- Clinical data 0%
- Efficacy 80%
- Security 70%
- Toxicity 30%
No information was found.
Clear, mobile, colourless to pale yellow liquid.
Major chemical constituents
The chief constituents of rosemary oil are camphor (5–31%), 1,8-cineol (15–55%), -pinene (9–26%), borneol (1.5–5.0%), camphene (2.5 12.0%),-pinene (2.0–9.0%), limonene (1.5–5.0%), verbenone (2.2–11.1%), -caryophyllene (1.8–5.1%) and myrcene (0.9–4.5%).
Medicinal uses Rosmarinus officinalis
Uses supported by clinical data
Uses described in pharmacopoeias and well established documents
Rosmarinus officinalis used orally for the treatment of dyspeptic complaints, and in external applications for supportive management of rheumatic complaints and circulatory disorders. Although one pilot study has indicated that the crude drug may enhance cognition, further data from randomized controlled clinical trials are required before any therapeutic recommendations can be made.
Uses described in traditional medicine
Used as a cholagogue, diaphoretic, digestant, diuretic, emmenagogue, laxative and a tonic. Also used in the management of headache, menstrual disorders, nervous menstrual complaints, tiredness, defective memory, prains and bruises.
The hepatoprotective and antimutagenic effects of the essential oil were compared to those of ethanol leaf extracts in vivo using carbon tetrachloride (CCl4) and cyclophosphamide as the hepatotoxic and mutagenic compounds. The results of the study showed that intragastric administration of 1.5 g/kg body weight (bw) of the essential oil or the leaf extract to rats for 3 weeks protected the animals against CCl4 induced hepatotoxicity.
The results were similar to those obtained using the control compound, silymarin. The results showed amelioration of most of the serum and liver parameters studied, and were confirmed by histopathological examination of the liver tissue. The hepatoprotectant activity of essential oil was not as great as that of the leaf extract. However, intragastric pretreatment of mice for 7 days with the essential oil (1.1 mg/g bw), reduced cyclophosphamide-induced mitodepression in bone marrow cells.
The essential oil weakly inhibited the growth of Acinetobacter iwoffi, Bacillus subtilis, Erwinia carotovora, Shigella flexneri, Staphylococcus aureus, Streptococcus pyogenes and Yersinia enterocolitica when added undiluted or in a 1:1 dilution to the agar medium.
The essential oil inhibited electrically stimulated muscular contractions in isolated guinea-pig ileum, but the effect of the lowest spasmolytic dose is preceded by an initial increase in the electrically stimulated contractile response. Pinene, which had weak spasmogenic properties, was considered to be the active constituent. In guinea-pig ileum, addition of the essential oil to the bath medium inhibited acetyl choline-induced contractions, with a median inhibitory concentration (IC50) of 465 nl/ml of the oil and 41 nl/ml of 1,8-cineole.
The essential oil, and its individual constituents, camphor, borneol, thymol, -pinene, -pinene and bornyl acetate, inhibited bone resorption when added to the food of rats. The monoterpenes borneol, thymol and camphor, were directly inhibitory in the osteoclast resorption pit assay.
Within 30 minutes, borneol inhibited the formation of actin rings, a characteristic of resorbing osteoclasts indicating cell polarization. Both the in vitro and the in vivo effects of borneol were reversible.
Modulation of cytochrome P450 isozymes and detoxification enzymes was compared after oral administration of the dried leaves, a dried dichloromethane leaf extract or the essential oil to rats. The animals received the leaves, extracts or essential oil in their rations at a concentration of 0.5% (w/w) for 2 weeks. The effects of the treatments were evaluated in assays for cytochrome P450 isozymes 1A, 2B, 2E1, glutathione S-transferase, nicotinamide adenine dinucleotide phosphate (NAD(P)H), quinone reductase and uridine diphosphate (UDP)-glucuronosyltransferase activities and on protein levels (immunoblot analyses). The results demonstrated that the essential oil selectively induced cytochrome P450, particularly isozyme 2B. The leaf extract enhanced both cytochrome P450 and detoxification enzymes. A dichloromethane extract of the leaves acted as a monofunctional inducer, inducing glutathione S-transferase, quinone reductase and UDP-glucuronosyltransferase, in particular UDP-glucuronosyltransferase 1A6.
