Hepatic Mixed-function Oxidases
Hepatic Mixed-function Oxidases - Related Videos
10:42
Bioluminescence Imaging of NADPH Oxidase Activity in Different Animal Models
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Cited by 16 •
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NADPH oxidase is the major source of reactive oxygen species (ROS) in phagocytes. Because of the ephemeral nature of ROS, it is difficult to measure and monitor ROS levels in living animals. A minimally invasive method for serial quantification of ROS in living mice is described.
09:12
Surface Functionalization of Hepatitis E Virus Nanoparticles Using Chemical Conjugation Methods
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Cited by 15 •
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We have engineered the capsid protein of hepatitis E virus as a theranostic nanoparticle (HEVNP). HEVNP self-assembles into a stable icosahedral cage in mucosal delivery. Here, we describe the modification of HEVNPs for tumor targeting by mutating surface-exposed residues to cysteines, which conjugate synthetic ligands that specifically bind tumor cells.
09:35
Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle
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Cited by 2 •
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08:45
Generation of Functional Endodermal Hepatic Organoids
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Cited by 1 •
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This protocol describes the generation of fast and reproducible endodermal hepatic organoids (eHEPOs). With this protocol, eHEPOs can be produced within 2 weeks and expand long-term (more than 1 year) without losing their differentiation and functionality.
10:40
Visualization and Analysis of Blood Flow and Oxygen Consumption in Hepatic Microcirculation: Application to an Acute Hepatitis Model
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Cited by 10 •
2012
An optical system was developed to visualize hepatic microcirculation with FITC-labeled erythrocytes and to measure the partial pressure of oxygen in the microvessels with laser-assisted phosphorimetry. This method can be used to investigate physiological and pathological mechanisms by analyzing microvascular structure, diameter, blood flow velocity, and oxygen tension.
FAQs
The catalytic cycle coordinates molecular oxygen with electrons supplied by NADPH. One oxygen atom is inserted into the drug or other substrate, while the second oxygen atom is reduced to water. This reaction chemically modifies the compound rather than simply transporting it, producing a form that is easier for the body to eliminate and thereby influencing its clinical persistence.
Lipid-soluble drugs, steroids, and related compounds are major substrates because the enzyme systems chemically alter them in the liver. That modification supports elimination and connects hepatic biochemistry with both pharmacology and steroid handling. Consequently, changes in oxidase activity can affect the disposition of therapeutic compounds as well as other biologically relevant substances.
Induction and inhibition are contrasting influences on oxidase activity. Either change can modify how rapidly a drug undergoes hepatic chemical transformation, which may alter its plasma concentration. The resulting change can affect therapeutic response or toxicity, making regulation of these enzyme systems an important mechanism behind clinically significant variation in drug effects.
Oxidation changes the chemical structure of lipid-soluble drugs so that they become easier to eliminate. The extent of this transformation contributes to drug clearance, meaning the removal of the compound from the body. Changes in oxidase activity can therefore alter how long a drug remains available in circulation and how strongly or persistently it acts.
A drug-drug interaction can arise when one drug changes the activity of hepatic mixed-function oxidases that process another compound. The second drug may then undergo a different degree of chemical transformation, producing altered plasma concentrations. Such changes can modify the intended therapeutic response or increase the possibility of toxicity, depending on the clinical situation.
Changes in oxidase activity are clinically relevant because they connect enzyme function with drug clearance, plasma concentration, therapeutic response, and toxicity. When activity is altered by induction or inhibition, clinicians and researchers must consider that the same administered drug may produce a different exposure or effect. These relationships help explain variability in pharmacological outcomes.