Biliverdin was reduced to bilirubin in pregnant and foetal guinea pigs, and the 100000 g supernatant from homogenates of foetal liver, placenta and maternal liver showed high biliverdin reductase activity. The placental transport of unconjugated bilirubin and biliverdin was compared by injecting unlabelled and radiolabelled pigments into the foetal or maternal circulation and analysing blood collected from the opposite side of the placenta. Injected bilirubin crossed the placenta from foetus to mother and vice versa, but injected biliverdin did not appear to cross without prior reduction to bilirubin. The guinea-pig placenta is apparently more permeable to bilirubin than biliverdin. Reduction of biliverdin to bilirubin in the foetus may, therefore, be essential for efficient elimination of haem catabolites from the foetus in placental mammals.
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http://dx.doi.org/10.1042/bj1940273 | DOI Listing |
Genes (Basel)
November 2024
Clinic for Small Animal Internal Medicine, Vetsuisse Faculty University of Zürich, 8057 Zürich, Switzerland.
In heme degradation, biliverdin reductase catalyzes the conversion of biliverdin to bilirubin. Defects in the biliverdin reductase A gene () causing biliverdinuria are extraordinarily rare in humans, and this inborn error of metabolism has not been reported in other mammals. The objective of this study was to diagnose biliverdinuria and identify the causal variants in two adult mixed-breed dogs with life-long green urine.
View Article and Find Full Text PDFiScience
December 2024
Poltava State Medical University, Department of Pathophysiology, Poltava, Ukraine.
5-Aminolevulinic acid (5-ALA) is an essential compound in the biosynthesis of heme, playing a critical role in various physiological processes within the human body. This review provides the thorough analysis of the latest research on the molecular mechanisms and potential therapeutic benefits of 5-ALA in managing metabolic disorders. The ability of 5-ALA to influence immune response and inflammation, oxidative/nitrosative stress, antioxidant system, mitochondrial functions, as well as carbohydrate and lipid metabolism, is mediated by molecular mechanisms associated with the suppression of the transcription factor NF-κB signaling pathway, activation of the transcription factor Nrf2/heme oxygenase-1 (HO-1) system leading to the formation of heme-derived reaction products (carbon monoxide, ferrous iron, biliverdin, and bilirubin), which may contribute to HO-1-dependent cytoprotection through antioxidant and immunomodulatory effects.
View Article and Find Full Text PDFAm J Hypertens
December 2024
Department of Physiology & Biophysics, Cardiovascular-Renal Research Center, Cardiorenal, and Metabolic Diseases Research Center, University of Mississippi Medical Center, Jackson, MS 39216 USA.
Background: Increased circulating bilirubin attenuates angiotensin (Ang) II-induced hypertension and improves renal hemodynamics. However, the intrarenal mechanisms that mediate these effects are not known. The goal of the present study was to test the hypothesis that bilirubin generation in the renal medulla plays a protective role against Ang II-induced hypertension.
View Article and Find Full Text PDFJ Phys Chem B
December 2024
Department of Chemistry, University of North Carolina, Chapel Hill, North Carolina 27599, United States.
Sandercyanin is a mildly fluorescent biliprotein with a large Stokes shift, a tetrameric quaternary structure, and a biliverdin (BV) chromophore that does not covalently bond to the protein. To adapt this promising protein for use in bioimaging, it is necessary to produce monomeric mutants that retain the spectroscopic properties while increasing the fluorescence quantum yield. Modulating these properties through the protonation state of BV's propionic tails is a possible avenue, if detailed mechanistic information on the role of such chains becomes available.
View Article and Find Full Text PDFMetabolism
February 2025
Drug & Disease Discovery D3 Research Center, Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY, USA. Electronic address:
The rising rates of obesity worldwide have increased the incidence of cardiovascular disease (CVD), making it the number one cause of death. Higher plasma bilirubin levels have been shown to prevent metabolic dysfunction and CVD. However, reducing levels leads to deleterious outcomes, possibly due to reduced bilirubin half-life that escalates the production of its catabolized product, urobilinogen, produced by gut bacteria and naturally oxidized to urobilin.
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