Protective effect of ascorbic acid against oxidative damage induced by hydrogen peroxide in cultured human peripheral blood lymphocytes

Siddique, Yasir Hasan; Beg, Tanveer; Afzal, Mohammad

doi:10.1007/s12291-009-0055-5

Cited by 12 publications

(5 citation statements)

References 31 publications

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“…These brain biomarkers correlated with histopathology signs. These findings agree with the study of Siddique et al (2009) CAT: catalase; SOD: superoxyde dismutase; GPx: Glutathion peroxydase; GSH: reduced glutathion; GST: Glutathion S-transferase; LPO: lipid peroxidation. *Significant when compared to the high dose H…”

Section: Discussionsupporting

confidence: 90%

Hydrogen peroxide-induced oxidative stress, acetylcholinesterase inhibition, and mediated brain injury attenuated byThymus algeriensis

Guesmi

Houda²,

Landoulsi

2018

Appl. Physiol. Nutr. Metab.

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The aim of the current study was to evaluate acetylcholinesterase (AChE) inhibition, antioxidant enzyme activities, and malondialdehyde (MDA) levels induced by hydrophobic fractions of Thymus algeriensis (HFTS) growing in Tunisia. The results showed that hydrogen peroxide (HO), an oxidative stress inducer, acts by decreasing the body mass and brain mass of rats. Moreover, we found higher MDA levels in the group treated with HO (P < 0.05) and a significantly lower activity of catalase, glutathione peroxidase, glutathione S-transferase, and superoxide dismutase, as well as a reduction in reduced glutathione activity in the brain tissues of HO-treated rats when compared with those of the control group (P < 0.05); however, rats that received HFTS with HO experienced a decrease in MDA levels in the brain. In contrast, HFTS demonstrated neuroprotective effects in rat brain. Overall, exposure to HFTS prior to HO induced a marked dose-dependent increase in reactive oxygen species scavenger levels (P < 0.05) accompanied by a statistically significant decrease in MDA levels (P < 0.05) when compared with no exposure. Notably, the activity of AChE was affected by exposure to natural compounds; levels were significantly lower in HFTS-treated rats and in those treated with the combination of HFTS and a low or high dose of HO. Furthermore, histopathological analysis showed that brain injuries occurred with high doses of HO administered alone or with a low dose of HFTS, whereas a high dose of essential oil markedly alleviated neurone degeneration. The results suggest that HFTS alleviates neuroinflammation by acting as an AChE inhibitor and attenuates HO-induced brain toxicity.

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Section: Discussionsupporting

confidence: 90%

Hydrogen peroxide-induced oxidative stress, acetylcholinesterase inhibition, and mediated brain injury attenuated byThymus algeriensis

Guesmi

Houda²,

Landoulsi

2018

Appl. Physiol. Nutr. Metab.

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“…Mtb culture supernatants (0.45 µm filtered) from vit C-treated and untreated time matched control cultures were used for estimating H 2 O 2 concentrations using the Pierce™ Quantitative Peroxide Assay Kit (Thermo Scientific). Briefly, culture filtrates were diluted by the addition of freshly made Dubos medium (1:1, v/v) and 10 µl of this was added to 100 µl of Xylenol Orange-based reagent and incubated at room temperature for 4 h. This dilution nullified the observed quenching of H 2 O 2 in presence of 10 mM vit C (data not shown) as described by Siddique et al [26] . An aliquot each of the filtrate was treated with 10 units of catalase for 5 mins at room temperature before H 2 O 2 measurement.…”

