Planta Med 2010; 76 - P502
DOI: 10.1055/s-0030-1264800

Chemical and biological investigations of Manuka honey

C Bäcker 1, K Wende 1, U Meyer 2, U Lindequist 1
  • 1EMA University of Greifswald, Institute for Pharmacy, F.-L.-Jahnstr. 17, 17489 Greifswald, Germany
  • 2Wala Heilmittel GmbH, Dorfstr. 1, 73087 Bad Boll/Eckwälden, Germany

Manuka honey is mainly obtained from New Zealands endemic Myrtaceae Leptospermum scoparium J.R. et G.Forst. Its increasing clinical use in wound management originates from its antimicrobial effects. Recent work identified 1,2-dicarbonyl methylglyoxal (MGO) as a major antibacterial compound [1] which appears in Manuka honey in high levels and is formed from dihydroxyacetone during storage [2]. In this study several Manuka honeys were investigated for antibacterial activity, MGO content and phenolic compounds. Antibacterial testing was done by agar diffusion assay as well as in the epidermis model ‘cow udder teat’ [3]. Aqueous dilutions of Manuka honeys were able to inhibit growth of multi-resistant strains of Staphylococcus aureus, S. epidermidis, Escherichia coli and Pseudomonas aeruginosa. In these honeys, MGO amounts ranging from 400 to over 1000mg/kg were found. However, no hydrogen peroxide was detected in Manuka honeys. In comparison: a rape honey contained only 3mg/kg MGO but high amounts of hydrogen peroxide and showed inhibiting effects on both Staphylococcus strains. If MGO was added to a non Manuka honey the resulting bacterial inhibition was the same as for a Manuka honey with comparable MGO amount. Detected and quantified phenolic compounds such as phenyllactic acid or methyl syringate did not exert antimicrobial activity on the tested strains. Osmotic effects did not contribute to inhibiting effect. Therefore, it appears likely that observed clinical benefits of Manuka honeys are proportional to its 1,2-dicarbonyl methylglyoxal content.

References: 1. Mavric, E et al. (2008) Mol. Nutr. Food Res. 52:483–489.

2. Adams, CJ et al. (2009) Carbohydrate Research 343:1050–1053.

3. Lukowski, G. et al. (2008) Skin Pharmacol Physiol 21: 98–105.