Bilirubin (BL) is a bile pigment that arises from the catabolism of hemeproteins and it is an important
biochemical marker for diagnosis and monitoring of hepatic and hematologic diseases. The high
concentration of this metabolite in plasma may be associated with disturbances in production, metabolism
and/or excretion. Several in vivo in vitro studies have established the antioxidant, anti-inflammatory and
anti-tumoral bilirubin capacity. The main objective was to verify that the effects of certain drugs and
nutritional compounds on the metabolism of bilirubin, as well as studying the effects of radical substances
in the UGT1A1 gene in addition have also studied the effect of various enzymes on serum bilirubin. The
methodology was a detailed search online database, such as Pubmed, NCBI, ScienceDirect and books,
a five-month period. Several studies refer four botanical groups as associated to changes in bilirubin
concentrations Cruciferae (e.g., broccoli), Rutaceae (citrus), Liliaceae (e.g., onions), and Leguminosae
(legumes). In a hyperbilirubinemic condition, the best approach would include the increasing UGT1A1
expression and this can be achieved with foods from the botanical families Cruciferae, Rutaceae, Liliaceae,
and Leguminosae. Regulation of UGTs by phytochemicals has been investigated with a focus on cancer
prevention numerous inhibitors from plant origin. The strategy to rise SBL, inhibiting UGT1A1 activity
appears unreasonable. Several studies show that low serum bilirubin concentrations are associated with
an increased risk of chronic diseases, whereas slightly elevated serum bilirubin levels seems to provide
protection. The enzymes HO-1 and BLV will also have an important role in the development of therapeutic
strategies based on dietary compounds however for these two enzymes there was considerable less
information about their inducers and inhibitors. It is proven that the ingestion of certain foods affects the
metabolism of bilirubin and the expression of UGT1A1 gene. Thus, it is justified the need for further studies
to demonstrate the potential of food to control the maintenance of bilirubin in order to identify possible
functional foods.info:eu-repo/semantics/publishedVersio

Ferreira, Isabel C.F.R.

Monteiro, Sandrine

Pereira, Rosa

Rodrigues, Carina

Vaz, Josiana A.

Biblioteca Digital do IPB

Livro de Resumos Título I Congresso Nacional de Ciências Biomédicas Laboratoriais: Livro de Resumos Editores Josiana Vaz  Amadeu Ferro  Clarisse Pais  Helena Pimentel  Sara Ricardo Design e paginação Atilano Suarez  Serviços de Imagem do Instituto Politécnico de Bragança Editor Instituto Politécnico de Bragança ISBN 978-972-745-211-8 Handle http://hdl.handle.net/10198/13540Apoio46Dietary compounds that modify bilirubin levelsRosa PereiraSchool of Health, Polytechnic Institute of Bragança, Bragança, Avenida D. Afonso V - 5300-121 Bragança, Portugal – rosa_94_pereira@hotmail.comSandrine MonteiroSchool of Health, Polytechnic Institute of Bragança, Bragança, Avenida D. Afonso V - 5300-121 Bragança, Portugal – sandrine.isa@hotmail.comCarina RodriguesSchool of Health, Polytechnic Institute of Bragança, Bragança, Avenida D. Afonso V - 5300-121 Bragança, Portugal; Research Unit on Applied Molecular Biosciences - REQUIMTE,  Faculty of Pharmacy, University of Porto, Porto, Portugal – carina@ipb.ptJosiana VazSchool of Health, Polytechnic Institute of Bragança, Bragança, Avenida D. Afonso V - 5300-121 Bragança, Portugal; Mountain Research Centre (CIMO), Instituto Politécnico de Bragança, Campus de Santa Apolónia, Apartado 1172, 5301-855 Bragança, Portugal – josiana@ipb.ptIsabel C.F.R. FerreiraMountain Research Centre (CIMO), Instituto Politécnico de Bragança, Campus de Santa Apolónia, Apartado 1172, 5301-855 Bragança, Portugal – iferreira@ipb.ptResumoBilirubin (BL) is a bile pigment that arises from the catabolism of hemeproteins and it is an important biochemical marker for diagnosis and monitoring of hepatic and hematologic diseases. The high concentration of this metabolite in plasma may be associated with disturbances in production, metabolism and/or excretion. Several in vivo in vitro studies have established the antioxidant, anti-inflammatory and anti-tumoral bilirubin capacity. The main objective was to verify that the effects of certain drugs and nutritional compounds on the metabolism of bilirubin, as well as studying the effects of radical substances in the UGT1A1 gene in addition have also studied the effect of various enzymes on serum bilirubin. The methodology was a detailed search online database, such as Pubmed, NCBI, ScienceDirect and books, a five-month period. Several studies refer four botanical groups as associated to changes in bilirubin concentrations Cruciferae (e.g., broccoli), Rutaceae (citrus), Liliaceae (e.g., onions), and Leguminosae (legumes). In a hyperbilirubinemic condition, the best approach would include the increasing UGT1A1 expression and this can be achieved with foods from the botanical families Cruciferae, Rutaceae, Liliaceae, and Leguminosae. Regulation of UGTs by phytochemicals has been investigated with a focus on cancer prevention numerous inhibitors from plant origin. The strategy to rise SBL, inhibiting UGT1A1 activity appears unreasonable. Several studies show that low serum bilirubin concentrations are associated with an increased risk of chronic diseases, whereas slightly elevated serum bilirubin levels seems to provide protection. The enzymes HO-1 and BLV will also have an important role in the development of therapeutic strategies based on dietary compounds however for these two enzymes there was considerable less information about their inducers and inhibitors. It is proven that the ingestion of certain foods affects the metabolism of bilirubin and the expression of UGT1A1 gene. Thus, it is justified the need for further studies to demonstrate the potential of food to control the maintenance of bilirubin in order to identify possible functional foods. Palavras-chave:Bilirubin levels, hyperbilirubinemia, oxidative stress, prevention, acquired factors, genetic, dietary compounds

