Effect of vitamin B12 on the oxidative stress of Sitophilus oryzae under different time course

Although the original data on systemic oxidative stress in COVID-19 patients have recently started to emerge, we are still far from a complete profile of changes in patients’ redox homeostasis. We aimed to assess the extent of oxidative damage of proteins, lipids and DNA during the course of acute disease, as well as their association with CT pulmonary patterns. In order to obtain more insight into the origin of the systemic oxidative stress, the observed parameters were correlated with inflammatory biomarkers and biomarkers of multiorgan impairment. In this prospective study, we included 58 patients admitted between July and October 2020 with COVID-19 pneumonia. Significant changes in malondialdehyde, 8-hydroxy-2’-deoxyguanosine and advanced oxidation protein products levels exist during the course of COVID-19. Special emphasis should be placed on the fact that the pattern of changes differs between non-hospitalized and hospitalized individuals. Our results point to the time-dependent relation of oxidative stress parameters with inflammatory and multiorgan impairment biomarkers, as well as pulmonary patterns in COVID-19 pneumonia patients. Correlation between redox biomarkers and immunological or multiorgan impairment biomarkers, as well as pulmonary CT pattern, confirms the suggested involvement of neutrophils networks, IL-6 production, along with different organ/tissue involvement in systemic oxidative stress in COVID-19.

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Time course of skeletal muscle loss and oxidative stress in rats with walker 256 solid tumor

Muscle & Nerve ◽

10.1002/mus.21798 ◽

2010 ◽

Vol 42 (6) ◽

pp. 950-958 ◽

Cited By ~ 38

Author(s):

Flávia A. Guarnier ◽

Alessandra L. Cecchini ◽

Andréia A. Suzukawa ◽

Ana Leticia G.C. Maragno ◽

Andréa N.C. Simão ◽

...

Keyword(s):

Oxidative Stress ◽

Skeletal Muscle ◽

Solid Tumor ◽

Time Course ◽

Muscle Loss ◽

Skeletal Muscle Loss ◽

Walker 256 ◽

And Oxidative Stress

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Mediators of mineralocorticoid receptor-induced profibrotic inflammatory responses in the heart

Clinical Science ◽

10.1042/cs20080247 ◽

2009 ◽

Vol 116 (9) ◽

pp. 731-739 ◽

Cited By ~ 30

Author(s):

Peter Wilson ◽

James Morgan ◽

John W. Funder ◽

Peter J. Fuller ◽

Morag J. Young

Keyword(s):

Oxidative Stress ◽

Mrna Expression ◽

Mineralocorticoid Receptor ◽

Time Course ◽

Cardiac Fibrosis ◽

Inflammatory Responses ◽

Receptor Activation ◽

Mrna Levels ◽

Tissue Remodelling ◽

Perivascular Inflammation

Coronary, vascular and perivascular inflammation in rats following MR (mineralocorticoid receptor) activation plus salt are well-characterized precursors for the appearance of cardiac fibrosis. Endogenous corticosterone, in the presence of the 11βHSD2 (11β hydroxysteroid dehydrogenase type 2) inhibitor CBX (carbenoxolone) plus salt, produces similar inflammatory responses and tissue remodelling via activation of MR. MR-mediated oxidative stress has previously been suggested to account for these responses. In the present study we thus postulated that when 11βHSD2 is inhibited, endogenous corticosterone bound to unprotected MR in the vessel wall may similarly increase early biomarkers of oxidative stress. Uninephrectomized rats received either DOC (deoxycorticosterone), CBX or CBX plus the MR antagonist EPL (eplerenone) together with 0.9% saline to drink for 4, 8 or 16 days. Uninephrectomized rats maintained on 0.9% saline for 8 days served as controls. After 4 days, both DOC and CBX increased both macrophage infiltration and mRNA expression of the p22phox subunit of NADPH oxidase, whereas CBX, but not DOC, increased expression of the NOX2 (gp91phox) subunit. eNOS [endothelial NOS (NO synthase)] mRNA expression significantly decreased from 4 days for both treatments, and iNOS (inducible NOS) mRNA levels increased after 16 days of DOC or CBX; co-administration of EPL inhibited all responses to CBX. The responses characterized over this time course occurred before measurable increases in cardiac hypertrophy or fibrosis. The findings of the present study support the hypothesis that endogenous corticosterone in the presence of CBX can activate vascular MR to produce both inflammatory and oxidative tissue responses well before the onset of fibrosis, that the two MR ligands induce differential but overlapping patterns of gene expression, and that elevation of NOX2 subunit levels does not appear necessary for full expression of MR-mediated inflammatory and fibrogenic responses.

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Time course of severe thyrotoxicosis in rats is marked by intense muscular oxidative stress and activation of chymotrypsin-like proteolysis

Free Radical Biology and Medicine ◽

10.1016/j.freeradbiomed.2012.08.324 ◽

2012 ◽

Vol 53 ◽

pp. S154-S155

Author(s):

S.S. Bernardes ◽

F.A. Guarnier⁎ ◽

P.C. Marinello ◽

A.N.C. Simão ◽

R. Cecchini ◽

...

