Bioconversion of lignocellulose: inhibitors and detoxification

Abstract

Bioconversion of lignocellulose by microbial fermentation is typically preceded by an acidic thermochemical pretreatment step designed to facilitate enzymatic hydrolysis of cellulose. Substances formed during the pretreatment of the lignocellulosic feedstock inhibit enzymatic hydrolysis as well as microbial fermentation steps. This review focuses on inhibitors from lignocellulosic feedstocks and how conditioning of slurries and hydrolysates can be used to alleviate inhibition problems. Novel developments in the area include chemical in-situ detoxification by using reducing agents, and methods that improve the performance of both enzymatic and microbial biocatalysts.

Figure 1

Formation of inhibitors. Scheme indicating main routes of formation of inhibitors. Furan aldehydes and aliphatic acids are carbohydrate degradation products, while lignin is the main source of phenolic compounds, as indicated by guaiacyl (4-hydroxy-3-methoxyphenyl) and syringyl (4-hydroxy-3,5-dimethoxyphenyl) moieties found in many phenolics. While the contents of furan aldehydes and aliphatic acids are relatively easy to determine, the quantification and identification of phenolic compounds remain challenging. The insert shows the variety of peaks representing phenolic compounds found in a hydrolysate of Norwegian spruce, as indicated by analysis using liquid chromatography-mass spectrometry (LC-MS).

Figure 2

Effects of genetic engineering for hyperresistance and chemical detoxification through alkaline treatment. Ethanol production by S. cerevisiae (control transformant and transformant overexpressing Yap1 [95]): in spruce hydrolysate medium (black triangle, Yap1 transformant; black square, Control transformant), in alkali-detoxified spruce hydrolysate (green triangle, Yap1 transformant; green square, Control transformant), and in inhibitor-free medium (blue triangle, Yap1 transformant; blue square, Control transformant).

Figure 3

Monosaccharide degradation in alkali. Initial phase of degradation of glucose during alkaline treatment. Calcium ions stabilize the reactive enol intermediate, which in turn is degraded to HMF, and further to formic and levulinic acids.