340 M. Ugliano and P.A. Henschke
uration of wine with flor yeast (Wurz et al. 1988). Gamma lactones, including-
butyrolactone, are quantitatively the most important. The sensory role of lactones
is not clear, although it has been suggested that these compounds contribute to the
aroma characteristics of Sherry wines. The role played by yeast in the formation of
other aliphatic-lactones (C 8 ;C 12 ) in wine (Ferreira et al. 2004) is not clear.
8D.4.4.2 Metabolism
Yeast-derived saturated short-medium chain and branched-chain aldehydes are
formed from sugar metabolism, fatty acid metabolism and branched-chain amino
acid metabolism (Fig 8D.7). In addition, hexanal, as well as hexenal isomers, are
formed during the pre-fermentative stages of winemaking by the sequential action
of grape lipoxygenase and hydroperoxide cleavage enzyme on linoleic and linolenic
acid, respectively (Crouzet 1986).
The major carbonyl, acetaldehyde, is formed as an intermediate in ethanol pro-
duction. In fermenting yeast, pyruvic acid is principally decarboxylated to acetalde-
hyde by pyruvate decarboxylase (Pdcp), which is encoded by the genesPDC1,5,6
(Flikweert et al. 1996). Acetaldehyde accumulation during fermentation is affected
by its rate of formation and the various reactions that consume it, with lowest levels
being found at end of fermentation. These reactions are summarised in Fig 8D.7.
The rate of acetaldehyde formation can be adversely affected by a deficiency of thi-
amine, a cofactor of Pdcp; thiamine depletion mainly results from wild yeast growth
during must processing (Bataillon et al. 1996). The main pathway for acetaldehyde
consumption is reduction to ethanol by alcohol dehydrogenase, which is encoded by
ADH1. This dehydrogenase reaction, which maintains redox balance in the cell by
oxidising NADH to NAD+, is essential for sugar metabolism (Flikweert et al. 1996).
Acetaldehyde is also oxidised to acetic acid by aldehyde dehydrogenase, encoded by
ALD4-6, as precursor for lipid biosynthesis and for regenerating NAD(P)H required
for biosynthetic and redox balancing reactions during cell growth.
Diacetyl, and its reduction products, acetoin and 2,3-butanediol, are also derived
from acetaldehyde (Fig 8D.7), providing additional NADH oxidation steps. Diacetyl,
which is formed by the decarboxylation of -acetolactate, is regulated by valine
and threonine availability (Dufour 1989). When assimilable nitrogen is low, valine
synthesis is activated. This leads to the formation of -acetolactate, which can be
then transformed into diacetyl via spontaneous oxidative decarboxylation. Because
valine uptake is suppressed by threonine, sufficient nitrogen availability represses
the formation of diacetyl. Moreover, the final concentration of diacetyl is deter-
mined by its possible stepwise reduction to acetoin and 2,3-butanediol, both steps
being dependent on NADH availability. Branched-chain aldehydes are formed via
the Ehrlich pathway (Fig 8D.7) from precursors formed by combination of acetalde-
hyde with pyruvic acid and -ketobutyrate (Fig 8D.7).
Finally, acetaldehyde can become bound to SO 2 , derived from the sulfate reduc-
tion pathway or added by winemakers as an antioxidant and antimicrobial com-
pound prior to fermentation (refer to Sect. 8D.4.5). Prefermentation additions of
SO 2 increase the concentration of the acetaldehyde-hydroxysulfonate adduct and