Substances & Homeopatic Remedies

Oleum santali

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Pharmacology

The oil is the part that is most often used in medicine so we will look at it from a chemical standpoint. The oil distilled from the sandalwood tree is made up of a several different volatile oils. You are already aware of the nature of scented oils; sandalwood oil is no different to the oils found in mint. 90% of the oil is comprised of alpha and beta santalol. These oils are responsible for the scent of the oil and its medicinal action.
Sandalwood oil has been found to be diuretic and to act as a urinary antiseptic, meaning that it kills bacteria that take up house in the urinary apparatus. One of its traditional uses is in gonorrhea and other urinary infections!


Carcinogenesis. 2005 Feb;26(2):369-80. Epub 2004 Nov 4.
Skin cancer chemopreventive agent, {alpha}-santalol, induces apoptotic death of human epidermoid carcinoma A431 cells via caspase activation together with dissipation of mitochondrial membrane potential and cytochrome c release.
Kaur M, Agarwal C, Singh RP, Guan X, Dwivedi C, Agarwal R.
Department of Pharmaceutical Sciences, School of Pharmacy, University of Colorado Health Sciences Center, Denver, CO 80262, USA.

alpha-Santalol, an active component of sandalwood oil, has been studied in detail in recent years for its skin cancer preventive efficacy in murine models of skin carcinogenesis; however, the mechanism of its efficacy is not defined. Two major biological events responsible for the clonal expansion of transformed/initiated cells into tumors are uncontrolled growth and loss of apoptotic death. Accordingly, in the present study, employing human epidermoid carcinoma A431 cells, we assessed whether alpha-santalol causes cell growth inhibition and/or cell death by apoptosis. Treatment of cells with alpha-santalol at concentrations of 25-75 microM resulted in a concentration- and a time-dependent decrease in cell number, which was largely due to cell death. Fluorescence-activated cell sorting analysis of Annexin V/propidium iodide (PI) stained cells revealed that alpha-santalol induces a strong apoptosis as early as 3 h post-treatment, which increases further in a concentration- and a time-dependent manner up to 12 h. Mechanistic studies showed an involvement of caspase-3 activation and poly(ADP-ribose) polymerase cleavage through activation of upstream caspase-8 and -9. Further, the treatment of cells with alpha-santalol also led to disruption of the mitochondrial membrane potential and cytochrome c release into the cytosol, thereby implicating the involvement of the mitochondrial pathway. Pre-treatment of cells with caspase-8 or -9 inhibitor, pan caspase inhibitor or cycloheximide totally blocked alpha-santalol-caused caspase-3 activity and cleavage, but only partially reversed apoptotic cell death. This suggests involvement of both caspase-dependent and -independent pathways, at least under caspase inhibiting conditions, in alpha-santalol-caused apoptosis. Together, this study for the first time identifies the apoptotic effect of alpha-santalol, and defines the mechanism of apoptotic cascade activated by this agent in A431 cells, which might be contributing to its overall cancer preventive efficacy in mouse skin cancer models.



J Nat Prod. 2005 Jun;68(6):819-24.  
Anti-Helicobacter pylori compounds from Santalum album.
Ochi T, Shibata H, Higuti T, Kodama KH, Kusumi T, Takaishi Y.
Graduate School of Pharmaceutical Sciences, University of Tokushima, Japan.

Six new sesquiterpenes, (Z)-2beta-hydroxy-14-hydro-beta-santalol (1), (Z)-2alpha-hydroxy-albumol (2), 2R-(Z)-campherene-2,13-diol (3), (Z)-campherene-2beta,13-diol (4), (Z)-7-hydroxynuciferol (5), and (Z)-1beta-hydroxy-2-hydrolanceol (6), together with five known compounds, (Z)-alpha-santalol (7), (Z)-beta-santalol (8), (Z)-lanceol (9), alpha-santaldiol (10), and beta-santaldiol (11), were isolated from Santalum album, by using bioassay-guided fractionation for Helicobacter pylori. The structures were determined by extensive NMR studies. The absolute configuration of compound 3 was determined by a modified Mosher method. The crude extracts as well as the isolated compounds showed antibacterial activity against H. pylori. Especially, compounds 7 and 8 have strong anti-H. pylori activities against a clarithromycin-resistant strain (TS281) as well as other strains.

Contact Dermatitis. 2005 Dec;53(6):320-3.  
Fragrance contact dermatitis in Korea: a joint study.
An S, Lee AY, Lee CH, Kim DW, Hahm JH, Kim KJ, Moon KC, Won YH, Ro YS, Eun HC.
AmorePacific Corporation, R&D Center, Yongin, Korea.

The purpose of this study is to determine the frequency of responses to selected fragrances in patients with suspected fragrance allergy and to evaluate the risk factors. 9 dermatology departments of university hospitals have participated in this study for the past 1 year. To determine allergic response to fragrances, 18 additional fragrances in addition to the Korean standard and a commercial fragrance series were patch-tested in patients with suspecting cosmetic contact dermatitis. Over 80% of the patients were women, and the most common site was the face. Cinnamic alcohol and sandalwood oil (Santalum album L.) showed high frequencies of positive responses. Of the specific fragrances, ebanol, alpha-isomethyl-ionone (methyl ionone-gamma) and Lyral (hydroxyisohexyl 3-cyclohexane carboxdaldehyde) showed high positive responses. We compared the results obtained during this study with those of other studies and concluded that including additional fragrance allergens may be useful for the detection of fragrance allergy.


Phytomedicine. 1999 May;6(2):119-23.
Antiviral activity of sandalwood oil against herpes simplex viruses-1 and -2.
Benencia F, Courreges MC.
Department of Biological Chemistry, Faculty of Sciences, University of Buenos Aires, Argentina.

Sandalwood oil, the essential oil of Santalum album L., was tested for in vitro antiviral activity against Herpes simplex viruses-1 and -2. It was found that the replication of these viruses was inhibited in the presence of the oil. This effect was dose-dependent and more pronounced against HSV-1. A slight diminution of the effect was observed at higher multiplicity of infections. The oil was not virucidal and showed no cytotoxicity at the concentrations tested.