Pathways

Oxybutynin is an antimuscarinic agent used to relax the bladder and prevent the urge to void. It can be taken either orally or intravenously. The bioavailability and the elimination half-life are both increased in the elderly. When taken orally, oxybutynin enters the intestine and is transported into the intestinal wall by the transporter solute carrier family 15 member 1. It is heavily metabolized by cytochrome P450 3A4 in both the intesine wall and the liver. In the endoplasmic reticulum of the intestine wall oxybutynin is metabolized by cytochrome P450 3A4 into N-desethyloxybutynin, an active metabolite. Oxybutynin is also metabolized into 2-cyclohexyl-2-phenylglycolic acid or phenylcyclohexylglycolic acid also by cytochrome P450 3A4. Both metabolites and the remaining original oxybutynin are transported into the blood by organic cation transporters. N-Desethyloxybutynin is an active metabolite that circulates the blood along with Oxybutynin. N-Desethyloxybutynin is active at muscarinic receptors in the bladder and salavary glands as well. Oxybutynin travels to the liver where it is transported in via organic cation transporters and metabolized again in the endoplasmic reticulum in the same way it was in the intestine wall. Oxybutynin is heavily cleared by the liver. The majority is metabolized into the inactive metabolite phenylcyclohexylgycolic acid. The metabolites are transported out of the liver and back into the blood where they are eliminated renally. Less than 0.1% is excreted as the active metabolite N-desethyloxybutynin, and less than 0.1% of the dose is excreted as the original oxybutynin. The majority is excreted as the inactive metabolite 2-cyclohexyl-2-phenylglycolic acid.

Oxycodone (also known as OxyContin or Dihydrohydroxycodeinone) is analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of oxycodone will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Hyperpolarization of neuron is caused by inactivation of calcium channels and activation of potassium channels via facilitated by G-protein.

Oxycodone is an opioid used in the management of moderate to severe pain. There is also an extended release formulation indicated for chronic moderate to severe pain requiring continuous opioid analgesics for an extended period. Oxycodone acts directly on a number of tissues not related to its analgesic effect. These tissues include the respiratory centre in the brain stem, the cough centre in the medulla, muscles of the pupils, gastrointestinal tract, cardiovascular system, endocrine system, and immune system. Oxycodone's effect on the respiratory centre is dose dependant respiratory depression. The action on the cough centre is suppression of the cough reflex.\ Pupils become miopic or decrease in size, peristalsis of the gastrointestinal tract slows, and muscle tone in the colon may increase causing constipation. In the cardiovascular system histamine may be released leading to pruritis, red eyes, flushing, sweating, and decreased blood pressure. Endocrine effects may include increased prolactin, decreased cortisol, and decreased testosterone. It is not yet known if the effects of opioids on the immune system are clinically significant. Oxycodone is an opioid used in the management of moderate to severe pain. There is also an extended release formulation indicated for chronic moderate to severe pain requiring continuous opioid analgesics for an extended period. Oxycodone acts directly on a number of tissues not related to its analgesic effect. These tissues include the respiratory centre in the brain stem, the cough centre in the medulla, muscles of the pupils, gastrointestinal tract, cardiovascular system, endocrine system, and immune system. Oxycodone's effect on the respiratory centre is dose dependant respiratory depression. The action on the cough centre is suppression of the cough reflex.\ Pupils become miopic or decrease in size, peristalsis of the gastrointestinal tract slows, and muscle tone in the colon may increase causing constipation. In the cardiovascular system histamine may be released leading to pruritis, red eyes, flushing, sweating, and decreased blood pressure. Endocrine effects may include increased prolactin, decreased cortisol, and decreased testosterone. It is not yet known if the effects of opioids on the immune system are clinically significant. Oxycodone binds to mu opioid receptors, stimulating the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as GABA is inhibited. Opioids close N-type voltage-operated calcium channels and open calcium-dependent inwardly rectifying potassium channels. This results in hyperpolarization and reduced neuronal excitability. Oxycodone acts at A delta and C pain fibres in the dorsal horn of the spinal cord. By decreasing neurotransmitter action there is less pain transmittance into the spinal cord. This leads to less pain perception. Oxycodone may also bind to delta and kappa opioid receptors.

Metabolites of Oxycodone are predicted with biotransformer.

Photosynthesis involves the transfer and harvesting of energy from sunlight and the fixation of carbon dioxide into carbohydrates. This process occurs in higher plants, including Solanum lycopersicum. Oxygenic photosynthesis requires water, which acts as an electron donor molecule. The reactions which involve the trapping of sunlight are known as "light reactions", and result in the production of NADPH, adenosine triphosphate, and molecular oxygen. The "dark reactions" are known as the Calvin cycle, and involve the use of the products of the light reactions to fix carbon dioxide and produce carbohydrates.