The ammonium cation is a positively charged polyatomic ion with the chemical formula NH4+. Ammonium ions are a waste product of the metabolism of animals. In fish and aquatic invertebrates, it is excreted directly into the water. In mammals, sharks, and amphibians, it is converted in the urea cycle to urea, because urea is less toxic and can be stored more efficiently. In birds, reptiles, and terrestrial snails, metabolic ammonium is converted into uric acid, which is solid and can therefore be excreted with minimal water loss. Ammonium is an important source of nitrogen for many plant species, especially those growing on hypoxic soils. However, it is also toxic to most crop species and is rarely applied as a sole nitrogen source. The ammonium ion (NH4+) in the body plays an important role in the maintenance of acid-base balance. The kidney uses ammonium (NH4+) in place of sodium (Na+) to combine with fixed anions in maintaining acid-base balance, especially as a homeostatic compensatory mechanism in metabolic acidosis. When a loss of hydrogen ions (H+) occurs and serum chloride (Cl–) decreases, sodium is made available for combination with bicarbonate (HCO3–). This creates an excess of sodium bicarbonate (NaHCO3) which leads to a rise in blood pH and a state of metabolic alkalosis. The therapeutic effects of Ammonium (as Ammonium Chloride) depend upon the ability of the kidney to utilize ammonia in the excretion of an excess of fixed anions and the conversion of ammonia to urea by the liver, thereby liberating hydrogen (H+) and chloride (Cl–) ions into the extracellular fluid.

Sodium sulfate anhydrous is an electrolyte replenisher and is used in isosmotic solutions so that administration does not disturb normal electrolyte balance and does not lead to absorption or excretion of water and ions. It is indicated for bowel cleansing prior to colonoscopy or barium enema X-ray examination. Sodium Sulfate, Potassium Sulfate and Magnesium Sulfate Oral Solution is indicated for cleansing of the colon as a preparation for colonoscopy in adults.

Atropine inhibits the muscarinic actions of acetylcholine on structures innervated by postganglionic cholinergic nerves, and on smooth muscles which respond to endogenous acetylcholine but are not so innervated. As with other antimuscarinic agents, the major action of atropine is a competitive or surmountable antagonism which can be overcome by increasing the concentration of acetylcholine at receptor sites of the effector organ (e.g., by using anticholinesterase agents which inhibit the enzymatic destruction of acetylcholine). The receptors antagonized by atropine are the peripheral structures that are stimulated or inhibited by muscarine (i.e., exocrine glands and smooth and cardiac muscle). Responses to postganglionic cholinergic nerve stimulation also may be inhibited by atropine but this occurs less readily than with responses to injected (exogenous) choline esters. Atropine is relatively selective for muscarinic receptors. Its potency at nicotinic receptors is much lower, and actions at non-muscarinic receptors are generally undetectable clinically. Atropine does not distinguish among the M1, M2, and M3 subgroups of muscarinic receptors.

Arsenic trioxide (ATO) is used to treat acute promyelocytic leukemia in people who have not been helped by other types of chemotherapy or whose condition has improved but then worsened following treatment with other types of chemotherapy. Arsenic trioxide acts through activation of Jun N-terminal kinase (JNK), activator protein-1, and inhibition of dual-specificity phosphatases. Although the exact mechanisms under which ATO exerts its therapeutic effect in acute promyelocytic leukemia cancer cells are not well elucidated. It was shown that apoptotic mechanisms involved the induction of phosphatidylserine externalization, caspase-3 activation, and nucleosomal DNA fragmentation. Adverse reactions described are leukocytosis, nausea, vomiting, diarrhea, and abdominal pain, fatigue, edema, hyperglycemia, dyspnea, cough, rash or itching, headaches, and dizziness.

SULFATE (as sodium sulfate, potassium sulfate, and magnesium sulfate) is a component of SUPREP Bowel Prep Kit. It is an osmotic laxative indicated for cleansing of the colon in preparation for colonoscopy in adults. Sulfate salts provide sulfate anions, which are poorly absorbed. The osmotic effect of unabsorbed sulfate anions and the associated cations causes water to be retained within the gastrointestinal tract. SUPREP Bowel Prep Kit, when ingested with a large volume of water, produces copious watery diarrhea.

