selenium etc.docx

Selenium Sources = meat, nuts, seafood Two forms/species: inorganic and organic Inorganic = selenite, selenate Organic = Selenocysteine, selenomethionine They have properties such as: antioxidant and anticarcinogenic Enzymes of Se-cys; Se-Met Glutathione peroxidase; Iodothyronine deiodinase; Thi...

Selenium Sources = meat, nuts, seafood Two forms/species: inorganic and organic Inorganic = selenite, selenate Organic = Selenocysteine, selenomethionine They have properties such as: antioxidant and anticarcinogenic Enzymes of Se-cys; Se-Met Glutathione peroxidase; Iodothyronine deiodinase; Thioredoxin reductase Cardiac muscle = associated with Glutathione Oxidation Reduction Cycle The glutathione oxidation-reduction cycle is a crucial cellular process that involves the interconversion of two forms of glutathione: reduced glutathione (GSH) and oxidized glutathione (GSSG). Here's a simple and brief explanation: Reduced Glutathione (GSH): Function: GSH is the active, antioxidant form of glutathione. Role: It helps protect cells from damage caused by reactive oxygen species (ROS) and other oxidative stressors. Oxidized Glutathione (GSSG): Formation: GSH can become oxidized to form GSSG in the presence of oxidative stress. Accumulation: Elevated levels of GSSG indicate oxidative stress and potential damage to the cell. Glutathione Recycling (Reduction): Enzyme Involvement: The enzyme glutathione reductase/glutathione peroxidase facilitates the reduction of GSSG back to GSH. Coenzyme: NADPH (nicotinamide adenine dinucleotide phosphate) provides the necessary reducing power for this reaction. NADPH Involvement: Role: NADPH acts as a coenzyme to regenerate GSH from GSSG. Source: NADPH is often produced in cellular processes like the pentose phosphate pathway. Antioxidant Defense: Continuous Cycle: The glutathione cycle is a continuous process, maintaining a balance between GSH and GSSG. Cellular Defense: This cycle is vital for the cell's defense against oxidative stress and maintaining a reducing environment. In summary, the glutathione oxidation-reduction cycle involves the dynamic balance between reduced (GSH) and oxidized (GSSG) forms of glutathione. This cycle helps protect cells from damage caused by oxidative stress, contributing to the overall health and function of the cell. Deiodination and reduction = Iodothyronine deiodinase  Deiodination: Definition: Deiodination refers to the removal of iodine atoms from thyroid hormones. Importance in Selenium Metabolism: Some selenoproteins, known as deiodinases, play a crucial role in the regulation of thyroid hormones. These enzymes contain selenium at their active sites in the form of selenocysteine. Function: Deiodinases catalyze the removal of iodine from thyroxine (T4) and triiodothyronine (T3), converting them into inactive forms or activating them, depending on the specific deiodinase. Deiodination, facilitated by selenoproteins like deiodinases, is involved in the regulation of thyroid hormones. Reduction, carried out by selenoproteins like glutathione peroxidases, plays a vital role in antioxidant defense, protecting cells from oxidative stress. These processes highlight the significance of selenium and selenoproteins in maintaining cellular homeostasis and overall health. Thioredoxin reductase (TrxR) is an enzyme that plays a crucial role in cellular redox homeostasis, and its activity is closely linked to the presence of the trace element selenium. Thioredoxin reductase is a selenoprotein, meaning it contains selenium in the form of the amino acid selenocysteine. Here's how thioredoxin reductase is related to selenium: Selenoprotein Structure: Thioredoxin reductase belongs to a family of selenoproteins, and its active site contains the amino acid selenocysteine (Sec). Selenocysteine is encoded by the UGA codon, which is typically a stop codon. However, in the presence of specific sequence elements called SECIS (selenocysteine insertion sequence), the UGA codon is recoded to incorporate selenocysteine. Reduction of Thioredoxin: Thioredoxin reductase is involved in the reduction of thioredoxin, another protein involved in cellular redox reactions. Thioredoxin acts as a key regulator of cellular redox balance by participating in the reduction of disulfide bonds in proteins. Thioredoxin, once oxidized, can be reduced back to its active form by thioredoxin reductase, using NADPH as a cofactor. Antioxidant Defense: The activity of thioredoxin reductase is essential for maintaining a reduced cellular environment and protecting cells from oxidative stress. It contributes to the overall antioxidant defense system in cells. Cellular Redox Homeostasis: Thioredoxin reductase, by participating in the thioredoxin system, helps regulate the redox status of cellular proteins, influencing processes such as cell growth, apoptosis, and the response to oxidative damage. Selenocysteine and Selenium: The presence of selenocysteine in thioredoxin reductase makes selenium an essential component for its function. Selenium, in the form of selenocysteine, is directly incorporated into the catalytic site of the enzyme. Physiological Roles: Thioredoxin reductase has been implicated in various physiological processes, including the protection against oxidative stress, DNA synthesis, and the regulation of cell proliferation. Diseases related to Selenium Keshan Disease Abnormal ECG Cargiogenic shock Cardiac enlargement Congestive heart failure Keshan disease is a potentially serious heart condition associated with selenium deficiency. It is characterized by an increased susceptibility to viral infections and a higher incidence of dilated cardiomyopathy (DCM). Dilated cardiomyopathy is a condition in which the heart's muscle becomes weakened and enlarged. This leads to a decrease in the heart's pumping ability, and the chambers of the heart (particularly the left ventricle) become dilated or stretched. • Impaired Pumping Function: As the heart becomes weakened, it struggles to pump blood efficiently to the rest of the body. This can lead to symptoms such as fatigue, shortness of breath, and fluid retention.  