Bilirubin

Found 33 Sample Hits

m/z	Adducts	Species	Organ	Scanning	Sample
567.2679	[M+H-H2O]+ PPM:13.6	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito03_17 - MTBLS58 Resolution: 17μm, 208x108 Description 1 male adult wild-type rat was obtained from Inserm U1085 - Irset Research Institute (University of Rennes1, France). Animals were age 60 days and were reared under ad-lib conditions. Care and handling of all animals complied with EU directive 2010/63/EU on the protection of animals used for scientific purposes. The whole epididymis was excised from each animal immediately post-mortem, loosely wrapped rapidly in an aluminum foil and a 2.5% (w/v) carboxymethylcellulose (CMC) solution was poured to embed the epididymis to preserve their morphology. To remove air bubbles, the filled aluminum molds was gently freezed by depositing it on isopentane or dry ice, then on the nitrogen vapors and finally by progressively dipping the CMC/sample coated with aluminum foil into liquid nitrogen (or only flush with liquid nitrogen). Frozen tissues were stored at -80 °C until use to avoid degradation.
584.2937	[M-H2O+NH4]+ PPM:11.9	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito03_17 - MTBLS58 Resolution: 17μm, 208x108 Description 1 male adult wild-type rat was obtained from Inserm U1085 - Irset Research Institute (University of Rennes1, France). Animals were age 60 days and were reared under ad-lib conditions. Care and handling of all animals complied with EU directive 2010/63/EU on the protection of animals used for scientific purposes. The whole epididymis was excised from each animal immediately post-mortem, loosely wrapped rapidly in an aluminum foil and a 2.5% (w/v) carboxymethylcellulose (CMC) solution was poured to embed the epididymis to preserve their morphology. To remove air bubbles, the filled aluminum molds was gently freezed by depositing it on isopentane or dry ice, then on the nitrogen vapors and finally by progressively dipping the CMC/sample coated with aluminum foil into liquid nitrogen (or only flush with liquid nitrogen). Frozen tissues were stored at -80 °C until use to avoid degradation.
567.2679	[M+H-H2O]+ PPM:13.6	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito03_18 - MTBLS58 Resolution: 17μm, 208x104 Description
584.2937	[M-H2O+NH4]+ PPM:11.9	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito03_18 - MTBLS58 Resolution: 17μm, 208x104 Description
567.2679	[M+H-H2O]+ PPM:13.6	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_43 - MTBLS58 Resolution: 17μm, 298x106 Description
584.2635	[M]+ PPM:1	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_43 - MTBLS58 Resolution: 17μm, 298x106 Description
584.2938	[M-H2O+NH4]+ PPM:12.1	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_43 - MTBLS58 Resolution: 17μm, 298x106 Description
585.271	[M+H]+ PPM:0.4	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_43 - MTBLS58 Resolution: 17μm, 298x106 Description
567.2679	[M+H-H2O]+ PPM:13.6	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_44 - MTBLS58 Resolution: 17μm, 299x111 Description
584.2937	[M-H2O+NH4]+ PPM:11.9	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_44 - MTBLS58 Resolution: 17μm, 299x111 Description
567.2678	[M+H-H2O]+ PPM:13.4	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_46 - MTBLS58 Resolution: 17μm, 298x106 Description
584.2937	[M-H2O+NH4]+ PPM:11.9	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_46 - MTBLS58 Resolution: 17μm, 298x106 Description
567.2679	[M+H-H2O]+ PPM:13.6	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_47 - MTBLS58 Resolution: 17μm, 301x111 Description
584.2937	[M-H2O+NH4]+ PPM:11.9	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_47 - MTBLS58 Resolution: 17μm, 301x111 Description
585.271	[M+H]+ PPM:0.4	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_47 - MTBLS58 Resolution: 17μm, 301x111 Description
567.2679	[M+H-H2O]+ PPM:13.6	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_48 - MTBLS58 Resolution: 17μm, 294x107 Description
584.2937	[M-H2O+NH4]+ PPM:11.9	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito08_48 - MTBLS58 Resolution: 17μm, 294x107 Description
567.2679	[M+H-H2O]+ PPM:13.6	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito01_04 - MTBLS58 Resolution: 17μm, 178x91 Description
584.2938	[M-H2O+NH4]+ PPM:12.1	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito01_04 - MTBLS58 Resolution: 17μm, 178x91 Description
567.2679	[M+H-H2O]+ PPM:13.6	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito01_03 - MTBLS58 Resolution: 17μm, 159x110 Description
584.2937	[M-H2O+NH4]+ PPM:11.9	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito01_03 - MTBLS58 Resolution: 17μm, 159x110 Description
