigated the effect of carnosine on MAP kinase cascade of cerebellum neurons under HC-induced oxidative stress in vitro.…”

Section: Introductionmentioning

confidence: 98%

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Carnosine protects neurons against oxidative stress and modulates the time profile of MAPK cascade signaling

et al. 2011

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Carnosine is a known protector of neuronal cells against oxidative injury which prevents both apoptotic and necrotic cellular death. It was shown earlier that carnosine serves as an intracellular buffer of free radicals. Using the model of ligand-dependent oxidative stress in neurons, we have shown that homocysteine (HC) initiates long-term activation of extracellular signal regulated kinase, isoforms 1 and 2 (ERK 1/2) and Jun N-terminal kinase (JNK) which corresponds to exitotoxic effect resulting in cellular death. L-carnosine (β-alanyl-L-histidine) protects neurons from both excitotoxic effect of homocysteine and cellular death. Its analogs, β-alanyl-D-histidine (D-carnosine) and L-histidyl-β-alanine, restricted accumulation of free radicals and delayed activation of ERK1/2 and JNK in neuronal cells, but did not promote neuronal viability.

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Section: Discussionmentioning

confidence: 91%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

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Carnosine protects neurons against oxidative stress and modulates the time profile of MAPK cascade signaling

et al. 2011

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“…Hyperhomocysteinemia is a risk factor in normal pregnancy. The administration of carnosine (100 mg/Kg) to pregnant rats that their pups were suffering from toxic effects of methionine induced prenatal hyper-homocysteinemia, restored the superoxide dismutase levels and prevented the cognitive decline and protected cerebellar neurons in the pubs from oxidative stress [ 648 ]. Carnosine prevented the oxidative stress in human erythrocytes that is induced by homocysteine and its by-product, homocysteic acid [ 649 ].…”

Section: Introductionmentioning

confidence: 99%

Resolving Geroplasticity to the Balance of Rejuvenins and Geriatrins

Tabibzadeh¹

2022

Aging and disease

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According to the cell centric hypotheses, the deficits that drive aging occur within cells by age dependent progressive damage to organelles, telomeres, biologic signaling pathways, bioinformational molecules, and by exhaustion of stem cells. Here, we amend these hypotheses and propose an eco-centric model for geroplasticity (aging plasticity including aging reversal). According to this model, youth and aging are plastic and require constant maintenance, and, respectively, engage a host of endogenous rejuvenating (rejuvenins) and gero-inducing [geriatrin] factors. Aging in this model is akin to atrophy that occurs as a result of damage or withdrawal of trophic factors. Rejuvenins maintain and geriatrins adversely impact cellular homeostasis, cell fitness, and proliferation, stem cell pools, damage response and repair. Rejuvenins reduce and geriatrins increase the age-related disorders, inflammatory signaling, and senescence and adjust the epigenetic clock. When viewed through this perspective, aging can be successfully reversed by supplementation with rejuvenins and by reducing the levels of geriatrins.

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