Causes: In the context of Keshan disease, selenium deficiency has been identified as a contributing factor. In areas where soil selenium levels are low, selenium deficiency may contribute to the development of DCM, as observed in Keshan disease. Kashin-Beck disease / osteoarthritis Antioxidant Protection: Selenium is an essential component of selenoproteins, including glutathione peroxidases, which play a role in antioxidant defense. Oxidative stress has been implicated in the development and progression of osteoarthritis. Antioxidant enzymes like those containing selenium may help protect joint tissues from oxidative damage.  Inflammation Modulation: Selenium has anti-inflammatory properties, and inflammation is a key factor in the pathogenesis of osteoarthritis. Selenoproteins may modulate inflammatory responses, and selenium deficiency could potentially contribute to an imbalance in inflammatory processes within the joints.  In cases of selenium deficiency, there may be an impact on the integrity and health of cartilage, which could contribute to the development or progression of osteoarthritis.  GSH-Px Enzymes: Glutathione peroxidases (GSH-Px) are a family of selenoproteins with antioxidant functions. These enzymes help neutralize reactive oxygen species (ROS) that can damage joint tissues. Selenium deficiency may reduce the activity of GSH-Px enzymes, potentially leaving joint tissues more susceptible to oxidative damage. The disease often manifests in childhood, leading to stunted growth and skeletal deformities. Children in endemic areas may exhibit short stature and abnormalities in limb development. Cobalt Important for Vitamin B12-cobalamin Cobalt toxicity = results in cardiomyopathy; Beer-Drinker's Cardiomyopathy; Cardiotoxic Effects: High levels of cobalt can lead to cardiotoxic effects, including inflammation and damage to heart muscle cells. Cobalt and Iron Interaction: Cobalt can interfere with the body's utilization of iron, leading to the accumulation of iron in the heart. This iron overload may contribute to oxidative stress and damage to cardiac tissues. Molybdenum Sources: legumes; beans; nuts Enzymes: xanthine oxidase, aldehyde oxidase, sulfite oxidase Xanthine oxidase participates in PURINE METABOLISM It catalyzes the oxidation of hypoxanthine to xanthine and xanthine to uric acid. CuSO4 decrease Mo retention Molybdenum is high in liver, skeleton and kidneys It is eliminated via urine Increased Mo is linked to increased level of uric acid & development of gout Gout is a type of arthritis caused by the deposition of urate crystals (formed from uric acid) in joints and other tissues. It is characterized by sudden and severe attacks of pain, swelling, and redness in the affected joints, often the big toe. Increase in molybdenum levels may somehow be associated with higher levels of uric acid in the blood, and this, in turn, may contribute to the development of gout. Nickel Found in metal alloys, batteries, oils Fe; Ni(CO)4 Nickel and ATPases: ATPases: ATPases are enzymes that hydrolyze ATP (adenosine triphosphate) to ADP (adenosine diphosphate) and inorganic phosphate, releasing energy. Nickel is a cofactor for a class of ATPases known as Ni-dependent ATPases. Examples: One well-known example of a Ni-dependent ATPase is urease. Urease is an enzyme that catalyzes the hydrolysis of urea to produce ammonia and carbon dioxide. Certain bacterial and plant ureases contain nickel ions in their active sites, and nickel is essential for their catalytic activity. Nickel and RNA Polymerases: RNA Polymerases: RNA polymerases are enzymes responsible for synthesizing RNA molecules from DNA templates during transcription. In some bacteria, a class of RNA polymerases known as nickel-dependent RNA polymerases exists. Example: An example of a nickel-dependent RNA polymerase is found in Helicobacter pylori, a bacterium associated with gastric ulcers. The RNA polymerase of H. pylori contains nickel in its active site, and nickel is required for its transcriptional activity. Nickel can be toxic: Pulmonary congestion Inability to oxygenate Hb Development of lesions in liver, lungs, kidneys, spleen and adrenals Lithium Anti-manic element Used in treatment of manic-depressive patients; mental diseases - BPD Fluoride Sources: water and tea Anti-cariogenic element Used to prevent tooth decades Increases remineralization and suppresses microbial period Iodine Sources: Seafood, Dairy products, iodized salt (most common) Synthesis of thyroid hormones – triiodothyronine T3 and tetraiodothyronine T4 Regulation of cell metabolism and metabolic rate In iodine deficiency – thyroid enlargement – goitre Along with Se – essential for thyroid gland functioning, biosynthesis and metabolism PHARMACOLOGICALLY BENEFICIAL ELEMENTS Bismuth – Helicobacter pylori infection Fluorine – tooth decay Germanium – cancer Gold – rheumatoid arthritis Lithium – bipolar disorder Molybdenum – Wilson’s disease Selenium – HP-associated Gastric Disease Selenium – Alzheimer disease Strontium – osteoporosis Zinc – depression