Conditional Expression of 15-Lipoxygenase-1 Inhibits the Selenoenzyme Thioredoxin Reductase

Yu, Margaret K.; Moos, Philip J.; Cassidy, Pamela B.; Wade, Mark; Fitzpatrick, Francis A.

doi:10.1074/jbc.m313939200

Cited by 36 publications

(32 citation statements)

References 47 publications

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“…No appreciable decrement in absorbance was noted for 1 mol/L peroxide. These data confirm and expand on prior published data that show co-oxidation of BC under these conditions (25).…”

Section: Methodssupporting

confidence: 82%

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Fiberoptic Resonance Raman Spectroscopy to Measure Carotenoid Oxidative Breakdown in Live Tissues

Bentz¹,

Diaz²,

Ring³

et al. 2010

Cancer Prevention Research

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Based on compelling epidemiologic and corroboratory in vitro studies, carotenoids are thought to have great potential as dietary prevention against cancer. Yet, carotenoid-based chemopreventive trials have found very contradictory results. Definitive conclusions from these trials are hampered by an inability to accurately and safely measure carotenoids in specific tissues at risk of cancer development. Raman spectroscopy has been proposed as an optical technology with which to analyze various molecules in live tissues. One major obstacle that impedes the clinical use of this powerful technology is the lack of a fiberoptic Raman probe suitable for endoscopic tissue evaluation. A single-fiber resonance Raman Spectroscope capable of noninvasive "optical biopsies" to measure carotenoid concentrations in live tissues has been developed. The accuracy of this Raman instrument was confirmed by comparison with more standard methods of spectrophotometry and high-pressure liquid chromatography using solubilized β-carotene (BC) and BC-loaded cells before use in a small patient cohort. This Raman instrument detected intact BC as well as BC oxidative breakdown as a decrement of its Raman signal in cells. Use of the Raman instrument in our small cohort study showed its feasibility for measuring human tissues and raised some potentially intriguing possibilities about BC tissue pharmacokinetics and oxidative biology. Based on these results, our newly developed single fiberoptic resonance Raman instrument may provide a very useful method of measuring carotenoids and their oxidative breakdown within live tissue during future carotenoid chemopreventive trials. This proof-of-concept study provides the foundation to justify future validation of our Raman prototype.

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“…No appreciable decrement in absorbance was noted for 1 mol/L peroxide. These data confirm and expand on prior published data that show co-oxidation of BC under these conditions (25).…”

Section: Methodssupporting

confidence: 82%

“…15-LOX-1-engineered ERC293 cells were grown to 80% confluence in media with or without 10 μmol/L ponasterone A as previously described (25). These cells were then exposed overnight to 0.3% (max) methyl-β-cyclodextrin (MβCD) alone or in combination with 0.2 or 1.0 μmol/L BC (26).…”

Section: Methodsmentioning

confidence: 99%

Fiberoptic Resonance Raman Spectroscopy to Measure Carotenoid Oxidative Breakdown in Live Tissues

Bentz¹,

Diaz²,

Ring³

et al. 2010

Cancer Prevention Research

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“…We also found that ectopic expression of 15-LOX-1 induces apoptosis in HCT-116 cells (data not shown). Other results by our group and others supporting the present finding that 15-LOX-1 expression inhibits proliferation and tumorigenesis and restores apoptosis include the following: (a) 13-S-HODE induced apoptosis and cell cycle arrest in transformed colonic cells (12); (b) 15-LOX-1 expression was crucial to apoptosis induced by nonsteroidal antiinflammatory drugs in colonic, esophageal, and gastric cancer cells (7,11,22,23); (c) the transient expression of 15-LOX-1 inhibited the proliferation of human osteosarcoma cells (24); and (d) ectopic expression of 15-LOX-1, but not 5-LOX, promoted apoptosis in virally transformed 293 kidney cells (25).…”

Section: Discussionmentioning

confidence: 99%

The Critical Role of 15-Lipoxygenase-1 in Colorectal Epithelial Cell Terminal Differentiation and Tumorigenesis

Shureiqi

Wu²,

Chen³

et al. 2005

Cancer Research

100

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Terminal differentiation is an important event for maintaining normal homeostasis in the colorectal epithelium, and the loss of apoptosis is an important mechanism underlying colorectal tumorigenesis. The very limited current data on the role of lipoxygenase (LOX) metabolism in tumorigenesis suggests that the oxidative metabolism of linoleic and arachidonic acid possibly shifts from producing antitumorigenic 15-LOX-1 and 15-LOX-2 products to producing protumorigenic 5-LOX and 12-LOX products. We examined whether this shift occurs in vitro in the human colon cancer cell line Caco-2 in association with the loss of terminal differentiation and apoptosis, or in vivo during the formation of colorectal adenomas in patients with familial adenomatous polyposis (FAP). Restoring terminal differentiation and apoptosis of Caco-2 cells increased the mRNA levels of 5-LOX, 15-LOX-2, and 15-LOX-1, but the only significant increases in protein expression and enzymatic activity were of 15-LOX-1. In FAP patients, 15-LOX-1 expression and activity were significantly down-regulated in adenomas (compared with paired nonneoplastic epithelial mucosa), whereas 5-LOX and 15-LOX-2 protein expressions and enzymatic activities were not. We conducted a validation study with immunohistochemical testing in a second group of FAP patients; 15-LOX-1 expression was down-regulated in colorectal adenomas (compared with nonneoplastic epithelial mucosa) in 87% (13 of 15) of this group. We confirmed the mechanistic relevance of these findings by demonstrating that ectopically restoring 15-LOX-1 expression reestablished apoptosis in Caco-2 cells. Therefore, 15-LOX-1 down-regulation rather than a shift in the balance of LOXs is likely the dominant alteration in LOX metabolism which contributes to colorectal tumorigenesis by repressing apoptosis. (Cancer Res 2005; 65(24): 11486-92)