Dietary compounds that modify bilirubin levels

Imprimindo:Este pôster tem 122 cm de largura por 91 cm de altura. Ele foi projetado para ser impresso em uma impressora de grandes formatos.Personalizando o Conteúdo:Os espaços reservados deste pôster estão formatados para você. Digite nos espaços reservados para adicionar texto ou clique em um ícone para adicionar uma tabela, gráfico, elemento gráfico imagem ou arquivo multimídia.Para adicionar ou remover marcadores do texto, basta clicar no botão Marcadores da guia Página Inicial.Se precisar de mais espaços reservados para títulos, conteúdo ou texto do corpo, faça uma cópia do que você precisa e arraste para o lugar. Os Guias Inteligentes do PowerPoint o ajudarão a alinhátodo o resto.Quer usar suas próprias imagens em vez das nossas? Não tem problema! Basta clicar com o botão direito do mouse em uma imagem e escolher Alterar Imagem. Mantenha a proporção das imagens ao redimensionar arrastando um canto.DIETARY COMPOUNDS THAT MODIFY BILIRUBIN LEVELSRosa Pereiraa*, Sandrine Monteiroa*, Carina Rodriguesa,b*, Josiana Vaza,c and Isabel C.F.R. Ferreiraca School of Health, Polytechnic Institute of Bragança, Bragança, Avenida D. Afonso V - 5300-121 Bragança, Portugal.b Research Unit on Applied Molecular Biosciences - REQUIMTE,  Faculty of Pharmacy, University of Porto, Porto, Portugal.cMountain Research Centre (CIMO), Polytechnic Institute of Bragança, Campus de Santa Apolónia, Apartado 1172, 5301-855 Bragança, Portugal. REFERENCES1. Fevery J. Bilirubin in clinical practice: a review. Liver Int Off J Int Assoc Study Liver [Internet].2008;28(5):592–605.2. Sticova E, Jirsa M. New insights in bilirubin metabolism and their clinical implications. World Journal ofGastroenterology. 2013. p. 6398–407.3. Bosma PJ, Chowdhury JR, Bakker C, Gantla S, de Boer a, Oostra B a, et al. The genetic basis of thereduced expression of bilirubin UDP-glucuronosyltransferase 1 in Gilbert’s syndrome. N Engl J Med.1995;333(18):1171–5.4. Rodrigues C, Vieira E, Santos R, de Carvalho J, Santos-Silva A, Costa E, et al. Impact of UGT1A1 genevariants on total bilirubin levels in Gilbert syndrome patients and in healthy subjects. Blood Cells, MolDis. 2012;48(3):166–72.5. Canu G, Minucci A, Zuppi C, Capoluongo E. Gilbert and Crigler Najjar syndromes: An update of theUDP-glucuronosyltransferase 1A1 (UGT1A1) gene mutation database. Blood Cells, Mol Dis [Internet].Elsevier Inc.; 2013;50(4):273–80.6. Rodrigues C, Costa E, Vieira E, De Carvalho J, Santos R, Rocha-Pereira P, et al. Bilirubin dependence onUGT1A1 polymorphisms, hemoglobin, fasting time and body mass index. Am J Med Sci [Internet].2012;343(2):114–8.7. Neuzil J, Stocker R. Free and albumin-bound bilirubin are efficient co-antioxidants for ??- tocopherol,inhibiting plasma and low density lipoprotein lipid peroxidation. J Biol Chem. 1994;269(24):16712–9.8. Strassburg CP, Lankisch TO, Manns MP, Ehmer U. Family 1 uridine-5???-diphosphateglucuronosyltransferases (UGT1A): From Gilbert’s syndrome to genetic organization and variability.Arch Toxicol. 2008;82:415–33.9. Katoh M, Yoshioka Y, Nakagawa N, Yokoi T. Effects of Japanese herbal medicine, Kampo, on humanUGT1A1 activity. Drug Metab Pharmacokinet. 2009;24(3):226–34.10. Saracino MR, Bigler J, Schwarz Y, Chang J-L, Li S, Li L, et al. Citrus fruit intake is associated with lowerserum bilirubin concentration among women with the UGT1A1*28 polymorphism. J Nutr [Internet].2009;139(3):555–60.11. Peterson S, Bigler J, Horner NK, Potter JD, Lampe JW. Cruciferae interact with the UGT1A1*28polymorphism to determine serum bilirubin levels in humans. J Nutr. 2005;135(December 2004):1051–5.12. LC AMR. Soy feeding induces phase II enzymes in rat tissues. Nutr Cancer. 