Definition
Description
Top Gene Interactions
Related Pathways
Methoxsalen Health Effects
- Anti aflatoxin
- Anti dermatitic
- Anti feedant
- Anti histaminic
- Anti inflammatory
- Anti keratotic
- Anti mitotic
- Anti pruritic
- Anti spasmodic
- Artemicide
- Bufocide
- Calcium antagonist
- Cancer preventive
- Cytotoxic
- Dermatitigenic
- Emetic
- Fungistat
- Hepatoprotective
- Herbicide
- Hypertrichotic
- Insecticide
- Lipolytic
- Molluscicide
- Phytoalexin
- Piscicide
- Anti leucodermic
- Anti mutagenic
- Anti pityriasic
- Anti scleromyxoedemic
- Antitumor promoter
General Information
- Metabolism: Route of Elimination: In both mice and man, methoxsalen is rapidly metabolized. Approximately 95% of the drug is excreted as a series of metabolites in the urine within 24 hours (Pathak et al. 1977). Half Life: Approximately 2 hours
- Uses/Sources: It is used to increase skin pigmentation with sunlight in the treatment of depigmentation conditions such as vitiligo and may cause skin burns and liver damage. (L579). It is als used for the treatment of psoriasis and vitiligo.
- Health Effects: Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides. Furocoumarins can cause photosensitization dermatitis especially if these compounds come into contact with the skin. Some furocoumarins, especially bifunctional furocoumarins, are known to be carcinogenic (A15105). Furocoumarin photochemotherapy is known to induce a number of side-effects including erythema, edema, hyperpigmentation, and premature aging of skin. All photobiological effects of furocoumarins result from their photochemical reactions. Because many dietary or water soluble furocoumarins are strong inhibitors of cytochrome P450s, they will also cause adverse drug reactions when taken with other drugs. Limited evidence of carcinogenic effect. (L579)
- Symptoms: Harmful if swallowed. May cause sensitisation by skin contact. (L579)
- Treatment: If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.
Mechanism of Action
Target Name | Mechanism of Action | References |
---|---|---|
Cytochrome P450 3A4 Acetylcholinesterase DNA Amine oxidase [flavin-containing] A Cytochrome P450 2C9 |
6504703 17016423 17995595 11374978 16451079 17139284 6746605 20419242 |
Methoxsalen Interacts with Diseases
Disease | Inference Score | References/Inference Genes |
Breast carcinoma | 44.88 |
|
Prostatic Neoplasms | 41.03 |
|
Colorectal cancer | 26.93 |
|
Lung Neoplasms | 22.86 |
|
Diabetes Mellitus, Experimental | 22.84 |
|
Stomach Neoplasms | 21.0 |
|
Adenocarcinoma | 20.81 |
|
Hepatocellular carcinoma | 20.23 |
|
Pancreatic carcinoma | 19.91 |
|
Diabetes Mellitus, Type 2 | 18.69 |
|
Osteosarcoma | 17.9 |
|
Brain Ischemia | 16.99 |
|
Liver Neoplasms, Experimental | 16.02 |
|
Cardiac hypertrophy | 15.11 |
|
Acute lymphoblastic leukemia | 15.1 |
|
Esophageal Neoplasms | 14.95 |
|
Male infertility | 14.87 |
|
Obesity | 14.56 |
|
Drug-induced liver injury | 13.98 |
|
Carcinoma, Small Cell | 13.96 |
|