The embryotoxic effects of d-camphor were investigated in rats and rabbits after intragastric administration for the treatment of hypotonic circulatory dysregulations. No evidence of teratogenicity was observed when d-camphor was administered orally to pregnant rats during the fetal period of organogenesis, at doses up to 1 g/kg bw per day, and to pregnant rabbits at doses up to 681 mg/kg bw per day. For rats, the no-observedeffect level for the fetal organism was above 1 mg/kg bw, and for rabbits, above 681 mg/kg bw. In rat dams a dose dependent reduction in food intake and salivation was noted at doses of 464 mg/kg bw and higher. The high dose of 1 mg/kg bw per day resulted in pronounced signs of toxicity such as clonic convulsion, pilo-erection, reduced motility and body weight gain. In rabbit dams, intragastric administration of a high dose (681 mg/kg bw per day) resulted in reduced body weight gain and food consumption. No increased incidence of variations, retardations or malformations was observed in any of the offspring at any of the doses, not even at the highest dose tested (rat: 1000 mg/kg bw per day; rabbit: 681 mg/kg bw per day). The daily maximum dose of camphor for human therapeutic use is approximately 1.43 mg/kg bw. Hence, under the present test conditions the therapeutic ratio is above 450 for the end point of embryotoxicity, reflecting a wide margin of safety. Since d-camphor is only one of the chemical constituents of the essential oil, the relevance of these data to the toxicology of the essential oil needs to be investigated.
A clinical study to assess the olfactory impact of the essential oils of lavender (Lavandula angustifolia) and rosemary (Rosmarinus officinalis) on cognitive performance and mood in healthy volunteers was performed. One hundred and forty-four participants were randomly assigned to one of three independent groups. Each of the subjects was asked to take the Cognitive Drug Research (CDR) computerized cognitive assessment battery in a cubicle containing one of the two odours or no odour (control). Visual analogue mood questionnaires were completed before exposure to the odour and after completion of the test battery. The participants were misled as to the genuine aim of the study until the completion of testing to prevent expectancy effects from possibly influencing the data. The outcome variables from the nine tasks that constitute the CDR core battery feed into six factors that represent different aspects of cognitive functioning. Analysis of performance revealed that lavender produced a significant decrement in performance of working memory, and impaired reaction times for both memory and attention-based tasks compared to the performance of the controls. In contrast, rosemary produced a significant enhancement of performance for overall quality of memory and secondary memory factors, but also impaired speed of memory compared to controls. With regard to mood, comparisons of the change in ratings from baseline to post-test revealed that following the completion of the cognitive assessment battery, both the control group and the group exposed to lavender were significantly less alert than the subjects exposed to rosemary; however, subjects in the control group were significantly less content than subjects who received the rosemary and lavender treatments.
Frontal electroencephalogram asymmetry shifting from baseline was examined in adults and infants exposed to lavender and rosemary oils by re-analysing previously published data from two studies. The results from 39 adults revealed significant electroencephalogram shifting in the lavender-treated group, with greater relative left frontal electroencephalogram activation (associated with greater approach behaviour and less depressed affect). The participants in the two groups exposed to the two aromas were further grouped by those with greater baseline, relative to left frontal electroencephalogram activation versus those with a greater baseline relative to right frontal activation. Collapsing across aroma groups, those with greater baseline, relative to right frontal activation, shifted left during exposure to the aroma. Those with greater baseline relative to left frontal activation did not change. In the group subjected to the rosemary aroma, those with greater baseline relative to right frontal electroencephalogram activation shifted left during exposure to the aroma, while those with greater baselines relative to left frontal electroencephalogram activation shifted right. The second study, involving 27 full-term newborns revealed no significant shifts in asymmetry in response to either aroma. However, when the aroma groups were collapsed, the right frontal electroencephalogram group exhibited significant shifting relative to left frontal electroencephalogram activation. This finding was similar to the findings in adults, suggesting that both lavender and rosemary may induce left frontal electroencephalogram shifting in adults and infants who show greater baselines relative to right frontal electroencephalogram activation.
The effects of lavender and rosemary oils on electroencephalogram activity, alertness and mood were assessed in 40 adults given 3 minutes of aromatherapy. Participants were also given simple mathematical computations to do before and after the therapy. The lavender-treated group showed increased beta power, suggesting increased drowsiness; they also had less depressed mood and reported feeling more relaxed and performed the mathematical computations faster and more accurately following aromatherapy. The rosemary-treated group, on the other hand, showed decreased frontal alpha and beta power, suggesting increased alertness. They also had lower anxiety scores, reported feeling more relaxed and alert and they were only faster, not more accurate, at completing the mathematical computations after the aromatherapy session.
Following oral use gastrointestinal complaints and hypersensitivity reactions may occur rarely. Inhalation can occasionally cause irritation and very rarely laryngospasm.
External use may worsen bronchospasm. Rarely hypersensitivity reactions of the skin may occur. Photoaggravated allergic contact dermatitis and cheilitis have been reported.
Aetheroleum Rosmarini is contraindicated in cases of hypersensitivity or allergy to the plant material. It should not be used in patients suffering from bronchial asthma or bronchitis or on damaged skin, such as in cases of burns, lesions or skin rashes.