1997;28(3):270–5.13. Condezo-Hoyos L, Abderrahim F, Conde MV, Sus??n C, D??az-Gil JJ, Gonz??lez MC, et al. Antioxidantactivity of liver growth factor, a bilirubin covalently bound to albumin. Free Radic Biol Med [Internet].Elsevier Inc.; 2009;46(5):656–62.14. Brodersen R. Bilirubin. Solubility and interaction with albumin and phospholipid. J Biol Chem.1979;254(7):2364–9.15. Roca L, Calligaris S, Wennberg RP, Ahlfors CE, Malik SG, Ostrow JD, et al. Factors affecting the bindingof bilirubin to serum albumins: Validation and application of the peroxidase method. Pediatr Res.2006;60(6):724–8.16. Hong AL, Huo D, Kim HJ, Niu Q, Fackenthal DL, Cummings S a., et al. UDP-glucuronosyltransferase1A1 gene polymorphisms and total bilirubin levels in an ethnically diverse cohort of women. Drug MetabDispos. 2007;35(8):1254–61.17. Jansen T, Daiber A. Direct antioxidant properties of bilirubin and biliverdin. Is there a role for biliverdinreductase? Front Pharmacol. 2012;3 MAR.18. Zucker SD, Goessling W. Mechanism of hepatocellular uptake of albumin-bound bilirubin. BiochimBiophys Acta - Biomembr. 2000;1463:197–208.19. Wolkoff AW, Goresky CA, Sellin J, Gatmaitan Z, Arias IM. Role of ligandin in transfer of bilirubin fromplasma into liver. Am J Physiol [Internet]. 1979;236(6):E638–48.20. Roberts MS, Magnusson BM, Burczynski FJ, Weiss M. Enterohepatic circulation: physiological,pharmacokinetic and clinical implications. Clin Pharmacokinet. 2002;41(10):751–90.21. Belo L, Nascimento H, Kohlova M, Bronze-da-Rocha E, Fernandes J, Costa E, et al. Body fat percentageis a major determinant of total bilirubin independently of UGT1A1*28 polymorphism in young obese.PLoS One. 2014;9(6).BRIEF DESCRIPTION OF BILIRUBIN METABOLISM In human plasma there are 4 main forms of circulating BL: unconjugatedbilirubin (UCB), also known as -bilirubin or indirect bilirubin (IB);monoconjugate bilirubin (bilirubin-) or monoglucorunide (MGB) or conjugatedbilirubin (CB); diconjugated bilirubin (bilirubin ) or diglucorunide (DGB) ordirect bilirubin, also known as hepatic growth factor covalently bound toalbumin, irreversibly. Another BL fraction to consider is the free BL that is notbound to albumin. BL is transported in plasma bound to Alb with a high affinitybond to the Alb primary binding site. The free BL correlates better with BLtoxicity than any other fraction. The main source of BL is the heme group ofhemoglobin from the destruction of senescent erythrocytes, which contributesaround 80-85% of total production. The remaining 15 to 20% of BL productionresults from the tournover of other liver hemeproteins such as myoglobin,catalase and cytochrome. A small proportion (1-5%) results from the prematuredestruction of premature erythrocytes in bone marrow or spleen. The hemecatabolism, resulting in BL production occurs within macrophages of the spleen,bone marrow and in Kupffer cells. After the heme breakdown BL is released intothe plasma. In this mechanism, the ring of ferroprotoporfirina IX heme group, theprosthetic group of proteins such as hemoglobin, myoglobin and cytochrome P-450, suffers the catalytic action of heme oxygenase (HO-1). This enzymeconsumes three molecules of oxygen and requires a reducing agent, nicotinamideadenine dinucletídeo phosphate (NADPH). The enzyme HO-1 acts at the centralbridge methionine, forming biliverdin (BLV) and is located in the plasmamembrane of the endoplasmic reticulum, nucleus and mitochondria. Its synthesisis induced by stimuli associated with oxidative stress, including free oxygen andbacterial lipopolysaccharide radicals by increasing the intracellular concentrationof hepatic heme induced by various drugs, natural compounds, cytokines andgrowth factors. From the oxidation of heme it also results iron (Fe3 +), carbonmonoxide (CO) and BLV. The BLV is, in turn reduced to BL in a reaction that iscatalyzed by biliverdin reductase (BVR), dependent on NADPH. BL at this stage,is called UCB and circulates in the blood bound to albumin.Alb greatly enhances their solubility due