Camphor, (pronounced /ˈkæmfə/) is a waxy, white or transparent solid with a strong, aromatic odor. It is a terpenoid with the chemical formula C10H16O. It is found in wood of the camphor laurel (Cinnamomum camphora), a large evergreen tree found in Asia (particularly in Sumatra, Borneo and Taiwan) and also of Dryobalanops aromatica, a giant of the Bornean forests. It also occurs in some other related trees in the laurel family, notably Ocotea usambarensis. Dried rosemary leaves (Rosmarinus officinalis), in the mint family, contain up to 20% camphor. It can also be synthetically produced from oil of turpentine. It is used for its scent, as an ingredient in cooking (mainly in India), as an embalming fluid, for medicinal purposes, and in religious ceremonies. A major source of camphor in Asia is camphor basil.
Norcamphor is a camphor derivative with the three methyl groups replaced by hydrogen.
In biosynthesis, camphor is produced from geranyl pyrophosphate, via cyclisation of linaloyl pyrophosphate to bornyl pyrophosphate, followed by hydrolysis to borneol and oxidation to camphor.
Camphor has been used in ancient Sumatra to treat sprains, swellings, and inflammation.
Camphor is readily absorbed through the skin and it produces a feeling of cooling similar to that of menthol, and acts as slight local anesthetic and antimicrobial substance. There are anti-itch gels and cooling gels with camphor as the active ingredient. Camphor is an active ingredient (along with menthol) in vapor-steam products, such as Vicks VapoRub.
Camphor may also be administered orally in small quantities (50 mg) for minor heart symptoms and fatigue.
In the 18th century, camphor was used by Auenbrugger in the treatment of mania.
Based on Hahnemann's writings, Camphor (dissolved in alcohol) was also successfully used to treat cholera epidemics in Naples, 1854-1855.
Camphor is also used as a nasal decongestant and cough suppressant.
Camphor is also commonly applied to the skin for antipruritic, analgesic, and counterirritant properties.
Analgesic Effects on the body
Camphor, capsaicin (the pungent ingredient in chili peppers), and menthol are plant-derived natural products well known for their sensory effects. Capsaicin and menthol are known to excite and subsequently desensitize sensory neurons by acting on two members of transient receptor potential (TRP) channel superfamily, TRP vanilloid subtype 1 (TRPV1) and TRP channel M8 (TRPM8), respectively. Thermo-sensitive transient receptor potential (Thermo-TRPs) cation channels are a subgroup of the transient receptor potential (TRP) superfamily of ion channels. They are understood to play a critical role in transduction of thermal and nociceptive information to the central nervous system. These thermoTRPs detect a wide range of temperatures spanning from noxious cold and heat as well as cool and warmth. Interestingly, all thermoTRP channels are apparently also chemosensitive, potentially enabling these channels to detect multiple sensory modalities.
Effects of camphor on TRPV1
TRPV1 receptors are found mainly in the nociceptive neurons of the peripheral nervous system, but they have also been described in many other tissues, including the central nervous system. TRPV1 is involved in the transmission and modulation of pain (nociception), as well as the integration of diverse painful stimuli.
Camphor activates TRPV1 and a TRPV1-like current in dorsal root ganglion (DRG) neurons but inhibits the TRPA1 channel , which is expressed in most nociceptive DRG neurons (Nagata et al., 2005). Chemosensitive and thermosensitive TRP channels often exhibit desensitization after prolonged or repeated stimulations to adapt to changing stimulus levels.
TRPV1 exhibits two types of desensitization response to activation: acute desensitization, during which TRPV1 currents decline despite the continued presence of agonist, and tachyphylaxis, in which repeated short-duration applications of agonist lead to smaller responses (Koplas et al., 1997; Bhave et al., 2002). Agonists of TRPV1 can induce a long-lasting analgesic effect after an initial activation; this analgesic effect can be especially pronounced in inflammatory conditions (Menendez et al., 2004).
Camphor-activated TRPV1 currents underwent significant desensitization and tachyphylaxis, which, together with inhibition of TRPA1, might generate the antipruritic, analgesic, and counterirritant properties of camphor.
The efficacy of camphor could be increased if other TRPV1 agonists act on the channel synergistically, for example, at physiological temperatures and under inflamed conditions.
