Fatty acid oxidation intracellular mechanism

As a general mechanism, the degradation of PVA starts outside the cells via enzymatic attack on the polymer. The resulting products are a mixture of acetoxy hydroxy and hydroxy fatty acids. Upon intracellular enzymatic deacetylation, hydroxy fatty acids are generated that can be further metabolised via the classical p-oxidation pathway and TCA cycle. 

Figure 1 depicts the sequence of events associated with the cellular uptake of fatty acids and fatty acid oxidation. Fatty acid uptake by the cell takes place by mechanisms not completely understood. Fatty acid analogues such as bromo-palmitate have been reported to inhibit the intracellular accumulation of long-chain fatty acids (Mahadevan and Saver, 1971) suggesting that their transport may depend on specific transport systems. Once inside the cell, the fatty acids may be bound to anionic binding proteins such as described by Arias and others (Ockner t, 1972 ... 

Aspartate is thought to reduce ammonia or increase the TCA cycle flux, and then deliver the potassium and magnesium to the subcellular locations to normalize intracellular concentrations." These conditions could increase fatty acid oxidation, spare glycogen, and reduce ammonia-induced fatigue — and thus increase the time to exhaustion. However, there are no proven action mechanisms. 

Figure 9.2. Mechanisms of aminoglycoside toxicity. This schematic representation summarizes the principles of aminoglycoside toxicity discussed in the text. Treatment with the drugs leads to the formation of reactive oxygen species through a redox-active complex with iron and unsaturated fatty acid or by triggering superoxide production by way of NADPH oxidase. An excess of reactive oxygen species, not balanced by intracellular antioxidant systems, will cause an oxidative imbalance potentially severe enough to initiate cell death pathways. Augmenting cellular defenses by antioxidant therapy can reverse the imbalance and restore homeostasis to protect the cell.

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