Transamination or Metabolism of Amino Acids of Various Types is essential for Homeostasis. Herein the various Pathways for Amino Acids and Transamination Thereof: 1) Tryptophan is the Substrate of Niacin (Vitamin B 3) which goes onto building Nicotinamide Adenine Dinucleotide (NAD+), important in ATP Synthesis, and Nicotinamide Adenine Dinucleotide Phosphate (NADP+), a Reduction Agent, via the catalytic action of Pyridoxine (Vitamin B6) and Riboflavin (Vitamin B2); 2) In the Biosynthesis of Serotonin (5-HT), Tryptophan is Activated for Conversion by Cofactors Pyridoxine (B6) and Tetrahydrobiopterin (BH4) and ultimately to 5 Hydroxyindoleacetic Acid (5-HIAA), a Measurable Metabolite of Serotonin Degradation excreted within the Urine. The Catalyzing Enzyme is Monoamine Oxidase and the inhibition of this enzyme is the Mechanism of Action of Pharmacologic Antipsychotic Drugs. Serotonin Syndrome (SS) can be an Adverse Drug Reaction due to the Pharmacodynamics of MOA Inhibitors. Excessive Serotonin in the Body (Serotoninosis) is typically ascertained via a Urinalysis where Metabolite 5-HIAA will be Elevated (DDx: Pheochromocytoma, Carcinoid Tumor et al). 2) Histidine is converted into Neurotransmitter and an Immunogenic agent (Immune Response Mediator) Histamine via Histidine Decarboxylase (HDC) and Pyridoxine Cofactor (Vitamin B6) as all Decarboxylations in Biosynthesis. Histamines vasodilatory properties are due to the acitivation of Nitric Oxide Synthase (NOS); 3) Glutamate, an Excitatory Neurotransmitter and essential for Memory Brain Processes, Transamination goes to Gamma Aminobutyric Acid (GABA), an important inhibitor Neurotransmitter, via the catalysis of Glutamate Decarboxylase (GAD) and Cofactor Pyridoxine. Isoniazid, an Antituberculosis Agent, can inhibit this Reaction (B6 Complexes) and thereby manifesting as Peripheral Neuropathy because of Elevated Glutamate, Isoniazid Toxicity (Supplementation with B6 is Standard for Tuberculosis Isoniazid Chemotherapy). Glutamate and Cysteine combine to make Glutathione, an Antioxidant (Mechanisim of binding and neutralizing Reactive Oxygen Species [ROS]), 4) Glycine combines with Succinyl Coenxyme A to form Delta Aminolevulinic Acid (D-ALA), which is important for Heme Synthesis via Delta Aminolevulinic Acid Synthase (D-ALAS) and Cofactor Pyridoxine goes onto make Heme Synthesis (Caveat of INH Toxicity is Sideroblastic Anemia due to Pyridoxine Inhibition). In X-Linked Sideroblastic Anemia, a Congenital Deficiency of Delta Aminolevulinic Acid Synthase impedes Heme Synthesis. 5) Argine Metabolism: 1) Creatine generates Adenosine Triphosphate as Phosphorylated Creatine via Creatine Kinase (Phosphorylating Enzyme). Myocardial Infarction (CK-MB) and Rhabdomyolysis (CK 5 Times Upper Normal Limit); 2) Ornithine with Urea as a By-Product; and 3) Nitric Oxide with a Citrulline Product. The Catalyst is Nitric Oxide Synthase (NOS) along with Tetrahydrobiopterin (BH4) Cofactor et al. The Nitric Oxide Pathway and the Mechanism of Action in Endothelial Cells (NO Synthesis Site) to Smooth Muscle Effect occurs when Nitric Oxide Synthase acts on Arginine creating the Vasodilatory Product Nitric Oxide (NO) to Guanylyl Cyclase to Cyclic Guanosine Monophosphate (cGMP) from Guanosine Triphosphate (GTP) and activating Protein Kinase G (PKG) inducing Vasodilation in the Arteries. The Regulation of cGMP occurs with Phosphodiesterase (PDE) where 5' Guanosine Monophosphate is produced. The Phosphodiesterase Inhibitors Class of Medications antagonize ( PDE5 Inhibition) the metabolism of cGMP, allowing vasodilation to occur. Sildenafil (Viagra) and Tadalafil are a commonly used PDE Inhibitors for Erectile Dysfunction (ED). Pulmonary Hypertension (PH) can be treated using this Mechanism. Nitrate and Nitroprusside (Nitric Oxide) are indicated for Coronary Vasodilation in Myocardial Infarction and Hypertensive Crisis respectively. Bradykinin Buildup as with Angiotensin Converting Enzyme Inhibiton (ACEi) can create the excessive vasodilatation seen in Angioedema via the Mechanism of Nitric Oxide Synthase. In a Metabolic Acidosis Scenario, the Kidney takes Carbon Dioxide (CO2) and Water (H2O) and turns it into Bicarbonate (HCO3-) and liberating Hydrogen. Exchanged Hydrogen is bond with Ammonia (NH3) to Ionic Ammonia (NH4+), thereby buffering the Acidosis. Buffering Acidity necessitates Amino Acids Glutamine and Glutamate where Alpha Ketogluterate is Synthesis which is Component of the Tricarboxylic Acid Cycle in the Mitochondrion for Cellular Respiration and ATP Synthesis. Goodness Gracious. I have just treated my first INH Induced Peripheral Neuropathy with a simple Pyridoxine Supplementation. Sadly, this patient had Active Tuberculosis apparently misdiagnosed as Latent TB (Isoniazid Therapy). MD Paul Bolin du bist herrlich und toll. Prost! Uberall Gesundheit und Friede!
