Lipid oxidation predominates over protein hydroperoxide formation in human monocyte-derived macrophages exposed to aqueous peroxyl radicals

Firth, Carole A.; Yang, Ya-Ting; Gieseg, Steven P.

doi:10.1080/10715760701416442

Cited by 23 publications

(11 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Oxidative stress is a fundamental underpinning of a number of neurodegenerative diseases, including HAD, the most severe form of HAND. Several studies point to HIV‐1 Tat's mediation of oxidative stress in astrocytes as possibly leading to cell death (Firth et al,2007). One mechanism through which oxidative stress is able to impact signaling pathways and their downstream transcription factors is via a respiratory burst orchestrated by the activation of NADPH oxidase.…”

Section: Discussionmentioning

confidence: 99%

15‐deoxy‐Δ^12,14‐prostaglandin J₂ inhibits human immunodeficiency virus‐1 tat‐induced monocyte chemoattractant protein‐1/CCL2 production by blocking the extracellular signal‐regulated kinase‐1/2 signaling pathway independently of peroxisome proliferator‐activated receptor‐γ and heme oxygenase‐1 in rat hippocampal slices

Kim

Lee

Yang

et al. 2012

J of Neuroscience Research

View full text Add to dashboard Cite

Iodine deficiency is an important nutritional deficiency, with more than 2 billion people worldwide estimated to be at risk. The developing fetus and young children are particularly at risk. During pregnancy and lactation, iodine requirements increase, whether in iodine‐poor or iodine‐sufficient countries, making the mother and the developing fetus vulnerable. The American Thyroid Association (ATA) recommends 250 micrograms per day of iodine intake for pregnant and lactating women. The thyroid gland is able to adapt to the changes associated with pregnancy as long as sufficient iodine is present. Dietary intake is the sole source of iodine, which is essential to the synthesis of thyroid hormones. Iodine is found in multiple dietary sources including iodized salt, dairy products, seaweed, and fish. Prenatal vitamins containing iodine are a good source of iodine, but iodine content in multivitamin supplements is highly variable. Congenital hypothyroidism is associated with cretinism. Clinical hypothyroidism has been associated with increased risk of poor perinatal outcome including prematurity, low birth weight, miscarriage, preeclampsia, fetal death, and impaired fetal neurocognitive development. Subclinical hypothyroidism is also associated with poor pregnancy outcomes and potential fetal neurocognitive deficits, but the data are more variable than those for clinical hypothyroidism. We concur with the ATA recommendation that all pregnant and lactating women should ingest (through diet and supplements) 250 micrograms of iodine daily. To achieve this goal, we recommend that all pregnant and lactating women take daily iodine supplementation of 150 micrograms. Birth Defects Research (Part A) 94:677–682, 2012. © 2012 Wiley Periodicals, Inc.

show abstract

Section: Discussionmentioning

confidence: 99%

15‐deoxy‐Δ^12,14‐prostaglandin J₂ inhibits human immunodeficiency virus‐1 tat‐induced monocyte chemoattractant protein‐1/CCL2 production by blocking the extracellular signal‐regulated kinase‐1/2 signaling pathway independently of peroxisome proliferator‐activated receptor‐γ and heme oxygenase‐1 in rat hippocampal slices

Kim

Lee

Yang

et al. 2012

J of Neuroscience Research

View full text Add to dashboard Cite

show abstract

“…Human peripheral blood monocytes were isolated from the blood of healthy volunteers using Lymphoprep, as described previously [38]. This project has been reviewed by the University of Reading Research Ethics Committee and has been given a favourable opinion for conduct.…”