Lithium is an alkali metal widely used in industry. Lithium salts are indicated in the treatment of manic episodes of Bipolar Disorder. The use of lithium in psychiatry goes back to the mid-19th century. Early work, however, was soon forgotten, and John Cade is credited with reintroducing lithium to psychiatry for mania in 1949. Mogens Schou undertook a randomly controlled trial for mania in 1954, and in the course of that study became curious about lithium as a prophylactic for depressive illness. In 1970, the United States became the 50th country to admit lithium to the marketplace. The specific mechanisms by which lithium exerts its mood-stabilizing effects are not well understood. Lithium appears to preserve or increase the volume of brain structures involved in emotional regulation such as the prefrontal cortex, hippocampus and amygdala, possibly reflecting its neuroprotective effects. At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission; however, these broad effects are underpinned by complex neurotransmitter systems that strive to achieve homeostasis by way of compensatory changes. For example, at an intracellular and molecular level, lithium targets second-messenger systems that further modulate neurotransmission. For instance, the effects of lithium on the adenyl cyclase and phospho-inositide pathways, as well as protein kinase C, may serve to dampen excessive excitatory neurotransmission. In addition to these many putative mechanisms, it has also been proposed that the neuroprotective effects of lithium are key to its therapeutic actions. In this regard, lithium has been shown to reduce the oxidative stress that occurs with multiple episodes of mania and depression. Further, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces apoptotic processes through inhibition of glycogen synthase kinase 3 and autophagy.

Since its discovery as component of the tea leaf by Albert Kossel in 1888, the history of theophylline (CAS 58-55-9) has been a long and successful one. At the turn of the century, theophylline became less expensive due to chemical synthesis and was primarily used as diuretic in subsequent years. It was Samuel Hirsch who discovered the bronchospasmolytic effect of theophylline in 1992, however, despite this pioneering discovery theophylline continued to be used primarily as diuretic and cardiac remedy. The molecular mechanism of bronchodilatation is inhibition of phosphodiesterase(PDE)3 and PDE4, but the anti-inflammatory effect may be due to histone deacetylase (HDAC) activation, resulting in switching off of activated inflammatory genes. Theophylline is indicated for the treatment of acute exacerbations of the symptoms and reversible airflow obstruction associated with asthma and other chronic lung diseases, e.g., emphysema and chronic bronchitis.

Pentaerythritol tetranitrate is an organic nitrate that has been used for the treatment of angina pectoris. Upon administration, the drug undergoes exstensive metabolism to NO which causes vasodilation and the relaxation of smooth muscle cells. The compound belongs to a familiy of explosive substances and may be used accordingly.

COPPER is a heavy metal trace element with the atomic symbol Cu. It is commonly used in contraceptive intrauterine devices (IUD) which birth control effectiveness is enhanced by COPPER continuously released into the uterine cavity. Mechanism(s) by which COPPER enhances contraceptive efficacy include interference with sperm transport and fertilization of an egg, and possibly prevention of implantation.

Glucose is a sugar with the molecular formula C6H12O6. The D-isomer (D-glucose), also known as dextrose, occurs widely in nature, but the L-isomer (L-glucose) does not. Glucose is made during photosynthesis from water and carbon dioxide, using energy from sunlight. The reverse of the photosynthesis reaction, which releases this energy, is a very important source of power for cellular respiration. Glucose is stored as a polymer, in plants as starch and in animals as glycogen, for times when the organism will need it. Glucose circulates in the blood of animals as blood sugar. Glucose can be obtained by hydrolysis of carbohydrates such as milk, cane sugar, maltose, cellulose, glycogen etc. It is however, manufactured by hydrolysis of cornstarch by steaming and diluting acid. Glucose is the human body's key source of energy, through aerobic respiration, providing about 3.75 kilocalories (16 kilojoules) of food energy per gram. Breakdown of carbohydrates (e.g. starch) yields mono- and disaccharides, most of which is glucose. Use of glucose as an energy source in cells is by either aerobic respiration, anaerobic respiration, or fermentation. All of these processes follow from an earlier metabolic pathway known as glycolysis. The insulin reaction, and other mechanisms, regulate the concentration of glucose in the blood. Glucose supplies almost all the energy for the brain, so its availability influences psychological processes. When glucose is low, psychological processes requiring mental effort (e.g., self-control, effortful decision-making) are impaired. Ingested glucose is absorbed directly into the blood from the intestine and results in a rapid increase in the blood glucose level. Glucose is used to manage hypoglycemia and for intravenous feeding. Nausea may occur after ingesting glucose, but this also may be an effect of the hypoglycemia which is present just prior to ingestion. Other adverse effects include increased blood glucose, injection site leakage of fluid (extravasation), injection site inflammation, and bleeding in the brain.