Transamination or Metabolism of Amino Acids of Various Types is essential for Homeostasis. Herein the various Pathways for Amino Acids and Transamination Thereof: 1) Tryptophan is the Substrate of Niacin (Vitamin B 3) which goes onto building Nicotinamide Adenine Dinucleotide (NAD+), important in ATP Synthesis, and Nicotinamide Adenine Dinucleotide Phosphate (NADP+), a Reduction Agent, via the catalytic action of Pyridoxine (Vitamin B6) and Riboflavin (Vitamin B2); 2) In the Biosynthesis of Serotonin (5-HT), Tryptophan is Activated for Conversion by Cofactors Pyridoxine (B6) and Tetrahydrobiopterin (BH4) and ultimately to 5 Hydroxyindoleacetic Acid (5-HIAA), a Measurable Metabolite of Serotonin Degradation excreted within the Urine. The Catalyzing Enzyme is Monoamine Oxidase and the inhibition of this enzyme is the Mechanism of Action of Pharmacologic Antipsychotic Drugs. Serotonin Syndrome (SS) can be an Adverse Drug Reaction due to the Pharmacodynamics of MOA Inhibitors. Excessive Serotonin in the Body (Serotoninosis) is typically ascertained via a Urinalysis where Metabolite 5-HIAA will be Elevated (DDx: Pheochromocytoma, Carcinoid Tumor et al). 2) Histidine is converted into Neurotransmitter and an Immunogenic agent (Immune Response Mediator) Histamine via Histidine Decarboxylase (HDC) and Pyridoxine Cofactor (Vitamin B6) as all Decarboxylations in Biosynthesis. Histamines vasodilatory properties are due to the acitivation of Nitric Oxide Synthase (NOS); 3) Glutamate, an Excitatory Neurotransmitter and essential for Memory Brain Processes, Transamination goes to Gamma Aminobutyric Acid (GABA), an important inhibitor Neurotransmitter, via the catalysis of Glutamate Decarboxylase (GAD) and Cofactor Pyridoxine. Isoniazid, an Antituberculosis Agent, can inhibit this Reaction (B6 Complexes) and thereby manifesting as Peripheral Neuropathy because of Elevated Glutamate, Isoniazid Toxicity (Supplementation with B6 is Standard for Tuberculosis Isoniazid Chemotherapy). Glutamate and Cysteine combine to make Glutathione, an Antioxidant (Mechanisim of binding and neutralizing Reactive Oxygen Species [ROS]), 4) Glycine combines with Succinyl Coenxyme A to form Delta Aminolevulinic Acid (D-ALA), which is important for Heme Synthesis via Delta Aminolevulinic Acid Synthase (D-ALAS) and Cofactor Pyridoxine goes onto make Heme Synthesis (Caveat of INH Toxicity is Sideroblastic Anemia due to Pyridoxine Inhibition). In X-Linked Sideroblastic Anemia, a Congenital Deficiency of Delta Aminolevulinic Acid Synthase impedes Heme Synthesis. 5) Argine Metabolism: 1) Creatine generates Adenosine Triphosphate as Phosphorylated Creatine via Creatine Kinase (Phosphorylating Enzyme). Myocardial Infarction (CK-MB) and Rhabdomyolysis (CK 5 Times Upper Normal Limit); 2) Ornithine with Urea as a By-Product; and 3) Nitric Oxide with a Citrulline Product. The Catalyst is Nitric Oxide Synthase (NOS) along with Tetrahydrobiopterin (BH4) Cofactor et al. The Nitric Oxide Pathway and the Mechanism of Action in Endothelial Cells (NO Synthesis Site) to Smooth Muscle Effect occurs when Nitric Oxide Synthase acts on Arginine creating the Vasodilatory Product Nitric Oxide (NO) to Guanylyl Cyclase to Cyclic Guanosine Monophosphate (cGMP) from Guanosine Triphosphate (GTP) and activating Protein Kinase G (PKG) inducing Vasodilation in the Arteries. The Regulation of cGMP occurs with Phosphodiesterase (PDE) where 5' Guanosine Monophosphate is produced. The Phosphodiesterase Inhibitors Class of Medications antagonize ( PDE5 Inhibition) the metabolism of cGMP, allowing vasodilation to occur. Sildenafil (Viagra) and Tadalafil are a commonly used PDE Inhibitors for Erectile Dysfunction (ED). Pulmonary Hypertension (PH) can be treated using this Mechanism. Nitrate and Nitroprusside (Nitric Oxide) are indicated for Coronary Vasodilation in Myocardial Infarction and Hypertensive Crisis respectively. Bradykinin Buildup as with Angiotensin Converting Enzyme Inhibiton (ACEi) can create the excessive vasodilatation seen in Angioedema via the Mechanism of Nitric Oxide Synthase. In a Metabolic Acidosis Scenario, the Kidney takes Carbon Dioxide (CO2) and Water (H2O) and turns it into Bicarbonate (HCO3-) and liberating Hydrogen. Exchanged Hydrogen is bond with Ammonia (NH3) to Ionic Ammonia (NH4+), thereby buffering the Acidosis. Buffering Acidity necessitates Amino Acids Glutamine and Glutamate where Alpha Ketogluterate is Synthesis which is Component of the Tricarboxylic Acid Cycle in the Mitochondrion for Cellular Respiration and ATP Synthesis. Goodness Gracious. I have just treated my first INH Induced Peripheral Neuropathy with a simple Pyridoxine Supplementation. Sadly, this patient had Active Tuberculosis apparently misdiagnosed as Latent TB (Isoniazid Therapy). MD Paul Bolin du bist herrlich und toll. Prost! Uberall Gesundheit und Friede!
Great sir.. Keep going with step 1 concepts... Thank you ❤️❤️❤️
God bless you paul
this is biochemistry right ?
Yes