567.2679	[M+H-H2O]+ PPM:13.6	Rattus norvegicus	normal	MALDI (DHB)	epik_dhb_head_ito01_05 - MTBLS58 Resolution: 17μm, 183x105 Description
584.2937	[M-H2O+NH4]+ PPM:11.9	Rattus norvegicus	normal	MALDI (DHB)	epik_dhb_head_ito01_05 - MTBLS58 Resolution: 17μm, 183x105 Description
567.2679	[M+H-H2O]+ PPM:13.6	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito01_06 - MTBLS58 Resolution: 17μm, 183x103 Description
584.2939	[M-H2O+NH4]+ PPM:12.3	Rattus norvegicus	Epididymis	MALDI (DHB)	epik_dhb_head_ito01_06 - MTBLS58 Resolution: 17μm, 183x103 Description
623.3672	[M+K]+ PPM:9.6	Mus musculus	Left upper arm	MALDI (CHCA)	357_l_total ion count - Limb defect imaging - Monash University Resolution: 50μm, 97x131 Description Diseased
585.2719	[M+H]+ PPM:2	Macropus giganteus	Brain	MALDI (BPYN)	170321_kangaroobrain-dan3-pos_maxof50.0_med1 - 170321_kangaroobrain-dan3-pos_maxof50.0_med1 Resolution: 50μm, 81x50 Description Sample information Organism: Macropus giganteus (kangaroo) Organism part: Brain Condition: Wildtype Sample growth conditions: Wild
607.2431	[M+Na]+ PPM:15.8	Macropus giganteus	Brain	MALDI (BPYN)	170321_kangaroobrain-dan3-pos_maxof50.0_med1 - 170321_kangaroobrain-dan3-pos_maxof50.0_med1 Resolution: 50μm, 81x50 Description Sample information Organism: Macropus giganteus (kangaroo) Organism part: Brain Condition: Wildtype Sample growth conditions: Wild
623.3496	[M+K]+ PPM:18.6	Homo sapiens	esophagus	DESI ()	LNTO22_1_4 - MTBLS385 Resolution: 17μm, 82x80 Description
549.2439	[M+H-2H2O]+ PPM:10.4	Mytilus edulis	gill	MALDI (DHB)	20190202_MS38_Crassostrea_Gill_350-1500_DHB_pos_A25_11um_305x210 - MTBLS2960 Resolution: 11μm, 305x210 Description single cell layer class_4 is the gill structure cells, metabolite ion 534.2956 is the top representive ion of this type of cell
602.3008	[M+NH4]+ PPM:5.8	Homo sapiens	esophagus	DESI ()	TO31T - MTBLS385 Resolution: 75μm, 56x54 Description
602.3017	[M+NH4]+ PPM:7.3	Homo sapiens	esophagus	DESI ()	TO29T - MTBLS385 Resolution: 75μm, 56x48 Description
584.2631	[M]+ PPM:0.3	Homo sapiens	esophagus	DESI ()	LNTO22_1_8 - MTBLS385 Resolution: 75μm, 69x61 Description

Bilirubin is a yellow bile pigment that is a degradation product of heme. It occurs in the normal catabolic pathway that breaks down heme in vertebrates. This catabolism is a necessary process in the bodys clearance of waste products that arise from the destruction of aged or abnormal red blood cells. Bilirubin has been found in all vertebrates and in certain plants including Strelitzia nicolai (PMID: 28573242). Bilirubin levels in humans are elevated in certain diseases such as jaundice and liver disease and it is responsible for the yellow color of bruises and the yellow discoloration in jaundice. Bilirubin breakdown products, such as stercobilin, cause the brown color of feces. A different breakdown product, urobilin, is the main component of the straw-yellow color in urine. Bilirubin consists of an open chain of four pyrroles (tetrapyrrole). It is formed by oxidative cleavage of a porphyrin in heme, which leads to biliverdin, a green tetrapyrrolic bile pigment that is also a product of heme catabolism. Biliverdin is then reduced to bilirubin via biliverdin reductase. After conjugation with glucuronic acid, bilirubin can be excreted in the urine. Bilirubin is structurally similar to the pigment phycobilin used by certain algae to capture light energy, and to the pigment phytochrome used by plants to sense light. Elevated bilirubin levels in humans are associated with Crigler-Najjar syndrome type I, which is an inborn error of metabolism. Crigler-Najjar syndrome is a rare genetic disorder characterized by an inability to properly convert and clear bilirubin from the body. Affected individuals cannot convert unconjugated bilirubin to the conjugated form because they lack a specific liver enzyme required to break down (metabolize) bilirubin. Since they cannot convert bilirubin, they develop abnormally high levels of unconjugated bilirubin in the blood (hyperbilirubinemia). Crigler-Najjar syndrome is caused by mutations in the UGT1A1 gene. The hallmark finding of Crigler-Najjar syndrome is a persistent yellowing of the skin, mucous membranes and whites of the eyes (jaundice). Elevation of both alanine aminotransferase and bilirubin levels in serum or plasma can be indicative of serious liver injury. High levels of bilirubin are indicative of jaundice, which is easily recognizable due to a yellowing of the skin and eyes. Bilirubin is also an antioxidant. Bilirubins antioxidant activity may be particularly important in the brain, where it prevents excitotoxicity and neuronal death by scavenging superoxide during N-methyl-D-aspartic acid neurotransmission (PMID: 31353321). Bilirubin