Rosemary has Anti-Carcinogenic Properties
Cindy L. A. Jones, Ph.D.
Published in Nutrition Science News, 1998.
The same rosemary (Rosmarinus officinalis L.) used by the Romans to improve memory is also under investigation as a potent anticancer therapy. These anticancer properties are probably associated with rosemary's antioxidant property, which is more effective than typical food additives such as BHT and BHA (tert-butyl-4-hydroxytoluene and tert-butyl-4-hydroxyanisol).1 Additionally, rosemary has anti-inflammatory activity, an activity that researchers are now finding often correlates with anticancer activity. This was demonstrated in an experiment that showed that carnosol, a component of rosemary, was able to reduce the amount of nitric oxide production in mice cells.2 Nitric oxide, which is released during inflammation, is a free radical that can damage DNA. Because cancer is often associated with states of chronic inflammation, some physicians recommend anti-inflammatory drugs such as aspirin and sulindac for the prevention of colon cancer. Active constituents of rosemary include carnosol, carnosic acid, ursolic acid, betulinic acid, rosmaridiphenol and rosmanol, most of which are present in the essential oil fraction.
Several studies have indicated that rosemary can prevent the binding of cancer causing chemicals (carcinogens) to cellular DNA. Binding of a carcinogen to DNA, leads to mutations in the DNA, and is an early step in the development of cancer. In one report, researchers compared the effects of whole rosemary extracts with the purified rosemary components, carnosol and ursolic acid, on breast cancer in rats. They found that whole rosemary extract given in the diet prevented the binding of the known carcinogen, 7,12-dimethylbenz[a]anthracene, (otherwise known as DMBA) to DNA in breast cells.4 Carnosol was also able to prevent binding, but to a lesser extent, whereas ursolic acid had little effect. Similar results were seen in the actual formation of breast tumors in these rats with both rosemary and carnosol decreasing tumor formation by 37%, while the groups receiving ursolic acid showed little reduction in the amount of tumors formed. These results are similar to previous results showing that rosemary extracts can decrease skin tumors in mice caused by certain carcinogens.
These results were confirmed by a later study also showing that rosemary could prevent breast cancer caused by administration of DMBA. Rats fed 1% rosemary in their diet for two weeks prior to the administration of DMBA had 76% less of the carcinogen bound to DNA compared to rats fed a control diet.5 This effect was also present when excess fat was added to the diet which increased the amount of carcinogen bound to DNA. High fat diets are known to be associated with a higher risk for breast cancer. Significant effects were also seen with only 0.5% rosemary in the diet. Similar results have been found using human bronchial cells and liver cells. In these experiments the DNA binding of the carcinogens aflatoxin and benzo(a)pyrene were also shown to be inhibited by rosemary extract. This indicates that the protective effect of rosemary is not just associated with DMBA and probably goes beyond just breast cancer.
Besides acting by preventing binding of carcinogens to the DNA, rosemary can also affect the metabolism of some carcinogens in a way that decreases their toxicity. Enzymes found in the liver, known as P450, glutathione S-transferases (GSH), and quinone reductases (QR) can affect the toxicity of some chemicals. Although the main role of the liver P450 enzymes is to detoxify compounds, the aromatic hydrocarbons such as DMBA are actually activated into much more potent carcinogens. Thus, DMBA, benzo[a]pyrene and aflatoxin are considered pro-carcinogens rather than direct acting carcinogens. The second group of enzymes, GSH and QR, act by detoxifying these active carcinogenic metabolites and thus protect against cancer. When rats were fed diets containing whole rosemary extract, the enzymes GST and QR were increased significantly compared to controls. 6 Animals fed carnosol in their diet did not exhibit an increase in these liver enzymes. These experiments show that rosemary has a protective effect by increasing the amount of enzymes that the liver uses for detoxification of cancer causing chemicals, and that the effect of whole rosemary is greater than that of its component, carnosol.
Similar experiments using human bronchial cells and liver cells in tissue culture have shown that rosemary extract, carnosol and carnosic acid were all able to reduce the levels of P450 enzymes after treatment with benzo(a)pyrene or aflatoxin B1.7 In bronchial cells, rosemary extract, carnosol and carnosic acid were able stimulate the QR and GST enzymes after treatment with benzo(a)pyrene. Therefore, by decreasing the enzymes that can convert procarcinogens to a more potent carcinogen and increasing enzymes that can inactivate carcinogens, rosemary components have a protective effect on cancers.
In summary, two separate mechanisms have been identified to explain the anti-carcinogenic properties of rosemary; blocking carcinogen binding to DNA, and modifying metabolic enzymes to decrease the toxicity of a carcinogen. Although the anticancer properties of rosemary have been clearly demonstrated in animal studies, these have not yet led to human trials. Since whole rosemary seems to be as beneficial or more beneficial than isolated components that have been examined to date, the addition of rosemary to one=s diet may have more benefit than just as a food flavoring or preservative.
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2. Offord, E.A., Mace, K., et al., Rosemary components inhibit benzo(a)pyrene-induced genotoxicity in human bronchial cells. Carcinogenesis 16:2057-2062.
3. Ho, C-H, Ferraro, T., et al, A Phytochemicals in tea and rosemary and their cancer-preventive properties, In Ho, C-T, Osawa, T., et al ed., Food Phytochemicals for Cancer Prevention II:2-19. Washington, DC: American Chemical Society, 1994.
4. Amagase, H., Sakamoto, K., et al, Dietary rosemary suppresses 7,12-dimethylbenz(a)anthracene binding to rat mammary cell DNA. J. Nutr. 126:1475-1480, 1996.
5. Singletary, K., MacDonald, C., and Wallig, M. Inhibition by rosemary and carnosol of 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat mammary tumorigenesis and in vivo DMBA-DNA adduct formation. Cancer Letters 104:43-48, 1996.
6. Singletary, K.W., Rosemary extract and carnosol stimulate rat liver glutathione-S-transferase and quinone reductase activities. Cancer Letters 100:139-144, 1996.
7. Offord, E. A., Mace, K. Et al. Mechanisms involved in the chemoprotective effects of rosemary extract studied in human liver and bronchial cells. Cancer Letters 114:275-281, 1997.