DGAT2-knockdown mice exhibit increased fatty acid (FA) oxidation through CYP2E1, leading to increased oxidative stress, inflammation, and tissue damage.
Instead, the delayed glycolysis activation reflects a long-term metabolic adaptation of neurons by excitotoxic insult; however, such an adaptation concurs with concomitant decrease in the rate of glucose oxidation through the PPP, hence, triggering oxidative stress and neurotoxicity.
These steps include conversion of glucose to pyruvate, subsequent oxidation through the tricarboxylic acid cycle to CO2, and oxidative phosphorylation, in which atmospheric O2 is used to produce H2O.
Expression and activation of either PPAR γ 1 or 2 reduced de novo lipogenesis and oxidative stress and mediated a switch from glucose to fatty acid oxidation through regulation of genes including Pdk4, Fabp4, Lpl, Acot1 and Cd36.
Instead of increasing the expression levels of oxidative TDORs, it may also be possible to increase their activity for substrate oxidation through enhanced reoxidation during catalysis.
Red cells metabolize glucose by breaking it down to lactic acid either via an anaerobic (oxygenless) pathway or by oxidation through a pathway called the pentose phosphate pathway.
It has been shown that ethylene inhibits ethane oxidation through depletion of lattice oxygen (O*).
Sulfide oxidation pathways within shallow-sea hydrothermal vents include chemical oxidation and biologically mediated oxidation through chemolithotrophy and phototrophy.
This may be due to direct or indirect oxidation through hydroxyl radicals generated by nanocatalysis (Fig. 1).
However, Blastocatella and Nitrospira were also increased, suggesting an increase in ammonia oxidation (Alma et al. 2016) and nitrite oxidation through the nitrification process (Wu et al. 2016).
