Chloride ions and hydrogen peroxide are the primary reactants that form hypochlorous acid (HOCl) in the presence of the enzyme myeloperoxidase (MPO).
Mast cell activation can lead to the release of myeloperoxidase (MPO) by certain immune cells (like neutrophils), which then generates hypochlorous acid (HOCl) from hydrogen peroxide and chloride ions. While this MPO-derived HOCl is a key part of the innate immune response, excessive generation of it can cause tissue damage.
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N-acetylcysteine (NAC) can cause anaphylactoid reactions, including skin flushing, through the non-IgE-mediated release of histamine from mast cells. This is distinct from a true allergic reaction (anaphylaxis).
Magnesium influences anaphylaxis by acting as a stabilizer for mast cells, which normally release histamine during an allergic reaction. In a state of anaphylaxis, mast cells are activated to release mediators like histamine, and research shows that magnesium can inhibit this process and stabilize the cells. Magnesium deficiency in rats has been shown to increase histamine levels in the blood and alter the number of mast cells.
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histamine mast cells cataracts
Mast cells are located in the eyes and release histamine, causing symptoms of allergic conjunctivitis that can worsen existing cataracts, though the direct link between mast cells/histamine and the formation of age-related cataracts is still being researched. While allergic inflammation can exacerbate cataract symptoms like blurriness and light sensitivity, research also suggests chronic inflammation related to mast cell activation could be a factor in age-related cataract progression.
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Electrolytes have antioxidant properties by interfering with damaging free radical reactions through chemical reactions like single electron transfer (SET) and hydrogen atom transfer (HAT).
Sodium bicarbonate has indirect antioxidant properties by acting as a buffer to neutralize acidity, support antioxidant enzymes for cellular protection.
Sodium bicarbonate can increase pH and buffer excess hydrogen ions, which helps protect cells from the damage caused by excess acidity.
It has been shown to improve the activity of antioxidant enzymes like superoxide dismutase, catalase, and ascorbate peroxidase.
By maintaining acid-base balance, it helps prevent cellular damage, such as reducing reactive oxygen species (ROS) and lipid peroxidation.
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Free Radical Cascade is a chain reaction where a free radical initiates a series of chemical reactions, such as cyclizations, to create new molecules.
A process where a single radical triggers a sequence of reactions to build complex structures.
A radical attacks a molecule, creating a new radical. This new radical then reacts with another molecule, and so on, often through a series of steps like radical additions and cyclizations.
When there are too many free radicals, they can steal electrons from other molecules, creating more free radicals and initiating a damaging cascade that leads to oxidative stress.
A free radical cascade contributes to cataracts by causing oxidative damage that leads to protein aggregation and lens opacification. Free radicals, particularly reactive oxygen species (ROS) and unstable molecules.
When pro-oxidant levels overwhelm the body's antioxidants, a chain reaction (cascade) of damage occurs, affecting lens proteins and leading to their aggregation and loss of transparency, which is the characteristic of a cataract.
Protein aggregation:
This damage causes the proteins to become unstable, unfold, and aggregate into large, insoluble clumps.
Iritis
Auto Immune Disorder
Mast Cell Activation
Histamine Release
Peroxide/Chloride
Reactive Oxygen Species
Oxidative Stress
Cataracts
Glaucoma
Transplant Rejection