The activation of TRPV1 can be further increased by proalgesic agents such as bradykinin and nerve growth factor, which are released after tissue injury or in irritated conditions (Chuang etal., 2001; Ji and Strichartz, 2004). Camphor is known as an effective counterirritant (Burkhart and Burkhart, 2003) but only weakly generates warmth sensations when applied in isolation. (Green, 1990). The effect of camphor might be stronger under irritated and inflamed conditions when the activity of TRPV1 is enhanced. Both type 1 muscarinic receptor (M1) and type II bradykinin receptor (B2R) are known to couple to PLC via their activation of Gαq/11. The resulting hydrolysis of phosphatidylinositol-4,5-bisphosphate (PIP2) and the activation of protein kinase C (PKC) are likely to combine to sensitize TRPV1.
The camphor-induced TRPV1-mediated response can be enhanced by PLC-coupled receptor stimulation, and this enhancement may increase the effectiveness of camphor in conditions in which TRPV1 is already sensitized. Enhanced camphor activation of TRPV1 is likely to lead to enhanced desensitization, perhaps making camphor a more effective counterirritant under inflamed conditions.
Capsaicin-induced TRPV1 channel desensitization has been proposed to mediate the capsaicin desensitization of nociceptive nerves.
Because camphor desensitizes TRPV1 even more strongly than capsaicin, it was proposed that camphor induced desensitization of TRPV1 contribute to the analgesic and counterirritant actions of camphor. In fact, the small inward currents activated by camphor suggest that, in the presence of a sufficient camphor concentration, significant pain relief might be attained without the initial painful experience that accompanies the application of topical capsaicin treatments.
Camphor activates and strongly desensitizes the transient receptor potential vanilloid subtype 1 channel in a vanilloid-independent mechanism, 2005
Effects on TRPV3
Transient receptor potential vanilloid-3 (TRPV3) is a thermo-sensitive ion channel expressed in
skin keratinocytes and in a variety of neural cells. TRPV3 is a member of thermo-TRPs, and a
structural homologue of transient receptor potential vanilloid-1 (TRPV1). It is heat-sensitive but capsaicin-insensitive. It is activated by warmth as well as monoterpenoids including camphor, menthol, dihydrocarveol and 1,8-cineol. Recently, it has been proposed that voltage, temperature and chemical cues act through independent mechanisms.
TRPV3 is predominantly expressed in human keratinocytes. In humans it is co-expressed with TRPV1 in skin, tongue, dorsal root ganglion, trigeminal ganglion, spinal cord and brain. TRPV3 is implicated in skin sensitization and hyperalgesia in inflamed tissues and shows increased expression in the case of peripheral nerve injury.
Camphor is known to produce a warm sensation (Green, 1990), consistent with the thermal activation range of TRPV3. However, repeated camphor applications sensitized TRPV3, apparently contradicting its analgesic role
In fact prolonged exposure (5-15 minutes) of monoterpenoids results in agonist-specific desensitization of TRPV3.
It was observed Ca2+independent desensitization of TRPV3 channels during prolonged incubation with camphor, 1,8-cineol, mentol.
While the bicyclic monoterpenoids (camphor or 1,8-cineol) induce both acute desensitization and tachyphylaxis,
monocyclic monoterpenoids (dihydrocarveol or menthol) preferentially induce only tachyphylaxis.
Monoterpenoids induce agonist-specific desensitization of transient receptor potential vanilloid-3 (TRPV3) ion channels, 2009
Its effects on the body include tachycardia, vasodilation in skin (flushing), slower breathing, reduced appetite, increased secretions and excretions such as perspiration, diuretic.
Large dose / toxicity
Camphor is poisonous. In large quantities, it produces symptoms of irritability, disorientation, lethargy, muscle spasms, vomiting, abdominal cramps, convulsions, seizures. Lethal doses in adults are in the range 50–500 mg/kg (orally). Generally, two grams cause serious toxicity and four grams are potentially lethal.
In 1980, the U.S. Food and Drug Administration set a limit of 11% allowable camphor in consumer products, and totally banned products labeled as camphorated oil, camphor oil, camphor liniment, and camphorated liniment (except "white camphor essential oil", which contains no significant amount of camphor). Since alternative treatments exist, medicinal use of camphor is discouraged by the FDA, except for skin-related uses, such as medicated powders, which contain only small amounts of camphor.