Pathways

Prunasin and amygdalin are cyanogenic glucosides, chemical compounds that can release toxic hydrogen cyanide after animal ingestion as a chemical defence. These compounds are also responsible for the bitter taste in many seeds, such as almonds, peaches or apples. Prunasin is transformed into amygdalin during fruit ripening. Cyanogenic glycosides are typically derived from amino acids, such as phenylalanine. This pathway involves the conversion of phenylalanine into prunasin and amygdalin by the enzyme L-phenylalanine N-monooxygenase (CYP79A2) and some other enzymes in the Arabidopsis thaliana species

Prussian blue is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Prussian blue passes through the liver and is then excreted from the body mainly through the kidney.

Pseudoephedrine is alpha and beta agonist used to treat nasal and sinus congestion as well as allergic rhinitis. It is in many cold and sinus medicines as well as allergy medicine. Pseudoephedrine's mechanism of action mainly occurs in the nose and sinuses. It primarily activates alpha adrenergic receptor 1A or 2A. Pseudoephedrine also inhibits sodium dependent noradrenaline receptors which prevents the reuptake of norepinephrine into the presynaptic neuron. This causes norepinephrine to accumulate in the synapse which also activates alpha adrenergic receptors. These receptors then activate the Gq protein cascade. This activates Phospolipase C which catalyzes Phosphatidylinositol 4,5-bisphosphate into Inositol 1,4,5-trisphosphate and Diacylglycerol. Diacylglycerol activates protain kinase C which activates the voltage-dependent calcium channel, allowing calcium to enter the cell. Inositol 1,4,5-trisphosphate activates Inositol 1,4,5-trisphosphate receptor on the sarcoplasmic reticulum which also allows calcium to enter the cell from the sarcoplasmic reticulum. This high concentration of calcium in the cytosol attaches to calmodulin which activates Myosin light chain kinase. This enzyme catalyzes Myosin light chain 3 into myosin LC-P which causes myosin to bind to actin and contract the muscle cell. The contraction of this smooth muscle causes the blood vessel to constrict. The contriction of blood vessels in the sinuses and nose lead to decongestion. Pseudophedrine also activates on beta receptors, and it inhibits sodium dependent dopamine and serotonin transporters, however not to the same effect or degree as it affects alpha receptors and the norepinephrine pathway.

Pseudoephedrine is a drug taken orally in cold and sinus medication or allergy medication. It is swallowed as a pill where it is digested then absorbed through the epithelial cells of the intestine without a transporter. Pseudoephedrine is a BSC class 1 compound, and therefore has high permiability and is able to pass through the membranes of the intestine and liver. It travels through the blood stream where only a small portion of Pseudoephedrine is metabolized in the liver. It is N-demethylated by Cytochrome P450 1A2 into the inactive metabolite Norpseudoephedrine. Both Pseudoephedrine and Norpseudoephedrine travel to the kidney where 55%-75% of the dose are excreted in the urine as unchanged Pseudoephedrine.

Pterin biosynthesis is a pathway located in the cytosol by which GTP becomes hydroxymethyldihydropterin (HMDHP), the pterin precursor of folate biosynthesis. Firstly, GTP cyclohydrolase (GCH) catalyzes the conversion of GTP and water to dihydroneopterin triphosphate, formic acid, and water. Secondly, nudix hydrolase from the Nudix (NUcleotide DIphosphates linked to some moiety X) protein family of phosphohydrolases uses water to eliminate a pyrophosphate from dihydroneopterin phosphate and releases a hydrogen ion in the process. However, this enzyme is non-specific for this reaction, and therefore the true dihydroneopterin triphosphate diphosphatase may yet to be found. Thirdly, dihydroneopterin phosphate phosphatase (Pase) dephosphorylates dihydroneopterin phosphate to 7,8-dihydroneopterin. This enzyme has not yet been identified in any organism, but it is possible that reaction is carried out by a nonspecific phosphatase. The fourth reaction is catalyzed by the enzyme dihydroneopterin aldolase (DHNA) whereby 7,8-dihydroneopterin is cleaved to form HMDHP and glycolaldehyde is released. The second function of DHNA is epimerizing 7,8-dihydroneopterin to form 7,8-dihydromonapterin. DHNA can also use 7,8-dihydromonapterin as a substrate to form HMDHP. HMDHP has two fates. It can either be pumped into the mitochondria by a yet to be discovered HMDHP transporter for use in folate biosynthesis, or be acted upon by cytosolic hydroxymethyldihydropterin pyrophosphokinase-dihydropteroate synthase (HPPK-DHPS). HPPK-DHPS is a bifunctional enzyme that requires magnesium as a cofactor and catalyzes consecutive steps in the pterin and folate biosynthesis pathways. The HPPK domain uses ATP to diphosphorylate HMDHP to HMDHP pyrophosphate, releasing AMP and a hydrogen ion in the process. The DHPS domain incorporates pABA, diffused out from the chloroplast, to form dihydropteroate and a diphosphate.