is a bile pigment that is a degradation product of heme. In particular, bilirubin is a yellow breakdown product of normal heme catabolism. Its levels are elevated in certain diseases and it is responsible for the yellow color of bruises. Bilirubin is an excretion product, and the body does not control levels. Bilirubin levels reflect the balance between production and excretion. Thus, there is no "normal" level of bilirubin. Bilirubin consists of an open chain of four pyrroles (tetrapyrrole); by contrast, the heme molecule is a closed ring of four pyrroles, called porphyrin. -- Wikipedia [HMDB]. Bilirubin is found in many foods, some of which are barley, mustard spinach, other bread, and sesbania flower. Bilirubin (BR) (from the Latin for "red bile") is a red-orange compound that occurs in the normal catabolic pathway that breaks down heme in vertebrates. This catabolism is a necessary process in the body's clearance of waste products that arise from the destruction of aged or abnormal red blood cells.[3] In the first step of bilirubin synthesis, the heme molecule is stripped from the hemoglobin molecule. Heme then passes through various processes of porphyrin catabolism, which varies according to the region of the body in which the breakdown occurs. For example, the molecules excreted in the urine differ from those in the feces.[4] The production of biliverdin from heme is the first major step in the catabolic pathway, after which the enzyme biliverdin reductase performs the second step, producing bilirubin from biliverdin.[5][6] Ultimately, bilirubin is broken down within the body, and its metabolites excreted through bile and urine; elevated levels may indicate certain diseases.[7] It is responsible for the yellow color of healing bruises and the yellow discoloration in jaundice. The bacterial enzyme bilirubin reductase is responsible for the breakdown of bilirubin in the gut.[8] One breakdown product, urobilin, is the main component of the straw-yellow color in urine.[9] Another breakdown product, stercobilin, causes the brown color of feces. Although bilirubin is usually found in animals rather than plants, at least one plant species, Strelitzia nicolai, is known to contain the pigment.[10] Bilirubin is created by the activity of biliverdin reductase on biliverdin, a green tetrapyrrolic bile pigment that is also a product of heme catabolism. Bilirubin, when oxidized, reverts to become biliverdin once again. This cycle, in addition to the demonstration of the potent antioxidant activity of bilirubin,[14] has led to the hypothesis that bilirubin's main physiologic role is as a cellular antioxidant.[15][16] Consistent with this, animal studies suggest that eliminating bilirubin results in endogenous oxidative stress.[17] Bilirubin's antioxidant activity may be particularly important in the brain, where it prevents excitotoxicity and neuronal death by scavenging superoxide during N-methyl-D-aspartic acid neurotransmission.[18] Bilirubin in plasma is mostly produced by the destruction of erythrocytes. Heme is metabolized into biliverdin (via heme oxygenase) and then into bilirubin (via biliverdin reductase) inside the macrophages. [11] Bilirubin is then released into the plasma and transported to the liver bound by albumin, since it is insoluble in water in this state. In this state, bilirubin is called unconjugated (despite being bound by albumin). [11] In the liver, unconjugated bilirubin is up-taken by the hepatocytes and subsequently conjugated with glucuronic acid (via the enzyme uridine diphosphate–glucuronyl transferase). In this state, bilirubin is soluble in water and it is called conjugated bilirubin. [11] Conjugated bilirubin is excreted into the bile ducts and enters the duodenum. During its transport to the colon, it is converted into urobilinogen by the bacterial enzyme bilirubin reductase.[8] Most of the urobilinogen is further reduced into stercobilinogen and is excreted through feces (air oxidizes stercobilinogen to stercobilin, which gives feces their characteristic brown color). [11] A lesser amount of urobilinogen is re-absorbed into portal circulation and transferred to the liver. For the most part, this urobilinogen is recycled to conjugated bilirubin and this process closes the enterohepatic circle. There is also an amount of urobilinogen which is not recycled, but rather enters the systemic circulation and subsequently the kidneys, where it is excreted. Air oxidizes urobilinogen into urobilin, which gives urine its characteristic color.[11][19] In parallel, a small amount of conjugated billirubin can also enter the systemic circulation and get excreted through urine. This is exaggerated in various pathological situations.[19]