Section: Methodsmentioning

confidence: 83%

Multifaceted remodeling by vitamin C boosts sensitivity of Mycobacterium tuberculosis subpopulations to combination treatment by anti-tubercular drugs

et al. 2018

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Bacterial dormancy is a major impediment to the eradication of tuberculosis (TB), because currently used drugs primarily target actively replicating bacteria. Therefore, decoding of the critical survival pathways in dormant tubercle bacilli is a research priority to formulate new approaches for killing these bacteria. Employing a network-based gene expression analysis approach, we demonstrate that redox active vitamin C (vit C) triggers a multifaceted and robust adaptation response in Mycobacterium tuberculosis (Mtb) involving ~ 67% of the genome. Vit C-adapted bacteria display well-described features of dormancy, including growth stasis and progression to a viable but non-culturable (VBNC) state, loss of acid-fastness and reduction in length, dissipation of reductive stress through triglyceride (TAG) accumulation, protective response to oxidative stress, and tolerance to first line TB drugs. VBNC bacteria are reactivatable upon removal of vit C and they recover drug susceptibility properties. Vit C synergizes with pyrazinamide, a unique TB drug with sterilizing activity, to kill dormant and replicating bacteria, negating any tolerance to rifampicin and isoniazid in combination treatment in both in-vitro and intracellular infection models. Finally, the vit C multi-stress redox models described here also offer a unique opportunity for concurrent screening of compounds/combinations active against heterogeneous subpopulations of Mtb. These findings suggest a novel strategy of vit C adjunctive therapy by modulating bacterial physiology for enhanced efficacy of combination chemotherapy with existing drugs, and also possible synergies to guide new therapeutic combinations towards accelerating TB treatment.

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“…Indeed, both lipid peroxidation and ROS are essential apoptosis mediators, devoted to eliminate pre-cancerous and cancerous, virus-infected or otherwise damaged cells [29]. However, the aldehydes generated from lipid peroxidation form DNA adducts and lipid hydro-peroxides inducing the extensive single and double strand breaks [30], which activate a variant of histone H2A, at Ser139. Hence, the membrane lipid peroxidation and DNA double-strand breaks are considered to be manifestations of the oxidative cell damage.…”

Section: Resultsmentioning

confidence: 99%

Differential Response of Two Human Breast Cancer Cell Lines to the Phenolic Extract from Flaxseed Oil

et al. 2016

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Many studies have evidenced that the phenolic components from flaxseed (FS) oil have potential health benefits. The effect of the phenolic extract from FS oil has been evaluated on two human breast cancer cell lines, MCF7 and MDA-MB231, and on the human non-cancerous breast cell line, MCF10A, by SRB assay, cellular death, cell cycle, cell signaling, lipid peroxidation and expression of some key genes. We have evidenced that the extract shows anti-proliferative activity on MCF7 cells by inducing cellular apoptosis, increase of the percentage of cells in G0/G1 phase and of lipid peroxidation, activation of the H2AX signaling pathway, and upregulation of a six gene signature. On the other hand, on the MDA-MB2131 cells we verified only an anti-proliferative activity, a weak lipid peroxidation, the activation of the PI3K signaling pathway and an up-regulation of four genes. Overall these data suggest that the extract has both cytotoxic and pro-oxidant effects only on MCF7 cells, and can act as a metabolic probe, inducing differences in the gene expression. For this purpose, we have performed an interactomic analysis, highlighting the existing associations. From this approach, we show that the phenotypic difference between the two cell lines can be explained through their differential response to the phenolic extract.

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Protective effect of ascorbic acid against oxidative damage induced by hydrogen peroxide in cultured human peripheral blood lymphocytes

Abstract: ABSTRACT

Cited by 12 publications

References 31 publications

Hydrogen peroxide-induced oxidative stress, acetylcholinesterase inhibition, and mediated brain injury attenuated byThymus algeriensis

Hydrogen peroxide-induced oxidative stress, acetylcholinesterase inhibition, and mediated brain injury attenuated byThymus algeriensis

Multifaceted remodeling by vitamin C boosts sensitivity of Mycobacterium tuberculosis subpopulations to combination treatment by anti-tubercular drugs

Differential Response of Two Human Breast Cancer Cell Lines to the Phenolic Extract from Flaxseed Oil

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