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Metabolism and Toxicity of Occupational Neurotoxicants: Genetic, Physiological, and Environmental Determinants
Published in Lucio G. Costa, Luigi Manzo, Occupatinal Neurotoxicology, 2020
Stefano M. Candura, Luigi Manzo, Anna F. Castoldi, Lucio G. Costa
UDP-glucuronosyltransferase activity is reduced in a number of inherited diseases known as familial hyperbilirubinemias. Gilbert’s syndrome is a mild form occurring in 2–5% of the population. The patients present chronic unconjugated hyperbilirubinemia and an impaired ability to metabolize menthol, which can thus be used as a probe drug to diagnose the disease. Glucuronidation of many other drugs and toxicants is also impaired.4 The large prevalence of Gilbert’s syndrome in the population makes it an important genetic deficiency when considering interindividual variation in neurotoxicant metabolism. Crigler-Najjar syndrome is a less common and more severe pathological condition. Infants often develop neurological damage from bilirubin encephalopathy (kernicterus) due to the immaturity of the blood-brain barrier. A proportion of patients (Type II) respond favorably to enzymatic inducers such as phenobarbital. The remaining patients (Type I) present higher unconjugated bilirubin levels (>20 mg/dl) and are not responsive to barbiturate therapy, suggesting a difference from Type II in the molecular basis of the genetic defect.4
Biotransformation of Xenobiotics in Living Systems—Metabolism of Drugs: Partnership of Liver and Gut Microflora
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Neonates are deficient in this conjugating system making them vulnerable to drugs such as chloramphenicol, which is inactivated by glucuronidation, resulting in “gray-baby” syndrome characterized by cyanosis, abdominal distention, vomiting, hypothermia, and cardiovascular collapse (Mulhall et al., 1983). Insufficient conjugation of bilirubin in neonates leads to increased serum concentration of lipid-soluble unconjugated bilirubin that may easily cross poorly established blood–brain barrier and cause kernicterus and neurotoxicity (Amin and Lamola, 2011).
Non-invasive and non-contact automatic jaundice detection of infants based on random forest
Published in Computer Methods in Biomechanics and Biomedical Engineering: Imaging & Visualization, 2023
Fatema-Tuz-Zohra Khanam, Ali Al-Naji, Asanka G. Perera, Danyi Wang, Javaan Chahl
Kernicterus can be avoided by early detection and treatment of jaundice or hyperbilirubinemia. High bilirubin can be controlled through phototherapy, a method that requires exposure of the affected newborn infant to particular wavelengths of blue light that transform bilirubin into a harmless, excretable form (Maisels 2015; Mreihil et al. 2018). On the other hand, excess bilirubin may need to be removed through Exchange transfusions (ET) in cases of extremely high levels (Women’s NCCf, Health Cs 2010). However, ET is an invasive technique where a calculated amount of the newborn’s blood is replaced by a donor’s blood to decrease the excess level of bilirubin. Therefore, phototherapy has been the most popular method for the treatment of jaundice or hyperbilirubinemia (Mreihil et al. 2018; Katti and Babu 2021).
Investigation of mutations (L41F, F17M, N57E, Y99F_Y134W) effects on the TolAIII-UnaG fluorescence protein's unconjugated bilirubin (UC-BR) binding ability and thermal stability properties
Published in Preparative Biochemistry & Biotechnology, 2022
Numan Eczacioglu, Yakup Ulusu, İsa Gokce, Jeremy H. Lakey
Bilirubin (C33H36N4O6) is an antioxidant tetrapyrrole molecule that is formed by the destruction of erythrocytes in the body (250–400 mg/day in an adult person), produced catabolically from heme, and available in the form of conjugated and unconjugated bilirubin structure (UC-BR).[4–6] It is a yellow-orange pigment that is strongly lipophilic in its unconjugated form and if UC-BR deposited in tissues may have a cytotoxic effect. If the level of bilirubin in blood plasma continues to rise due to the imbalance between bilirubin production rates and uptake or conjugation in the liver, hyperbilirubinemia may occur and the passing of bilirubin into brain tissue can be observed. This situation may cause kernicterus, a serious condition associated with permanent neurological damage in neonates.[4] Kernicterus disease is a condition where bilirubin exceeds the blood-brain barrier and causes damage to some nuclei of the brain cells when newborns have severe jaundice due to an increase in the amount of bilirubin in their blood. In addition to mental retardation and spasticity, damage to the brain is irreversible and may even result in death.[7]