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“…Kelavkar et al (2001) indicated that TRXR could directly reduce the lipid hydroperoxide 15-HPETE and potentially limit its accumulation in cells that express 15-LOX. In addition, 15-HPETE was previously shown to inhibit the activity of mammalian TRXR1 (Yu et al 2004). Therefore, we can infer that the protective effect of RA against oxidative damage is likely related to TRXR regulation of the release of ARA.…”

Section: Discussionmentioning

confidence: 90%

Retinoic acid attenuates oxidative injury in bovine mammary epithelial cells induced by hydrogen peroxide

Jin¹,

Yan²,

Shi³

et al. 2017

CZECH J ANIM SCI

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Jin L., Yan S., Shi B., Shi H., Guo X., Li J. (2017): Retinoic acid attenuates oxidative injury in bovine mammary epithelial cells induced by hydrogen peroxide. Czech J. Anim. Sci., 62, 539-548.The objective of this study was to explore how retinoic acid (RA) attenuates oxidative injury induced by hydrogen peroxide (H 2 O 2 ) in bovine mammary epithelial cells (BMEC). Subconfluence BMEC were randomly divided into four groups with six replicates: the control group (incubated in serum-free medium without RA or H 2 O 2 for 30 h), H 2 O 2 group (pre-incubated for 24 h without RA, then for another 6 h with 600 μM H 2 O 2 ), RA group (incubated with 1 mg/ml RA for 30 h without H 2 O 2 ), and RA + H 2 O 2 group (RA prevention group, pre-incubated with 1 mg/ml RA for 24 h and then for another 6 h with 600 mM H 2 O 2 ). The results showed that the H 2 O 2 treatment significantly decreased several measured traits, including the cell viability, glutathione peroxidase (GPX) and thioredoxin reductase (TRXR) activities, selenoprotein P (SELP) content, catalase and superoxide dismutase activities, total antioxidant capacity, and GPX1, TRXR1, and SELP gene expression, as well as GPX1 and TRXR1 protein expression. H 2 O 2 treatment also increased the malondialdehyde and reactive oxygen species contents and induced a marked increase of several measured traits, including the arachidonic acid (ARA) concentration, cytosolic phospholipase A2 and 5-lipoxygenase gene expression and activity, and 15-hydroxy twenty-four arachidonic acid and hydroxy peroxide tetracosenic arachidonic acid contents. RA pre-treatment prevented corresponding increases in parameters related to ARA metabolism and increased the activity of TRXR. Moreover, RA pre-treatment attenuated the phosphorylation levels of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase and effectively decreased the ARA content. These results suggest that RA protected BMEC from oxidative stress by elevating TRXR activity, which inhibited the MAPK signaling pathway and led to a decreased concentration of ARA.Keywords: vitamin A; thioredoxin reductase; oxidative injury; arachidonic acid; p38 mitogen-activated protein kinase List of abbreviations: RA = retinoic acid, ROS = reactive oxygen species, VA = vitamin A, BMEC = bovine mammary epithelial cells, GPX1 = glutathione peroxidase 1, TRXR1 = thioredoxin reductases 1, ARA = arachidonic acid, CPLA2 = cytosolic phospholipase A2, MAPK = mitogen-activated protein kinase, H 2 O 2 = hydrogen peroxide, DMSO = dimethyl sulfoxide, MTT = 5-diphenyltetrazolium bromide, DMEM/F12 = Dulbecco's Modified Eagle's Medium/F12, 5-LOX = 5-lipoxygenase, PGE2 = prostaglandin E2, COX-2 = cyclooxygenase-2, LTB4 = leukotriene B4, 12-or 15-HETE = 12-or 15-hydroxyeicosatetraenoic acid, 12-or 15-HPETE = 12-or 15-hydroperoxyeicosatetraenoic acid, ERK1/2 = extracellular signal-regulated kinase ½, JNK = c-Jun N-terminal kinase, PBS = phosphate buffered solution, RGR = relative growth rate, T-AOC = total antioxidant capacity, SOD = superoxide ...

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Conditional Expression of 15-Lipoxygenase-1 Inhibits the Selenoenzyme Thioredoxin Reductase

Cited by 36 publications

References 47 publications

Fiberoptic Resonance Raman Spectroscopy to Measure Carotenoid Oxidative Breakdown in Live Tissues

Fiberoptic Resonance Raman Spectroscopy to Measure Carotenoid Oxidative Breakdown in Live Tissues

The Critical Role of 15-Lipoxygenase-1 in Colorectal Epithelial Cell Terminal Differentiation and Tumorigenesis

Retinoic acid attenuates oxidative injury in bovine mammary epithelial cells induced by hydrogen peroxide

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