scholarly journals Dual Role of Dietary Curcumin Through Attenuating AFB1-Induced Oxidative Stress and Liver Injury via Modulating Liver Phase-I and Phase-II Enzymes Involved in AFB1 Bioactivation and Detoxification

2018 ◽  
Vol 9 ◽  
Author(s):  
Ishfaq Muhammad ◽  
He Wang ◽  
Xiaoqi Sun ◽  
Xinghe Wang ◽  
Meiyu Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Phase I ◽  
Phase Ii ◽  
Dual Role ◽  
Phase Ii Enzymes

Possible Mechanisms of Alteration in the Capacities of Carcinogen Metabolizing Enzymes during Schistosomiasis and Their Role in Bladder Cancer Induction

1993 ◽  
Vol 21 (6) ◽  
pp. 281-305 ◽  
Author(s):  
A F Badawi ◽  
M H Mostafa
Keyword(s):  
Bladder Cancer ◽  
Phase I ◽  
Phase Ii ◽  
Potential Role ◽  
Metabolizing Enzymes ◽  
Phase Ii Enzymes ◽  
Causative Agents ◽  
Host Metabolism ◽  
Common Malignancy

Carcinoma of the urinary bladder is the most common malignancy in many tropical and subtropical countries. There is a well documented association with chronic urinary schistosomal infection, and bladder cancer associated with schistosomiasis is a major cause of morbidity and mortality in the endemic areas. Many factors have been suggested as possible causative agents in schistosome-associated bladder carcinogenesis but theories concerning the possible role of schistosomal infection in altering host metabolism of chemical carcinogens have received most attention. In experimental schistosomiasis there is a common pattern of changes in the activities of several hepatic Phase I and Phase II enzymes. Phase I enzymes show increased activities in the early stages of infection but these activities are reduced to below their pre-infection levels in the intermediate and late chronic stages of the disease. The activities of Phase II enzymes are altered in favour of the deconjugation pathways in the later stages of the disease. The possible basic mechanisms that might be involved in such changes during parasitism and their potential role in the induction of bladder neoplasia are discussed. Le carcinome de la vessie est la forme de cancer la plus commune dans de nombreux pays tropicaux et sous-tropicaux. Il existe une association bien documentée avec l'infection schistosomale urinaire chronique, et le cancer de la vessie, associé à la schistosomiase, est une cause importante de morbidité et de mortalité dans les régions end miques. De nombreux facteurs ont été suggérés comme agents causatifs possibles dans la carcinogénétique de la vessie associée aux schistosomes mais les théories concernant le rôle possible de l'infection schistosomale dans l'altération du métabolisme de l'hôte de carcinogènes chimiques, ont été beaucoup plus écoutées. Dans le schistosomiase expérimentale, on observe un module commun dans les modifications de activités des plusieurs enzymes hépatiques de phase I et de phase II. Les enzymes de phase I présentent un accroissement d'activités aux stades précoces de l'infection mais ces activités diminuent pour tomber á des niveaux inférieurs á ceux préables á l'infection pendant les stades intermédiaires et chroniques de la maladie. Les activités des enzymes de phase II sont modifiées en faveur de voies de d conjugaison à des stades plus avancés de la maladie. Les mécanimses de base qui sont peut-être impliqués dans ces changements pendant le parasitisme et leur rôle potentiel dans le déclenchement d'une néoplasie de la vessie sont examinés.

scholarly journals Mycotoxins: cytotoxicity and biotransformation in animal cells

2016 ◽  
Vol 5 (2) ◽  
pp. 377-387 ◽  
Author(s):  
Jikai Wen ◽  
Peiqiang Mu ◽  
Yiqun Deng
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Phase I ◽  
Cell Cycle Arrest ◽  
Phase Ii ◽  
Animal Cells ◽  
Phase Ii Enzymes ◽  
Cycle Arrest

Mycotoxins can be biotransformed by phase I and phase II enzymes in animals. However, most of the mycotoxin at high dosage combined with their metabolites can cause carcinogenesis and various cytotoxicity, such as apoptosis, lipids oxidation and cell cycle arrest,etc., and most of which are related to oxidative stress.

scholarly journals The role of oxidative/nitrosative stress in pathogenesis of paracetamol-induced toxic hepatitis

2010 ◽  
Vol 63 (11-12) ◽  
pp. 827-832 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic ◽  
Rada Jesic-Vukicevic
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Kupffer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Severe Liver ◽  
Hepatocellular Necrosis

Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito?chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu?cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion radicals through the enzyme nicotinamide adenine dinucleotide phosphate oxidase. Hydrogen peroxide, which is influenced by the neutrophil-derived enzyme myeloperoxidase, generates hypochlorus acid as a potent oxidant. Role of peroxynitrite in paracetamol-induced oxidative stress. Superoxide can react with nitric oxide to form peroxynitrite, as a potent oxidant. Nitrotyrosine is formed by the reaction of tyrosine with peroxynitrite in paracetamol hepatotoxicity. Conclusion. Overdose of paracetamol may produce severe liver injury with hepatocellular necrosis. The most important mechanisms of cell injury are metabolic activation of paracetamol, glutathione depletion, alkylation of proteins, especially mitochondrial proteins, and formation of reactive oxygen/nitrogen species.

Dual role of cadmium in rat liver: inducing liver injury and inhibiting the progression of early liver cancer

2021 ◽  
Author(s):  
Honglong Zhang ◽  
Jun Yan ◽  
Ye Xie ◽  
Xuhong Chang ◽  
Junliang Li ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Cancer ◽  
Rat Liver ◽  
Dual Role

Activation of Polycyclic Aromatic Compounds by cDNA-Expressed Phase I and Phase II Enzymes

2002 ◽  
Vol 22 (3-4) ◽  
pp. 955-967 ◽  
Author(s):  
Hansruedi Glatt ◽  
Ulrike Pabel ◽  
Eva Muckel ◽  
Walter Meinl
Keyword(s):  
Phase I ◽  
Phase Ii ◽  
Aromatic Compounds ◽  
Polycyclic Aromatic Compounds ◽  
Phase Ii Enzymes ◽  
Polycyclic Aromatic
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