Pathways

Chlorophyll a degradation is the process in leaf senescence and fruit ripening observable due to its characteristic loss of green colouring. There are two pathways for chlorophyll a degradation. This first pathway, largely occurring in the chloroplast, is hypothesized to be operational during fruit senescence and as an immune respone. First, chlorophyllase catalyzes the conversion of chlorophyll a into chlorophyllide a and phytol. Second, the predicted enzyme magnesium dechelatase (coloured orange in the image) is theorized to release Mg2+ from chlorophyllide to form pheophorbide a. Pheophorbide a has two fates. Either it is transported out of the chloroplast by a predicted pheophorbide a transporter and converted into pyropheophorbide a by the probable pheophorbidase enzyme (coloured orange in the image) or it it continues on to eventually become a primary fluorescent chlorophyll catabolite. Continuing along the main branch, pheophorbide a oxygenase, localized to the chloroplast membrane (coloured dark green in the image), catalyzes the conversion of pheophorbide into epoxypheophorbide a. Next, epoxypheophorbide and water spontaneously converts into red chlorophyll catabolite. Last, red chlorophyll catabolite reductase (RCCR) converts red chlorophyll catabolite into primary fluorescent chlorophyll catabolite.

Chlorophyll a degradation is the process in leaf senescence and fruit ripening observable due to its characteristic loss of green colouring. There are two pathways for chlorophyll a degradation. This second pathway, occurring in the chloroplast, is possibly the primary route by which chlorophyll a undergoes degradation in senescing leaves. First, the predicted enzyme pheophytin a synthase (coloured orange in the image) is theorized to dechelate Mg2+ in chlorophyll a to form pheophytin a. Second, pheophytinase catalyzes teh conversion of pheophytin into pheophorbide a and phytol. Third, pheophorbide a oxygenase, localized to the chloroplast membrane (coloured dark green in the image), catalyzes the conversion of pheophorbide into epoxypheophorbide a. Fourth, epoxypheophorbide and water spontaneously converts into red chlorophyll catabolite. Fifth, red chlorophyll catabolite reductase (RCCR) converts red chlorophyll catabolite into primary fluorescent chlorophyll catabolite.

Chlorophyll a and chlorophyll b are important light harvesting pigments that capture photons and direct them to reaction centers within the plant. Both chlorophyll a and b have essentially the same structure with the exception of the methyl group on carbon 7 of chlorophyll a and a formyl group on carbon 7 of chlorophyll b. The process by which chlorophyll b is synthesized was only recently elucidated with the discovery of the enzyme chlorophyllide a oxygenase, or CAO, which showed that this enzyme was capable of catalyzing the chemical transition from chlorophyll a to chlorophyll b.

Chloroprocaine is a local hydrochloride anesthetic typically administered through intrathecal injection. This is commonly used during labor and delivery in order to block generation and conduction of nerve impulses. The mechanism of action is thought to increase the threshold for electrical excitation and slow propagation of nerve impulses. This is through inhibiting sodium influx through voltage gated sodium channels, with the sodium flux interrupted the action potential cannot occur. This receptor site is theorized to be within the cytoplasmic portion of the sodium channel. Chloroprocaine is also hypothesized to antagonize NMDA receptors, nicotinic acetylcholine receptors and serotonin receptor ion channel complex. Chloroprocaine also acts on blood vessels to stimulate vasoconstriction thus reducing any possible bleeding. Absorption of chloroprocaine is dependent on total dose and concentration as well as route, vascularity and or presence or absence of epinephrine at the administration site. Chloroprocaine is metabolized in the plasma through hydrolysis by the pseudocholinesterase and excreted through the urine.

Chloroprocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Chloroprocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore chloroprocaine preferentially inhibits neurons that are actively firing.

Metabolites of sildenafil are predicted with biotransformer.

Chloropyramine is a first-generation H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles. Allergies causes blood vessel dilation which causes swelling (edema) and fluid leakage. Chloropyramine also inhibits the H1 histamine receptor on bronchiole smooth muscle myocytes. This normally activates the Gq signalling cascade which activates phospholipase C which catalyzes the production of Inositol 1,4,5-trisphosphate (IP3) and Diacylglycerol (DAG). Because of the inhibition, IP3 doesn't activate the release of calcium from the sarcoplasmic reticulum, and DAG doesn't activate the release of calcium into the cytosol of the endothelial cell. This causes a low concentration of calcium in the cytosol, and it, therefore, cannot bind to calmodulin.Calcium bound calmodulin is required for the activation of myosin light chain kinase. This prevents the phosphorylation of myosin light chain 3, causing an accumulation of myosin light chain 3. This causes muscle relaxation, opening up the bronchioles in the lungs, making breathing easier.

Chloropyramine is a first-generation ethylenediamine H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.

Chloropyramine is a first-generation H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles. Allergies causes blood vessel dilation which causes swelling (edema) and fluid leakage. Chloropyramine inhibits the H1 histamine receptor on blood vessel endothelial cells. This normally activates the Gq signalling cascade which activates phospholipase C which catalyzes the production of Inositol 1,4,5-trisphosphate (IP3) and Diacylglycerol (DAG). Because of the inhibition, IP3 doesn't activate the release of calcium from the sarcoplasmic reticulum, and DAG doesn't activate the release of calcium into the cytosol of the endothelial cell. This causes a low concentration of calcium in the cytosol, and it, therefore, cannot bind to calmodulin. Calcium bound calmodulin is required for the activation of the calmodulin-binding domain of nitric oxide synthase. The inhibition of nitric oxide synthesis prevents the activation of myosin light chain phosphatase. This causes an accumulation of myosin light chain-phosphate which causes the muscle to contract and the blood vessel to constrict, decreasing the swelling and fluid leakage from the blood vessels caused by allergens.