This paper summarizes the findings obtained during my PhD research over the past three years. The results provide insights which help to understand the enhanced brown-rot decay resistance of acetylated wood with particular emphasis on the role of water. The protection acetylation provides is derived from moisture exclusion within the acetylated cell wall, but the exact mechanism by which water is excluded remained unclear. The first two studies conducted elucidate the moisture exclusion mechanism. It was demonstrated that hydroxyl (OH) accessibility is reduced in acetylated wood both by direct substitution of OH groups with acetyl groups and by hindering access of unmodified OH groups, due to steric hindrance. Characterisation of water in the various void structures of the wood anatomy by means of low-field nuclear magnetic resonance (LFNMR) relaxometry revealed that acetylation causes greater water mobility due to weaken interactions between water molecules and the acetylated pore walls. Both these initial studies also compared the moisture properties of the acetylated samples to samples modified with propionic anhydride. The idea was to demonstrate the importance of steric hindrance relative to direct OH substitution by modifying the wood with a larger anhydride molecule. However, the results indicated the propionylated cell walls were damaged in some way. The last two studies investigate acetylated wood decayed by the brown-rot fungus, Rhondonia placenta. Moisture development and chemical changes were assessed by means of LFNMR, OH accessibility and acetyl content throughout brown-rot degradation and revealed a markedly different degradation pattern for acetylated wood compared to unmodified samples, suggesting de-acetylation occurs within the cell wall prior to decomposition. Lastly, brown-rot decay in acetylated wood was investigated from the fungal perspective by determining how acetylation affects expression of fungal enzymes involved in oxidative chemistry and polysaccharide hydrolysis. Clear trends were difficult to observe for the oxidative genes selected, but genes involved in polysaccharide degradation showed a delayed response for acetylated samples and the most highly acetylated samples had the lowest overall expression levels.

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