Laurotetanine is an alkaloid isolated from the leaves of Peumus boldus and other plants. It was demonstrated that laurotetanine from Beilschmiedia species possess an anti-acetylcholinesterase (AChE), anti-α-glucosidase, anti-leishmanial and anti-fungal activities. Laurotetanine exhibits antiplasmodial activity and good antioxidant activities also. It relaxed the rat thoracic aorta mainly by suppressing the Ca2+ influx through both voltage- and receptor-operated calcium channels. It showed significant anti-tumor metastatic activities.

alpha-Solanine, a naturally occurring steroidal glycoalkaloid in potato sprouts, was found to possess anti-carcinogenic properties, such as inhibiting proliferation and inducing apoptosis of tumor cells. Human intake of high doses of alpha-Solanine has led to acute intoxication, in severe cases coma and death. The ratio of a-solanine to a-chaconine may determine the degree and nature of the glycoalkaloid toxicity in potatoes, as the toxicity of the two alkaloids act synergistically. alpha-Solanine can inhibit cholinesterase, disrupt cell membranes, and cause birth defects. Some studies suggests that the toxic mechanism of solanine is caused by the chemical's interaction with mitochondrial membranes. Experiments show that solanine exposure opens the potassium channels of mitochondria, decreasing their membrane potential. This, in turn, leads to K+ being transported from the mitochondria into the cytoplasm, and this increased concentration of K+ in the cytoplasm triggers cell damage and apoptosis.

Phenserine tartrate (phenserine), a phenylcarbamate analog of physostigmine, is a long-acting and centrally active inhibitor of acetylcholinesterase (AChE). In addition to being a potent inhibitor of AChE, it has been demonstrated that phenserine inhibits the formation of beta-APP, the source of neurotoxic beta-amyloid peptide which is a major component of the extraneuronal plaques that pathologically characterize Alzheimer’s disease (AD). Phenserine was developed as a potential therapy for AD by Axonyx, under license from the National Institutes of Health/National Institute on Aging. In March 2005, Axonyx suspended patient recruitment for the ongoing Phase III trials of phenserine, after the drug failed to meet the primary endpoints of the first of these trials.

Fensulfothion is an organophosphate insecticide/nematicide. Fensulfothion is highly toxic to man and other non-target terrestrial and aquatic organisms from acute oral and dermal routes of exposure. Fensulfothion is registered for use as preplant or at-planting soil application to tobacco and various fruits and vegetables. Postplant topical applications are permitted in addition to the at-planting application on corn, peanuts, and rutabagas. Topical application is also permitted on commercial and ornamental turf. Fensulfothion is an organophosphate insecticide/nematicide that kills primarily by contact action, but also provides some systemic control of insects attacking the foliage of treated plants. The mode of action is by phosphorylating the acetylcholinesterase enzyme of tissues, allowing accumulation of acetylcholine at nerve junctions, with subsequent blocking effects upon the central nervous system.

Methidathion is an organophosphate insecticide and acaricide (U.S. EPA, 1988). Methidathion and its oxygen analog produce their toxic reaction primarily through their inhibition of cholinesterase (ChE) enzymes, including acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). Methidathion is used to control a variety of insects and mites in many crops such as fruits, vegetables, tobacco, alfalfa and sunflowers. Methidathion is also used in greenhouses and on rose cultures. It is especially useful against scale insects.

Chelidonine is the major alkaloid component of Chelidonium majus. Chelidonine is an isolate of Papaveraceae with acetylcholinesterase and butyrylcholinesterase (a nonspecific cholinesterase) inhibitory activity. It showed strong cytotoxicity in cancer cells. While several modes of death have been identified, most of anti-cancer attempts have focused on stimulation of cells to undergo apoptosis. Chelidonine seems to trigger multiple mechanisms in MCF-7 breast cancer cells. It induces both apoptosis and autophagy modes of cell death in a dose dependent manner. Alteration of expression levels of bax/bcl2, and dapk1a by increasing concentration of chelidonine approves switching the death mode from apoptosis induced by very low to autophagy by high concentrations of this compound. On the other hand, submicromolar concentrations of chelidonine strongly suppressed telomerase at both enzyme activity and hTERT transcriptional level. Long exposure of the cells to 50 nanomolar concentration of chelidonine considerably accelerated senescence. Altogether, chelidonine may provide a promising chemistry from nature to treat cancer. Chelidonine exhibits a broad spectrum of pharmacological properties, such as anti-inflammatory and antiviral activities Its biological activities and clinical applications have been extensively investigated. Especially the usage of chelidonine as an anticancer drug is very important lately. It also has profound inhibitory effects on airway inflammation, which means chelidonine can improve allergic asthma in mice and may also work for human medicine.

CHOLINE is a basic constituent of lecithin that is found in many plants and animal organs. Choline was officially recognized as an essential nutrient by the Institute of Medicine in 1998.1 Its role in the body is complex. It is needed for neurotransmitter synthesis (acetylcholine), cell-membrane signaling (phospholipids), lipid transport (lipoproteins), and methyl-group metabolism (homocysteine reduction). It is the major dietary source of methyl groups via the synthesis of S-adenosylmethionine (AdoMet). At least 50 AdoMet-dependent reactions have been identified in mammals, and it is likely that the number is much higher. Choline is required to make the phospholipids phosphatidylcholine, lysophosphatidylcholine, choline plasmalogen, and sphingomyelin—essential components for all membranes. It plays important roles in brain and memory development in the fetus and appears to decrease the risk of the development of neural tube defects. The importance of choline in the diet extends into adulthood and old age. In a study of healthy adult subjects deprived of dietary choline, 77% of the men and 80% of the postmenopausal women developed signs of subclinical organ dysfunction (fatty liver or muscle damage). Less than half of premenopausal women developed such signs. Ten percent of the subjects studied developed fatty liver, muscle damage, or both when they consumed the Adequate Intake (AI) of choline. The damage was reversed when they consumed a high-choline diet. Plasma choline concentration has been found to vary in response to diet, decreasing approximately 30 percent in humans fed a choline-deficient diet for 3 weeks. Based on estimated dietary intakes and studies reporting liver damage with lower choline intakes, the Institute of Medicine, Food and Nutrition Board set the AI for choline at 425 milligrams/per day for women aged 19 and older, and 550 milligrams/per day for men aged 19 and older.