Response to H2O2-mediated and paraquatmediated
oxidative stress
Husain et al. [45] investigated global metabolic
responses in response to H2O2-mediated and paraquatmediated
oxidative stress in E. histolytica trophozoites. In
this study, they showed that oxidative stress caused
changes in the metabolites involved in glycolysis and
its associated pathways, as evidenced by the accumulation
of glycolytic intermediates upstream of pyruvate,
and reduced ethanol production. They have further
shown that oxidative stress inactivated several key
enzymes of glycolysis and its associated pathways such as
PFOR, phosphoglycerate mutase, and NAD+
-dependent
alcohol dehydrogenase, and resulted in the inhibition of
glycolysis and the redirection of metabolic flux toward
glycerol production, chitin biosynthesis, and the nonoxidative
branch of the pentose phosphate pathway. As
a result of the repression of glycolysis and fermentation,
the levels of nucleoside triphosphates were decreased
upon H2O2 stress, whereas the levels of nucleoside
monophosphates increased, in a manner opposite to the
decrement in their corresponding triphosphate counterparts.
Both paraquat and H2O2-mediated oxidative stress
led to a decrement in L-cysteine and L-cystine, and a
slight increment in cysteine S-sulfinate, in a time-dependent
manner. These findings suggest that L-cysteine
is involved in scavenging of ROS in E. histolytica.