Keyword(s):

Oxidative Stress ◽

Time Course

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Differential activation of heat-shock and oxidation-specific stress genes in chemically induced oxidative stress

Biochemical Journal ◽

10.1042/bj3090453 ◽

1995 ◽

Vol 309 (2) ◽

pp. 453-459 ◽

Cited By ~ 38

Author(s):

L Tacchini ◽

G Pogliaghi ◽

L Radice ◽

E Anzon ◽

A Bernelli-Zazzera

Keyword(s):

Oxidative Stress ◽

Heat Shock ◽

Time Course ◽

Consensus Sequence ◽

Single Agent ◽

Stress Protein ◽

Hsp 70 ◽

Activator Protein ◽

Chemically Induced ◽

Haem Oxygenase

Post-ischaemic reperfusion increases the level of the major heat-shock (stress) protein hsp 70 and of its mRNA by transcriptional mechanisms, and activates the binding of the heat-shock factor HSF to the consensus sequence HSE. In common with CoCl2 treatment, post-ischaemic reperfusion increases the level of haem oxygenase mRNA, an indicator of oxidative stress, but CoCl2 does not seem to induce the expression of the hsp 70 gene [Tacchini, Schiaffonati, Pappalardo, Gatti and Bernelli-Zazzera (1993) Lab. Invest. 68, 465-471]. Starting from these observations, we have now studied the expression of two genes of the hsp 70 family and of other possibly related genes under conditions of oxidative stress. Three different chemicals, which cause oxidative stress by various mechanisms and induce haem oxygenase, enhance the expression of the cognate hsc 73 gene, but do not activate the inducible hsp 70 gene. Expression of the other genes that have been studied seems to vary in intensity and/or time course, in relation to the particular mechanism of action of any single agent. The pattern of induction of the early-immediate response genes c-fos and c-jun observed during oxidative stress differs from that found in post-ischaemic reperfused livers. Oxidative-stress-inducing agents do not promote the binding of HSF to its consensus sequence HSE, such as occurs in heat-shock and post-ischaemic reperfusion, and fail to activate AP-1 (activator protein 1). With the possible exception of Phorone, the oxidative stress chemically induced in rat liver activates NFkB (nuclear factor kB) and AP-2 (activator protein 2) transcription factors.

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Altered maternal micronutrients (folic acid, vitamin B12) and omega 3 fatty acids through oxidative stress may reduce neurotrophic factors in preterm pregnancy

The Journal of Maternal-Fetal & Neonatal Medicine ◽

10.3109/14767058.2011.579209 ◽

2011 ◽

Vol 25 (4) ◽

pp. 317-323 ◽

Cited By ~ 40

Author(s):

Madhavi Dhobale ◽

Sadhana Joshi

Keyword(s):

Oxidative Stress ◽

Fatty Acids ◽

Folic Acid ◽

Vitamin B12 ◽

Neurotrophic Factors ◽

Omega 3 Fatty Acids ◽

Omega 3

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Methanol Extract of Usnea barbata Induces Cell Killing, Apoptosis, and DNA Damage against Oral Cancer Cells through Oxidative Stress

Antioxidants ◽

10.3390/antiox9080694 ◽

2020 ◽

Vol 9 (8) ◽

pp. 694

Author(s):

Jen-Yang Tang ◽

Kuang-Han Wu ◽

Yen-Yun Wang ◽

Ammad Ahmad Farooqi ◽

Hurng-Wern Huang ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Oral Cancer ◽

Cancer Cells ◽

Cell Lines ◽

Time Course ◽

Cell Killing ◽

Parp Cleavage ◽

Flow Cytometric ◽

Oral Cancer Cells

Some lichens provide the resources of common traditional medicines and show anticancer effects. However, the anticancer effect of Usnproliea barbata (U. barbata) is rarely investigated, especially for oral cancer cells. The aim of this study was to investigate the cell killing function of methanol extracts of U. barbata (MEUB) against oral cancer cells. MEUB shows preferential killing against a number of oral cancer cell lines (Ca9-22, OECM-1, CAL 27, HSC3, and SCC9) but rarely affects normal oral cell lines (HGF-1). Ca9-22 and OECM-1 cells display the highest sensitivity to MEUB and were chosen for concentration effect and time course experiments to address its cytotoxic mechanisms. MEUB induces apoptosis of oral cancer cells in terms of the findings from flow cytometric assays and Western blotting, such as subG1 accumulation, annexin V detection, and pancaspase activation as well as poly (ADP-ribose) polymerase (PARP) cleavage. MEUB induces oxidative stress and DNA damage of oral cancer cells following flow cytometric assays, such as reactive oxygen species (ROS)/mitochondrial superoxide (MitoSOX) production, mitochondrial membrane potential (MMP) depletion as well as overexpression of γH2AX and 8-oxo-2′deoxyguanosine (8-oxodG). All MEUB-induced changes in oral cancer cells were triggered by oxidative stress which was validated by pretreatment with antioxidant N-acetylcysteine (NAC). In conclusion, MEUB causes preferential killing of oral cancer cells and is associated with oxidative stress, apoptosis, and DNA damage.

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