Section: Methodsmentioning

confidence: 99%

Effect of low extracellular pH on NF-κB activation in macrophages

Gerry¹,

Leake

2014

Atherosclerosis

View full text Add to dashboard Cite

ObjectiveMany diseases, including atherosclerosis, involve chronic inflammation. The master transcription factor for inflammation is NF-κB. Inflammatory sites have a low extracellular pH. Our objective was to demonstrate the effect of pH on NF-κB activation and cytokine secretion.MethodsMouse J774 macrophages or human THP-1 or monocyte-derived macrophages were incubated at pH 7.0–7.4 and inflammatory cytokine secretion and NF-κB activity were measured.ResultsA pH of 7.0 greatly decreased pro-inflammatory cytokine secretion (TNF or IL-6) by J774 macrophages, but not THP-1 or human monocyte-derived macrophages. Upon stimulation of mouse macrophages, the levels of IκBα, which inhibits NF-κB, fell but low pH prevented its later increase, which normally restores the baseline activity of NF-κB, even though the levels of mRNA for IκBα were increased. pH 7.0 greatly increased and prolonged NF-κB binding to its consensus promoter sequence, especially the anti-inflammatory p50:p50 homodimers. Human p50 was overexpressed using adenovirus in THP-1 macrophages and monocyte-derived macrophages to see if it would confer pH sensitivity to NF-κB activity in human cells. Overexpression of p50 increased p50:p50 DNA-binding and in THP-1 macrophages inhibited considerably TNF and IL-6 secretion, but there was still no effect of pH on p50:p50 DNA binding or cytokine secretion.ConclusionA modest decrease in pH can sometimes have marked effects on NF-κB activation and cytokine secretion and might be one reason to explain why mice normally develop less atherosclerosis than do humans.

show abstract

“…Interestingly, in HIVE oxidative stress markers have been found to co-localize with glial cells and neurons (Pocernich et al 2005b). Several studies point to the effect of HIV-1 Tat in mediating oxidative stress in astrocytes (Blokhina et al 2003; Nath 2002; Pocernich et al 2005a; Pocernich et al 2005b; Saha and Pahan 2007; Viviani et al 2001) possibly leading to cell death (Firth et al 2007; Muscoli et al 2002; Viviani et al 2001). Furthermore, it has also been demonstrated that HIV-1 induced oxidative stress in astrocytes can regulate target genes that are under the control of NF-κB, one of the essential transcription factors responsible for CXCL10 induction (Song et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Cooperative induction of CXCL10 involves NADPH oxidase: Implications for HIV dementia

Williams

Yao

Peng

et al. 2009

Glia

View full text Add to dashboard Cite

With the increasing prevalence of HIV-associated neurocognititve disorders (HAND), understanding the mechanisms by which HIV-1 induces neuro-inflammation and subsequent neuronal damage is important. The hallmark features of HIV-encephalitis, the pathological correlate of HIV-associated Dementia (HAD), are gliosis, oxidative stress, chemokine dysregulation, and neuronal damage/death. Since neurons are not infected by HIV-1, the current thinking is that these cells are damaged indirectly by pro-inflammatory chemokines released by activated glial cells. CXCL10 is a neurotoxic chemokine that is up-regulated in astroglia activated by HIV-1 Tat, IFN-γ, and TNF-α. In this study we have demonstrated that HIV-1 Tat increases CXCL10 expression in IFN-γ and TNF-α stimulated human astrocytes via NADPH oxidase. We have shown that the treatment of astrocytes with a mixture of Tat and cytokines leads to a respiratory burst that is abrogated by apocynin, an NADPH oxidase inhibitor. Pre-treatment of Tat, IFN-γ, and TNF-α stimulated astrocytes with apocynin also resulted in concomitant inhibition of CXCL10 expression. Additionally, apocynin was also able to reduce Tat and cytokine-mediated activation of the corresponding signaling molecules Erk1/2, Jnk, and Akt with a decrease in activation and nuclear translocation of NF-κB, important regulators of CXCL10 induction. Understanding the mechanisms involved in reducing both oxidative stress and the release of proinflammatory agents could lead to the development of therapeutics aimed at decreasing neuroinflammation in patients suffering from HAD.

show abstract

Lipid oxidation predominates over protein hydroperoxide formation in human monocyte-derived macrophages exposed to aqueous peroxyl radicals

Cited by 23 publications

References 56 publications

Effect of low extracellular pH on NF-κB activation in macrophages

Cooperative induction of CXCL10 involves NADPH oxidase: Implications for HIV dementia

Contact Info

Product

Resources

About