Biomedical Engineering Reference
In-Depth Information
acetic acid inhibits yeasts by acidifying the cytoplasm, which causes physiological
stress or suppresses metabolic activity [
48
]. This especially happens when the pH of
the sourdough is below the pK
a
of acetic acid, 4.76. Non-dissociated acetic acid
decreased the leavening capacity of
C. milleri
when grown together with the hetero-
fermentative
L. brevis
compared to homofermentative species.
Candida milleri
adapts to a wide range of pH (3.5-6.0) and has a good inherent acid tolerance, the
leavening activity is obviously affected by the fermentation process [
7
] .
The leavening power of baker's yeast is strongly influenced by the environmen-
tal conditions of storage [
49
]. Pre-treatment at 30°C with organic acids (malic,
succinic and citric acids), under a wide range of pH values, was assayed before
use [
49
]. The treatment with organic acids variously increased the fermentative
activity. When the pH of baker's yeast, containing citric acid, was raised from 3.5
to 7.5, both the fermentative and maltase activities increased. Glycerol-3-phosphate
dehydrogenase activity and the levels of internal glycerol also increased in the
presence of citrate. On the contrary, baker's yeast containing succinic acid at pH
7.5, showed a decreased viability during storage, despite the maintenance of high
fermentative activity.
6.2.2.3
Osmotic Stress
A
w
is defined as the chemical potential of the free water in solution. Low and interme-
diate values of A
w
limit the growth of yeasts. The A
w
of the cytosol of yeast cells is
lower than that of the surrounding medium, corresponding to a higher osmotic pres-
sure (turgor pressure). This turgor pressure drives water into the cell based on the
concentration gradient. Turgor pressure is counteracted by the limited ability for
expansion of the cell wall and thus determines the shape of the cells [
50
] . The ability
to survive under rapid changes of A
w
is an intrinsic characteristic of the microbial cell.
Survival mechanisms in response to osmotic downshift or upshift allow passive water
loss or uptake. In response to altered osmolarity, yeasts cells develop mechanisms to
adjust to high external osmolarity and to maintain or to recover an inside-directed
driving force for water adaptation. These mechanisms are based on sensing the
osmotic changes [
50
] and accumulating chemically inert osmolytes, for example
glycerol. The high osmolarity glycerol (HOG) signalling system plays a central role
in the osmotic adaptation of yeasts.
Saccharomyces cerevisiae
monitors osmotic
changes through the sensor histidine kinase (
Slu1
) localised at the plasma membrane.
Under optimal environmental conditions,
Slu1
is active and inhibits signalling. Upon
loss of turgor pressure,
Slu1
is inactivated, and this results in the activation of the
nitrogen-activated protein (NAO) kinase cascade and phosphorylation of the NAP
kinase (Hog1). Active Hog1 accumulates in the nucleus, where it affects gene
expression. Two HOG target genes encode for enzymes involved in the synthesis of
glycerol. Because of the presence of three hydroxylic functions that attract water
clouds, glycerol serves as an osmolyte to increase the intra-cellular osmotic pressure
[
50
]. Since glycerol is more reduced than the substrate glucose, its s ynthesis also
affects the redox metabolism. Therefore, the redox metabolism needs to be adjusted
