Glutamine synthetase activity and glutamate uptake in hippocampus and frontal cortex in portal hypertensive rats.

AIM: To study glutamine synthetase (GS) activity and glutamate uptake in the hippocampus and frontal cortex (FC) from rats with prehepatic portal vein hypertension. METHODS: Male Wistar rats were divided into sham-operated group and a portal hypertension (PH) group with a regulated stricture of the portal vein. Animals were sacrificed by decapitation 14 d after portal vein stricture. GS activity was determined in the hippocampus and FC. Specific uptake of radiolabeled L-glutamate was studied using synaptosome-enriched fractions that were freshly prepared from both brain areas. RESULTS: We observed that the activity of GS increased in the hippocampus of PH rats, as compared to control animals, and decreased in the FC. A significant decrease in glutamate uptake was found in both brain areas, and was more marked in the hippocampus. The decrease in glutamate uptake might have been caused by a deficient transport function, significantly and persistent increase in this excitatory neurotransmitter activity. CONCLUSION: The presence of moderate ammonia blood levels may add to the toxicity of excitotoxic glutamate in the brain, which causes alterations in brain function. Portal vein stricture that causes portal hypertension modifies the normal function in some brain regions.

Does hepatomegaly alter iron-dependent oxidative effects in human plasma?

A four-fold increase in the iron content of normal subjects was detected in plasma after 5 hours of iron administration. Iron supplementation had a surprisingly erratic effect on four patients with hepatomegaly secondary to heart insufficiency, since the increase in the iron content in the plasma after iron-dextran administration was either within the control range or significantly lower, independently of the initial values. Thiobarbituric acid reactive substances (TBARS) content was 2.5 +/- 0.2 and 4.3 +/- 0.4 microM for control and hepatomegalic subjects, respectively. The TBARS basal level was increased by iron supplementation. The difference between TBARS content in hepatomegalic and control subjects, after 5 hours of iron administration, was increased by 50% as compared to the difference in the basal content of TBARS. alpha-Tocopherol (alpha-T) content in plasma from subjects with hepatomegaly showed a significant decrease (-41%) as compared to control subjects. No significant difference over the basal level of alpha-T was measured after 5 hours of iron administration in any subject. The data presented here suggest that abnormal liver condition affects iron-dependent oxidative stress in plasma. Moreover, alpha-T does not seem to be the main antioxidant to control iron-dependent oxidative stress in plasma.