Tea tree oil

The components of tea tree oil, particularly terpinen-4-ol and α-terpineol, mediate antimicrobial actions by disrupting the structural and functional integrity of bacterial membrane. Hydrocarbons are capable of partitioning into the cell and cytoplasmic membrane of microorganisms and disrupt their vital functions, which may result in leakage of ions such as potassium, and the inhibition of respiration. Eventually, cell lysis may occur due to weakening of the cell wall, and loss of turgor pressure and subsequent rupture of the cytoplasmic membrane. The loss of 260-nm-absorbing material may be indicative of a damaged cytoplasmic membrane and loss of nucleic acids. In E. coli, perturbed potassium homeostasis, glucose-dependent respiration, cell morphology, and ability to exclude propidium iodide was observed.

Tea tree oil also mediates its antifungal actions in a similar way, where it alters the permeability of Candida albicans and inhibits its respiration in a dose-dependent manner. Plasma and mitochondrial membranes of fungal species are also thought to be negatively affected by inhibition of glucose-induced medium acidification by tea tree oil, which involves inhibition of membrane ATPase responsible for the expulsion of protons. Tea tree oil also inhibits the formation of germ tubes, or mycelial conversion, in C. albicans, thereby disrupting cell morphogenesis. Water-soluble fraction of TTO, terpinen-4-ol, and α-terpineol, can inhibit the lipopolysaccharide-induced production of the inflammatory mediators such as TNF-α, IL-1β and IL-10 by human peripheral monocytes by approximately 50% and that of prostaglandin E2 by about 30% after 40 h. These components of tea tree oil may also suppress superoxide production by agonist-stimulated monocytes and decrease the production of reactive oxygen species by both stimulated neutrophils and monocytes.