Endogenous biochemical pathway

As noted above, ethanol makes use of endogenous biochemical pathways in the liver, and to a lesser extent in the brain and stomach, for its elimination. However, overloading any of the metabolic pathways with alcohol can lead to disequilibrium and redirection of normal metabolic processes. This usually results in the accumulation of harmful by-products. 

Many of the species involved in the endogenous metabolism can undergo a multitude of transformations, have many reaction channels open, and by the same token, can be produced in many reactions. In other words, biochemical pathways represent a multi-dimensional space that has to be explored with novel techniques to appreciate and elucidate the full scope of this dynamic reaction system. 

Many important food aromas originate from biochemical pathways. These pathways comprise microbial reactions, endogenous and exogenous enzymatic action, and plant metabolism. In the past, flavour research concentrated on characterising the important chemicals in foods responsible for their specific aroma. Less information is therefore available on the biogeneration of flavours. At present, however, a renaissance of studies of natural flavours, including their biogeneration can be observed [1]. 

Genetic. The differences between many susceptible and resistant cultivars are the abilities of the latter to appropriately respond quantitatively in time and in space to infection, rather than qualitative differences in biochemical pathways. This type of genetic resistance may be considered a form of an endogenous constitutively sensitized state. Genetic sensitization of a cultivar requires both a source of appropriate germplasm and a method of effective transfer and incorporation of the genetic material into the recipient cultivar. Both requirements cannot always be met. Furthermore, undesirable traits often accompany desired resistance traits. This very important area of plant sensitization, broadly construed, lies beyond the scope of this paper. 

PrPc s protective activity can be titrated against Dpi expression level by alterations in endogenous Prnp copy-number or transgene array copy-number but the highest levels of Dpi can out-compete PrPc-directed protective activity [122, 132, 133]. With generally similar results obtained with APrP expression, Dpi and APrP are assumed to modulate a shared, discrete biochemical pathway [126, 134],... 

These basic compounds are derived from various metabolic pathways, from endogenous tissue sources, from a deranged biochemical pathway involving normal intestinal flora, or from exogenous sources. Their retention in renal failure makes them potential uremic toxins. 

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