I. Specificity of the glutathione S-transferases in the conversion of leukotriene A4 to leukotriene C4

Chang, Mei Chi; Rao, Mukund Palat; Reddanna, Pallu; Li, C. H.; Tu, Chen‐Pei D.; Corey, E. J.; Reddy, C. Channa

doi:10.1016/0003-9861(87)90520-0

Cited by 31 publications

(11 citation statements)

References 22 publications

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“…The semi-enzymatic synthesis and purification of some of the linoleic and arachidonic acid oxidation products such as 9-HODE, 12-HpODE, 5-HETE, 9-HETE, 12-HETE, 15-HETE, 5-HpETE, 15-HpETE, 5,15-diHpETE and 5,6-diHETE were performed as described [18]. The authenticity of each of the lipid mediators was confirmed using co-chromatography as well as gas chromatography-mass spectrometric experiments.…”

Section: Reagentsmentioning

confidence: 99%

The oxidative stress mediator 4-hydroxynonenal is an intracellular agonist of the nuclear receptor peroxisome proliferator-activated receptor-β/δ (PPARβ/δ)

Coleman

Prabhu

Thompson

et al. 2007

Free Radical Biology and Medicine

104

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Liver insufficiency and damage is a major cause of death and disease worldwide and may result from exposure to environmental toxicants, specific combinations or dosages of pharmaceuticals and microbial metabolites. The generation of reactive intermediates, in particular 4-hydroxynonenal (4-HNE), is a common event in liver damage caused by a variety of hepatotoxic drugs and solvents. The peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that are involved in the transcriptional regulation of lipid metabolism as well as other biological functions. Importantly, we have observed that the PPARβ/δ −/− mouse is more susceptible to chemically-induced hepatotoxicity than its wildtype counterpart, and our objective in this study was to elucidate the mechanism(s) by which PPARβ/δ confers protection to hepatocytes. We hypothesized that PPARβ/ δ plays a protective role by responding to toxic lipids and altering gene expression accordingly. In support, oxidized-VLDL and constituents including 13-S-hydroxyoctadeca-dienoic acid (13(S)-HODE) and 4-HNE are PPARβ/δ ligands. A structure-activity relationship was established where 4-HNE and 4-hydroperoxynonenal (4-HpNE) enhanced the activity of the PPARβ/δ subtype while 4-hyroxy-hexenal (4-HHE), 4-oxo-2-Nonenal (4-ONE), and trans-4,5-epoxy-2(E)-decenal did not activate this receptor. Increasing PPARβ/δ activity with a synthetic agonist decreased sensitivity of hepatocytes to 4-HNE and other toxic agents, whereas inhibition of this receptor had the opposite result. Gene expression microarray analysis identified several important PPARβ/δ-regulated detoxification enzymes involved in 4-HNE metabolism that are regulated at the transcript level. This research established 4-HNE as an endogenous modulator of PPARβ/δ activity and raises the possibility that agonists of this nuclear receptor may be utilized to prevent or treat liver disease associated with oxidative damage.

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Section: Reagentsmentioning

confidence: 99%

The oxidative stress mediator 4-hydroxynonenal is an intracellular agonist of the nuclear receptor peroxisome proliferator-activated receptor-β/δ (PPARβ/δ)

Coleman

Prabhu

Thompson

et al. 2007

Free Radical Biology and Medicine

104

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“…The decreased level of GSH renders cell membranes more permeable by altering their lipid composition and it has been shown that synthesis of leukotrienes depend on GSH content. 27 We have demonstrated that PTX could show depolymerization of actin at nontoxic doses of 1.8 mM and 3.6 mM in a 2 hour exposure in B16F10 melanoma cells by fluorescence study (data not reported). Hence this investigation suggests that the receptors located on the surface of the B16F10 melanoma cells are connected via cytoskeletal elements.…”

Section: Discussionmentioning

confidence: 85%

“…27 Hydroxyalkenals are produced by lipid peroxide degradation being treated with electrophilic compounds. Our experimental data have shown that the increase in GST activity in melanoma cells after PTX treatment supports the production of hydroxyalkenals.…”

Section: Discussionmentioning

confidence: 99%

Potentiation of Antimetastatic Activity of Pentoxifylline in B16F10 and B16F1 Melanoma Cells Through Inhibition of Glutathione Content

Shukla

Gude

2003

Cancer Biotherapy and Radiopharmaceuticals

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“…Lowering of GSH levels could affect membrane permeability by increasing the susceptibility of membrane components to oxidative damage. Depletion of GSH alters the lipid composition of membranes as the synthesis of certain leukotrienes has been shown to be GSH-dependent [30], the main constituent of cytoskeletal system, that maintains the cell's integrity.…”

Section: Discussionmentioning

confidence: 99%

Potentiation of Lipid Peroxidation in B16F10 and B16F1 Melanoma Cells by Caffeine, a Methylxanthine Derivative: Relationship to Intracellular Glutathione

Shukla

Gude²

2003

Chemotherapy

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Background: Caffeine has shown an inhibitory role in invasion and proliferation in melanoma pulmonary metastasis as well as in high-grade tissue sarcoma. However, little is known about its mechanism and possible role in metastatic cell lines. Materials and Methods: B16F10 and B16F1 cell lines of high and low metastatic potential were treated with caffeine at different time intervals with different doses. Reduced glutathione, glutathione S-transferase and lipid peroxides were estimated to evaluate the effect of caffeine. Results: Caffeine treatment showed glutathione depletion and increased lipid peroxidation with higher glutathione S-transferase activity in both B16F10 and B16F1 cell lines. However the effect of caffeine was dependent on the time factor as well as on the dose. Conclusions: Caffeine was an effective inhibitor of metastatic activity. Glutathione depletion in conjunction with increased lipid peroxidation was a potent indicator in the regulation of metastatic behavior of B16F10 and B16F1 melanoma cell lines.

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I. Specificity of the glutathione S-transferases in the conversion of leukotriene A4 to leukotriene C4

Cited by 31 publications

References 22 publications

The oxidative stress mediator 4-hydroxynonenal is an intracellular agonist of the nuclear receptor peroxisome proliferator-activated receptor-β/δ (PPARβ/δ)

The oxidative stress mediator 4-hydroxynonenal is an intracellular agonist of the nuclear receptor peroxisome proliferator-activated receptor-β/δ (PPARβ/δ)

Potentiation of Antimetastatic Activity of Pentoxifylline in B16F10 and B16F1 Melanoma Cells Through Inhibition of Glutathione Content

Potentiation of Lipid Peroxidation in B16F10 and B16F1 Melanoma Cells by Caffeine, a Methylxanthine Derivative: Relationship to Intracellular Glutathione

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