to two binding sites for this moleculeand also prevents it is excreted into urine (15).METHODS AND MATERIALSome studies point out that UCB may prevent cardiovascular disease(CVD) and other chronic diseases. Clinical evidence indicates thathyperbilirubinaemic individuals with GS, with mild hyperbilirubinemia,are at reduced risk of developing cardiovascular and chronic kidneydisease. There are currently several studies that have established anassociation between low BL and the presence and severity of variouscardiovascular diseases and the respective causes or co-morbidities suchas, type 2 diabetes, metabolic syndrome, hypertension, chronic kidneydisease and albuminuria. It was observed the same association, asdescribed above, with other disease conditions which physiopathology isrelated to oxidative stress, such as rheumatoid arthritis, multiplesclerosis, cancer and overall mortality.RESULTSCONCLUSIONIn a hyperbilirubinemic condition, were it is important to lower serum bilirubinlevels, the best approach would include the increasing UGT1A1 expression andthis can be achieved with foods from the botanical families Cruciferae (e.g.,broccoli), Rutaceae (citrus), Liliaceae (e.g., onions), and Leguminosae(legumes). Regulation of UGTs by phytochemicals has been investigated with afocus on cancer prevention numerous inhibitors from plant origin (epicatechingallate, epigallocatechin gallate, octyl gallate, propyl gallate, quercetin, tannicacid, benzoin gum, capsaicin, dihydrocapsaicin, eugenol, gallocatechin gallate,geraniol, menthol, menthyl acetate, naringenin, allspice berry oil, N-vanillylnonanamide, clovebud oil, peppermint oil, silibinin, and silymarin). Thestrategy to rise SBL, inhibiting UGT1A1 activity appears unreasonable becauseUGT1A1 also glucuronides, estrogens and several dietary carcinogens.Several studies show that low serum bilirubin concentrations are associatedwith an increased risk of chronic diseases, whereas slightly elevated serumbilirubin levels seems to provide protection. The enzymes HO-1 and BLV willalso have an important role in the development of therapeutic strategies basedon dietary compounds however for these two enzymes there was considerableless information about their inducers and inhibitors.Fig. (1). Bilirubin hepatic uptake, conjugation and glucoronid transporters. SER: smooth endoplasmic reticulum; UCB:unconjugated bilirubin; Alb: albumin; MGB e DGB: mono and diglucuronid; Y: ligandin; UGT1A1: uridine 5'-diphospho-glucuronosyltransferase 1A1 (UDP-glucuronosyltransferase, UGT); UDPGlcUA: glucuronic acid residue; OATP1B1/3: organicanion transporter, 1B1 and 1B3; ABCC3: ATP-Binding Cassette transporter, (Sub-Family C, CFTR/MRP, Member 3); MRP2:Multidrug Resistance-associated Protein 2; ABCC2: ATP-Binding Cassette transporter (sub-family G member 2). The image alsoshows the location of UGT1A1 in the membrane of smooth endoplasmic reticulum membrane (SER); transport of unconjugatedbilirubin (UCB) into hepatocyte at the sinusoidal surface by the action of the organic anion basolateral transporters OATP1B1/3(organic anion transporter, 1B1 and 1B3); ligandin assembles and transport UCB to the SER; conjugation of UCB by UGT1A1results in bilirubin glucuronides (MGB, DGB); glucuronides are water soluble and are transported to the exterior of the hepatocyte,at the apical canalicular surface, by the MRP2 (Multidrug Resistance-Associated Protein 2) and ABCC2 (ATP-Binding Cassettetransporter - sub-family G member 2), and possibly by the ligandin (initially named Y protein) a glutathione-S-transferases (17),which despite being in much smaller quantity, can pass through the protein ABCC3 a ATP-Binding Cassette transporter, (Sub-FamilyC, CFTR/MRP, Member 3) and be again captured by OATP transporters.DRUG INTERACTION WITH BILIRUBIN METABOLISMMany exogenous substances, xenobiotics and drugs are substrates