EFFECT OF Plectranthus wightii METHANOL EXTRACT AGAINST GENTAMICIN-INDUCED NEPHROTOXICITY IN RATS
V. R. Mohan, A. Doss, P. S. Tresina in Ethnomedicinal Plants with Therapeutic Properties, 2019
Bilirubin is a yellow pigment produced when heme is catabolized. Hepatocytes render bilirubin water soluble and therefore easily excretable by conjugating it with glucoronic acid prior to secreting it into bile by active transport. Hyperbilirubinemia may result from the production of more bilirubin than the liver can process, damage to the liver impairing its ability to excrete normal amount of bilirubin or obstruction of excretory ducts of the liver (Olaleye et al., 2010). Serum bilirubin is considered as one of the true test of liver functions since it reflects the ability of the liver to take up and process bilirubin into bile. Elevated levels may indicate several illnesses. High levels of total bilirubin in CCl4-treated rats may be due to CCl4 toxicity. This may have resulted in hyperbilirubinemia. The significant reduction in the level of total bilirubin in the serum of E. floccosa leaf ethanol extracttreated rats suggested the hepatoprotective potential of leaf extract against CCl4 intoxication.
Cellular Components of Blood
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
With ageing, glycolysis – and hence ATP formation – decreases in the red cell, so that energy for the maintenance of cellular integrity is diminished. The old red cells are removed by the reticuloendothelial cells, especially in the spleen. The globin chains are broken down to amino acids and re-enter the amino acid pool. The iron is reutilized by the bone marrow for the synthesis of Hb. The protoporphyrin ring is opened to form biliverdin. A small fraction of protoporphyrin is converted to carbon monoxide. Biliverdin is metabolized to bilirubin, which is bound to albumin and carried to the liver. In the liver, bilirubin is conjugated with glucuronic acid and excreted in the bile and hence into the small gut. In the gut, the bilirubin is converted to stercobilin, some of which is reabsorbed into the plasma and excreted by the kidney as urobilinogen in the urine (Figure 51.7).
Physiology of blood
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
With ageing, glycolysis – and hence ATP formation – decreases in the red cell, so that energy for the maintenance of cellular integrity is diminished. The old red cells are removed by the reticuloendothelial cells, especially in the spleen. The globin chains are broken down to amino acids and re-enter the amino acid pool. The iron is reutilized by the bone marrow for the synthesis of Hb. The protoporphyrin ring is opened to form biliverdin. A small fraction of protoporphyrin is converted to carbon monoxide. Biliverdin is metabolized to bilirubin, which is bound to albumin and carried to the liver. In the liver, bilirubin is conjugated with glucuronic acid and excreted in the bile and hence into the small gut. In the gut, the bilirubin is converted to stercobilin, some of which is reabsorbed into the plasma and excreted by the kidney as urobilinogen in the urine (Figure 9.7).
Renal and Hepatic Disease: Cnidoscolus aconitifolius as Diet Therapy Proposal for Prevention and Treatment
Published in Journal of the American College of Nutrition, 2021
Maria Lilibeth Manzanilla Valdez, Maira Rubi Segura Campos
In addition to the guideline of Brunt and Tiniakos (52) shown in Table 2, another way to diagnose LD and specifically NAFLD is with hepatic biomarkers. The alterations in serum aminotransferases can show hepatic injury. Serum aminotransferases are alanine aminotransferase (ALT) and aspartate aminotransferase (AST). ALT is found in the liver parenchyma and AST is found in the liver, heart, skeletal muscle, pancreas, and lung. So, the AST is not as specific as the ALT. The elevation in serum levels usually indicates injury or necrosis in the hepatocytes (38).Alkaline phosphatase (ALP) and gamma-glutamyl-transpeptidase (GGT): GGT is an enzyme found in the hepatocyte and in the biliary epithelium. ALP is found in the liver, bone, intestine and placenta. An elevation of both is a sign of hepatic cholestasis.Bilirubin: it is a product of the degradation of the catabolism of hemoglobin. It is metabolized in the smooth endoplasmic reticulum of the hepatocyte, by glucuronyl-transferase.
Effects of hepatocyte growth factor gene-transfected mesenchymal stem cells on dimethylnitrosamine-induced liver fibrosis in rats
Published in Growth Factors, 2019
Soung Hoon Moon, Chang Min Lee, See-Hyoung Park, Myeong Jin Nam
The level of aspartate aminotransferase (AST) in the bloodstream is measured to evaluate liver damage. AST levels in blood are low in individuals with healthy livers. However, when the liver is impaired, AST levels in the blood are increased. High AST levels indicate that the liver is damaged and other organs, such as the heart and kidneys, may also be damaged. Alanine aminotransferase (ALT), an enzyme produced by liver cells, plays an essential role in metabolism. It aids the liver in degrading proteins for easy absorption. When the liver is impaired, ALT can be released into the bloodstream. Alkaline phosphatase (ALP) is an enzyme found in cells that comprise the liver and bone (Gowda et al. 2009). Liver diseases and bone disorders induce high ALP levels in the blood, and increased blood ALP levels are detected in liver cancer and fibrosis. Bilirubin is a waste product primarily produced by the breakdown of heme (Pearson 1967) and is ultimately processed by the liver. The amount of bilirubin in blood is a crucial indicator of liver condition (Kim et al. 2013). Taken together, measuring the levels of AST, ALT, ALP, and TBIL (total bilirubin) in blood can help doctors determine the underlying cause of a liver problem.
The relationship between UGT1A1 gene & various diseases and prevention strategies
Published in Drug Metabolism Reviews, 2022
Dan Liu, Qi Yu, Qing Ning, Zhongqiu Liu, Jie Song
Neurological diseases related to the UGT1A1 gene are mainly caused by bilirubin metabolism disorders. Hyperbilirubinemia may increase the risk of Neurological disease. Bilirubin is a pigment made during degradation of hemoglobin in RBC. The average life span of normal RBC is about 120 d, and a considerable number of RBC are naturally destroyed and apoptotic every day. Bilirubin has severe neurotoxicity. It produces glucuronate bilirubin under the action of UGT1A1 metabolizing enzyme, and then enters the small intestine together with bile, and is finally excreted. This is the only detoxification metabolic pathway of bilirubin in vivo. Yueh et al. demonstrate that neuroinflammation and reactive gliosis are prominent features of bilirubin brain toxicity, and a disturbed redox status resulting from activation of NADPH oxidase is an important contributing mechanism found in bilirubin-induced neurological dysfunction (Yueh et al. 2017). The schematic diagram of neurological diseases related to UGT1A1 gene is shown in Figure 1.