Due to its irritant properties, the essential oil should not be used on the face or mucosa, and contact with the eyes should be avoided. After application of the essential oil, wash hands to avoid accidental contact with the face and eyes. As with all essential oils, do not exceed the recommended dose. If there is persistence or worsening of rheumatic symptoms, e.g. in cases of redness, swelling or over-heating of joints, patients should seek advice from a health care practitioner.
References 1. European Pharmacopoeia, 5th ed, Strasbourg, Directorate for the Quality of Medicines of the Council of Europe (EDQM), 2005. 2. Bedevian AK. Illustrated polyglottic dictionary of plant names. Cairo, Medbouly Library, 1994. 3. Farnsworth NR, ed. NAPRALERT database. Chicago, University of Illinois at Chicago, IL (an online database available directly through the University of Illinois at Chicago or through the Scientific and Technical Network [STN] of Chemical Abstracts Services), 30 June 2005. 4. Youngken HW. Textbook of pharmacognosy, 6th ed. Philadelphia, PA, Blakiston, 1950. 5. Bruneton J. Pharmacognosy, phytochemistry, medicinal plants. Paris, Lavoisier, 1995. 6. Perry LM, Metzger J. Medicinal plants of east and southeast Asia: Attributed properties and uses. Cambridge, MA, MIT Press, 1980. 7. Wichtl M, eds. Herbal drugs and phytopharmaceuticals, English ed. (transl Bisset NR). Boca Raton, FL, Medpharm, 1994. 8. WHO guidelines for assessing quality of herbal medicines with reference to contaminants and residues. Geneva, World Health Organization, 2007. 9. Guidelines for predicting dietary intake of pesticide residues, 2nd rev. ed. Geneva, World Health Organization, 1997 (WHO/FSF/FOS/97.7). 10. Salido S et al. Chemical composition and seasonal variations of rosemary oil from southern Spain. Journal of Essential Oil Research, 2003, 15:10–14. 11. Domokos J et al. Essential oil of rosemary (Rosmarinus officinalis L.) of Hungarian origin. Journal of Essential Oil Research, 1997, 9:41–45. 12. Blumenthal M, Goldberg A, Brinckmann J, eds. Herbal medicine: Expanded Commission E monographs. Austin, TX, American Botanical Council, 2000. 13. Moss M et al. Aromas of rosemary and lavender essential oils differentially affect cognition and mood in healthy adults. International Journal of Neuroscience, 2003, 113:15–38. 14. Hagers Handbuch der Drogen (CD ROM). Heidelberg, Springer Verlag, 2003 [in German]. 15. Fahim FA et al. Allied studies on the effect of Rosmarinus officinalis L. on experimental hepatotoxicity and mutagenesis. International Journal of Food Sciences and Nutrition, 1999, 50:413–427. 16. Mangena T, Muyima NYO. Comparative evaluation of the antimicrobial activities of essential oils of Artemisia afra, Pteronia incana and Rosmarinus officinalis on selected bacteria and yeast strains. Letters in Applied Microbiology, 1999, 28:291–296. 17. Lis-Balchin M et al. Comparison of the pharmacological and antimicrobial actions of commercial plant essential oils. Journal of Herbs, Spices and Medicinal Plants, 1996, 4:69–82. 18. Hof S, Ammon PT. Negative inotropic action of rosemary oil, 1,8-cineol, and bornyl acetate. Planta Medica, 1989, 55:106–107. 19. Mühlbauer RC et al. Common herbs, essential oils, and monoterpenes potently modulate bone metabolism. Bone, 2003, 32:372–380. 20. Debersac P et al. Induction of cytochrome P450 and/or detoxication enzymes by various extracts of rosemary: description of specific patterns. Food and Chemical Toxicology, 2001, 39:907–918. 21. Leuschner J. Reproductive toxicity studies of D-camphor in rats and rabbits. Arzneimittelforschung, 1997, 47:124–128. 22. Sanders C et al. EEG asymmetry responses to lavender and rosemary aromas in adults and infants. International Journal of Neuroscience, 2002, 112:1305–1320. 23. Diego MA et al. Aromatherapy positively affects mood, EEG patterns of alertness and math computations. International Journal of Neuroscience, 1998, 96:217–224. 24. Blumenthal M et al., eds. The complete German Commission E monographs: Therapeutic guide to herbal medicines. Austin, TX, American Botanical Council, 1998. 25. Armisén M, Rodríguez V, Vidal C. Photoaggravated allergic contact dermatitis due to Rosmarinus officinalis cross-reactive with Thymus vulgaris. Contact Dermatitis, 2003, 48:52–53. 26. Fernandez L et al. Allergic contact dermatitis from rosemary (Rosmarinus officinalis L.). Contact Dermatitis, 1997, 37:248–249. 27. Guin JD. Rosemary cheilitis: one to remember. Contact Dermatitis, 2001, 45:63. 28. Reynolds JEF ed. Martindale: The extra pharmacopoeia, 13th ed. London, Pharmaceutical Press, 199 .