of UGT1A1enzyme. Genetic variations that alter the expression of UGT1A1 may be a dangeras they would increase toxicity for patients. The variant most studied in thisinteraction corresponds to the polymorphism UGT1A1 * 28, at the UGT1A1promoter responsible for the GS, characterized by hiperbilirubinemia. Examplesof UGT1A1 substrates are irinotecan (SN-38), acetaminophen (paracetamol) andsimvastatin (8).Dietary compounds or dietary sources intakeType of study Effect on bilirubin levelsSummaryRecord of food intake from fourbotanical groups: Cruciferae,Rutaceae, Liliaceae and Leguminosae.ObservationalDecreased SBL. Only homozygotes 7/7 showed decreased bilirubin concentrations after consuming cruciferous vegetables but not with the intake of other investigated botanical groups. Cruciferous, citrus and soy (doses adjustusd for body weight)Clinical Decreased SBL. The intake of cruciferous vegetables, soy foods and citrus fruit seems was associated to a decrease on SBL but only in women that are homozygous 7/7.Record of food intake Citrus fruit, cruciferous and soyObservationalDecreased SBL. Women homozygous 7/7 that consume citrus fruit may exhibit a higher activity of this gene than those who do not include it on their diet.Cruciferous, citrus and soy (Different quantities of Cruciferous supplementation)Clinical Decreased SBL within all of  three group of vegetable and it was observed in the three genotypes. Results suggest a dose-response.Soy In vivo DecreasedResveratrol(Resveratrol doses)Clinical Decreased SBL. UGT1A1 activities were minimally affected by the intervention. is more pronounced in individuals with low baseline enzyme activity.Dandelion In vivo Decreased Rooibos In vivo Decreased Honeybush tea In vivo DecreasedRosemery In vivo DecreasedEllagic acid (present in berryes, pomegranate, grapes, walnuts, and blackcurrants)In vivo DecreasedFerulic acid In vivo DecreasedCurcumin In vivo DecreasedAstaxanthin In vivo DecreasedGreen tea In vitro Increased Green tea In vitro IncreasedQuercetin In vitro IncreasedRutin In vitro IncreasedNaringenin In vitro IncreasedAllspice In vitro IncreasedPeppermint oil In vitro IncreasedCacao In vitro IncreasedTable 2. Sources or dietary compounds that can modulate serum bilirubin levels by interfering with UGT1A1 activity.Bilirubin (BL) is a yellow-orange pigment resulting from the catabolism ofhemeproteins. This tetrapirrolic metabolite belongs to one of the mostconserved superfamily of molecules in living, organisms. The BL has beensubject of study for more than three centuries. In clinical diagnosis, BL is amarker of liver function and used to monitoring hematological diseases. Theenzyme that catalyzes BL conjugation is the uridine diphosphate glucuronyltransferase 1A1 (UGT1A1). Unconjugated BL (UCB) is lipid solublemolecule but after conjugation (with one or two molecules of glucuronicacid) becomes water soluble (conjugated bilirubin: CB), allowing itsexcretion via the bile canaliculi. The most prevalent metabolic disorder inthe Caucasian population is Gilbert's syndrome (GS). It´s a benigncondition, characterized by moderate hyperbilirubinemia in the absence ofhemolysis or liver dysfunction. The common variant associated with thissyndrome is the TA duplication at position c.-41_-40dupTA (variantUGT1A1*28 or A(TA)7TAA allele) located in the promoter region of theUGT1A1 gene. The presence of hyperbilirubinemia, associated with GS, canlead to the worsening of clinical symptoms of individuals with chronichemolytic diseases.At high concentrations, as described in children with Crigler-Najjarsyndrome type I (SCN-I) or type II (SCN-II), BL can be extremely toxic.However, in the past 20 years, the possible antioxidant, anti-inflammatoryand anti-carcinogenic properties, observed in the presence of mild elevatedSBL, have been motivated researchers to conduct numerous epidemiologicaland