S-ADENOSYLMETHIONINE DECARBOXYLASE ACTIVITY IS DECREASED IN THE RAT CORTEX AFTER TRAUMATIC BRAIN INJURY

S-Adenosyl-L-methionine decarboxylase (SAMdc) and L-ornithine decarbox ylase (ODC) are major enzymes regulating polyamine synthesis. Followin g ischemia, putrescine content increases as a result of post-traumatic activation of ODC and inhibition of SAMdc. These alterations are thou ght to mediate edema and cell death. The purpose of this study was to quantify SAMdc activity and edema in the brain following controlled co rtical impact injury. Anesthetized adult male rats underwent a right p arietal craniectomy and were subjected to cortical impact injury. Tiss ues were obtained from three bilateral regions: parietal cortex, motor area (CPm); parietal cortex, somatosensory area (CPs); and the pyrifo rm cortex (CPF). SAMdc activity was determined in the postmitochondria l fraction from homogenates of fresh, unfrozen tissues by measuring th e decarboxylation of S-adenosyl-L-[carboxyl-C-14] methionine. Basal SA Mdc activity was determined in unoperated rats, and regional differenc es were noted: Activity was lower in the CPF than in the CPm and CPs. SAMdc activity decreased to the greatest extent in the ipsilateral CPm (impact site) from 1 to 72 h following traumatic brain injury. Signif icant edema was found in the ipsilateral CPm 1, 8, 16, 24, and 48 h af ter injury. Decreased SAMdc activity impairs the conversion of putresc ine to polyamines and may contribute to delayed pathological changes i n the brain after traumatic injury.