Abstract
This study examined the relationship between elevation of blood phenylalanine (Phe) concentrations often observed in trauma or infected patients without hepatic dysfunction and alterations of liver Phe catabolism. Rats underwent pathophysiologically different stresses, either sepsis or scald injury. The catalytic activity of hepatic Phe hydroxylase (PH) in the septic rats, as measured after preincubation with Phe, decreased to 60% of the control values; this in vitro result suggests a reduction of enzyme species activated by its substrate. Phe was degraded in the septic rats to a similar extent to that in controls, when measured by pulse administration of [1- 14C]-Phe. In the scalded rats whose plasma Phe level showed a comparable but transient increase, no significant alterations occurred in Phe catabolism and enzyme activities. The changes in plasma glucagon and catecholamine levels were consistent with those of the enzyme activities involved in Phe and tyrosine (Tyr) catabolism in the stressed groups. These results indicate that inadequate activation of native PH by regulatory mechanisms involving Phe in vivo was also associated with the accumulation of plasma Phe in infected rats during massive mobilization of amino acids from muscles under conditions of enhanced and sustained catabolism.
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