experimental studies to clarify the mechanisms involved in its potentialprotective effect.Observation of in vitro and in vivo studies suggest that certain dietarycompounds may increase or decrease BL levels. It is well known that drugsand other substances that can compete with BL for glucuronidation alsocontribute to the raising of SBL. Some herbal extracts can even exertinhibitory effects of UGT1A1 activity and thereby increase BL levels. Onthe other hand, there are dietary components that increase enzymatic activityof UGT1A1 , such as citrus fruit and some constituents of such Cruciferousvegetables (eg. cabbage and broccoli) by increasing the expression ofUGT1A1 gene. In animal models it was demonstrated that soy protein andsoy isoflavones enhance hepatic UGT activity.INTRODUCTIONAfter hepatic uptake and metabolism, BL may remain in the liver cells (storage)connected to cytoplasmic proteins. It can also move to the smooth endoplasmicreticulum of the hepatocyte and undergo conjugation with one or two residuesof glucuronic acid ( UDPGlcUA) by the catalytic action of UGT1A1 formingmonoglucorunídeo (MGB) or diglucorunídeo (DGB ), named as conjugatedbilirubin (CB). In the gut this CB undergoes oxidation by the action of intestinalenzymes and bacterial flora and urobilinogen is formed as other pigments. TheUrobilinogen may again be captured to the liver (enterohepatic circulation) andmay be conjugated.The liver plays a central role in the metabolism of BL. It is responsible for theircapture, storage, conjugation and excretion. The BNC circulates in plasma in acomplex bound to Alb ( BL- Alb ) entering the hepatocyte by its surfacesinusoidal (figure 1).An extensive variety of fruits and vegetables offer a range of nutrients anddifferent bioactive compounds including phytochemicals, vitamins, minerals,and fibers. Many dietary compounds, present in fruits, vegetables and spiceshave been isolated and evaluated for their therapeutic potential. Evidencesuggests that the health benefits of fruits and vegetables are attributed to theinteractions of the phytochemicals present in whole foods by modulatingseveral metabolic pathways. The impression that these compounds have healthpromoting effects emerged because their consumption was related to a reducedincidence of cancer, cardiovascular, neurological, respiratory, and age relateddiseases (21).

Bilirubin (BL) is a bile pigment that arises from the catabolism of hemeproteins and it is an important biochemical marker for diagnosis and monitoring of hepatic and hematologic diseases. The high concentration of this metabolite in plasma may be associated with disturbances in production, metabolism and/or excretion. Several in vivo and in vitro studies established the antioxidant, anti-inflammatory and anti- tumoral properties of bilirubin. Clinical and prospective studies show that slightly elevated serum bilirubin levels are positively correlated with a lower prevalence of oxidative stress-mediated diseases. In this review, detailed information on dietary compounds related to changes in serum bilirubin levels are provided. Most of the reviewed articles described compounds that inhibit or induces the most important enzymes in BL metabolism. Knowing how to modulate bilirubin levels by these compounds would be useful as a therapeutic approach, either to lowering serum bilirubin levels, in cases of hyperbilirubinemia, or to increase bilirubin concentration in order protect against oxidative stress. Several studies refer four botanical groups as associated to changes in bilirubin concentrations Cruciferae (e.g., broccoli), Rutaceae (citrus), Liliaceae (e.g., onions), and Leguminosae (legumes).info:eu-repo/semantics/publishedVersio

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Dietary compounds that modify bilirubin levels

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