Bilirubin: An Endogenous Product of Heme Degradation with Both Cytotoxic and Cytoprotective Properties: Fig. 1

Kapitulnik, Jaime

doi:10.1124/mol.104.002832

Cited by 216 publications

(189 citation statements)

References 81 publications

(67 reference statements)

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“…Hyperbilirubinemia is neurotoxic in the neonate leading to brain damage, known as 'kernicterus' [75]. It is tempting to speculate that evolution of the gtPBREM cluster of binding sites for a number of LATFs in the promoter of UGT1A1 [46,47] may be related to the need for perinatal UGT1A1 induction in primates.…”

Section: Page 9 Of 31mentioning

confidence: 99%

From differential induction of UDP-glucuronosyltransferases in rat liver to characterization of responsible ligand-activated transcription factors, and their multilevel crosstalk in humans

Bock¹

2011

Biochemical Pharmacology

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. From differential induction of UDP-glucuronosyltransferases in rat liver to characterization of responsible ligand-activated transcription factors, and their multilevel crosstalk in humans. Biochemical Pharmacology, Elsevier, 2011, 82 (1) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64

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Section: Page 9 Of 31mentioning

confidence: 99%

From differential induction of UDP-glucuronosyltransferases in rat liver to characterization of responsible ligand-activated transcription factors, and their multilevel crosstalk in humans

Bock¹

2011

Biochemical Pharmacology

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“…Following heme catabolism, bilirubin releases into the blood, where it binds to serum proteins and is transported to the liver, followed by metabolism through glucuronidation by UDP-glucuronosyltransferase 1A1 (UGT1A1) (1). Neonatal jaundice is mostly benign, but dangerously high levels of total serum bilirubin can be produced when newborns inherit inactivating gene polymorphisms in the UGT1A1 gene, as seen in Crigler Najjar diseases (2), which lead to encephalopathy and kernicterus (3).…”

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confidence: 99%

Developmental Onset of Bilirubin-induced Neurotoxicity Involves Toll-like Receptor 2-dependent Signaling in Humanized UDP-glucuronosyltransferase1 Mice

Yueh

Chen

Nguyen

et al. 2014

Journal of Biological Chemistry

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Background: Neonatal jaundice with dangerously high levels of serum bilirubin leads to neurological toxicity. Results: Toll-like receptor 2 signaling is essential for regulation of glia activation, neuroinflammation, and oxidative stress when neonatal mice experience severe hyperbilirubinemia. Conclusion: Toll-like receptor 2 signaling is linked to a protection mode against serum bilirubin-induced brain toxicity. Significance: Understanding how signaling from innate immunity contributes to bilirubin-induced pathology.

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“…HO-1 may also contribute to cellular survival through generation of its products CO, biliverdin (converted to bilirubin), and Fe 2ϩ . Both biliverdin and bilirubin are antioxidant molecules that may confer protection via their ability to quench peroxyl radicals and singlet oxygen, thus interfering with lipid peroxidation (28). CO has been recently recognized as a signaling molecule (29), which may provide additional resistance mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…8). Bilirubin, a secondary product of HO-1, was used because it is able to prevent H 2 O 2 -induced lipid peroxidation (28). Pretreatment of the L1 and A4 cells with SnPPIX significantly sensitized both lines to NO toxicity compared with the controls treated with NO alone (p Ͻ 0.001 for both L1 (control versus SnPPIX) and A4 (control versus SnPPIX)).…”

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confidence: 99%

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Resistance to Nitric Oxide-induced Necrosis in Heme Oxygenase-1 Overexpressing Pulmonary Epithelial Cells Associated with Decreased Lipid Peroxidation

Reiter

Pang

Dedon

et al. 2006

Journal of Biological Chemistry

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Increased expression of heme oxygenase-1 (HO-1) increases NO resistance in several cell types, although the biochemical mechanism for this protection is unknown. To address this issue, we have measured different molecular markers of nitrosative stress in three stably transfected cell lines derived from the human lung epithelial line A549: two lines that overexpress rat HO-1 (L1 and A4), and a control line with the empty vector (Neo). Compared with the control Neo cells, L1 and A4 cells had, respectively, 5.8-and 3.8-fold greater HO activity accompanied by increased resistance to NO-induced necrosis. Compared with the Neo control, the HO-1-overexpressing cells also showed significantly less lipid peroxide formation and decreased perturbation of transition metal oxidation and coordination states following a cytotoxic NO exposure. These effects were blocked by the HO-1 inhibitors Zn-and Sn-protoporphyrin IX. In contrast, HO-1 overexpression did not significantly affect total reactive oxygen or nitrogen species, the levels of the nucleobase deamination products in DNA (xanthine, inosine, and uracil) following NO exposure, or NO-induced protein nitration. While increased HO-1 activity prevented NO-induced fluctuations in transition metal homeostasis, addition of an iron chelator decreased NO toxicity only slightly. Our results indicate that lipid peroxidation is a significant cause of NO-induced necrosis in human lung epithelial cells, and that the increased NO survival of L1 cells is due at least in part to decreased lipid peroxidation mediated by HO-1-generated biliverdin or bilirubin.

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Bilirubin: An Endogenous Product of Heme Degradation with Both Cytotoxic and Cytoprotective Properties: Fig. 1

Cited by 216 publications

References 81 publications

From differential induction of UDP-glucuronosyltransferases in rat liver to characterization of responsible ligand-activated transcription factors, and their multilevel crosstalk in humans

From differential induction of UDP-glucuronosyltransferases in rat liver to characterization of responsible ligand-activated transcription factors, and their multilevel crosstalk in humans

Developmental Onset of Bilirubin-induced Neurotoxicity Involves Toll-like Receptor 2-dependent Signaling in Humanized UDP-glucuronosyltransferase1 Mice

Resistance to Nitric Oxide-induced Necrosis in Heme Oxygenase-1 Overexpressing Pulmonary Epithelial Cells Associated with Decreased Lipid Peroxidation

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