hyperammonemia/phosphatase

In the present work, we studied the effects of toxic ammonia levels on the cytoskeleton of neural cells, with emphasis in the homeostasis of the phosphorylating system associated with the intermediate filaments (IFs). We used in vivo and in vitro models of acute hyperammonemia in 10- and 21-day-old

An investigation of several neurochemical consequences of exposure of the rat to 3/4 of the estimated single injection LD50 quantity of trimethyltin chloride (TMT) indicated that a significant elevation in the levels of glutamine (Gln) and 5-hydroxyindole acetic acid (5-HIAA) occurred at post-dosing

Increased skeletal muscle ammonia uptake with loss of muscle mass adversely affects clinical outcomes in cirrhosis. Hyperammonemia causes reduced protein synthesis and sarcopenia but the cellular responses to impaired proteostasis and molecular mechanism of l-leucine induced adaptation to ammonia

Metabolic features of parenteral feeding with conventional amino acid solutions were examined in 47 patients over a long period. 30 patients were kept alive by artificial respiration. The metabolic parameters ammonium, blood urea nitrogen, GOT, alkaline phosphatase were carried out, in 6 patients

Triplicate groups of juvenile yellow catfish (1.98 ± 0.01 g) were fed diets supplemented with 0% and 1% alanyl-glutamine dipeptide (AGD) for 56 days under three ammonia concentrations (0.01, 5.70 and 11.40 mg L-1 total ammonia nitrogen). The results showed that ammonia poisoning could induce growth

The present study was aimed to investigate the antioxidant potential of Momordica charantia fruit extract (MCE) in ammonium chloride-induced (AC) hyperammonemic rats. Experimental hyperammonemia was induced in adult male Wistar rats (180-200 g) by intraperitoneal injections of ammonium chloride (100

Changes in oxidative metabolism were studied in hepatopancreas, muscle, and hemolymph of the edible crab Scylla serrata, exposed to a sublethal concentration (2.5 ppm) of cadmium chloride. A significant decrease in glycogen, total carbohydrates, and pyruvate and an increase in lactate levels in

An increased risk of valproate-induced toxicity has been reported in children, particularly in those younger than 2 years of age. Significant variations in valproate pharmacokinetics and shifts in the metabolic pathways towards CYP2C9-dependent metabolism seem to play some role in the age-related

The use of intestinal segments in the urinary tract can cause metabolic changes that depend on the intestinal segment utilized. The severity of these changes basically depends on the area of the intestinal mucosa in contact with urine, the duration of exposure to urine and renal function. The length

Hyperammonemia occurring following acute liver failure is the primary cause of hepatic encephalopathy. In the brain, ammonium is catabolised by glutamine synthetase expressed exclusively in astroglia; ammonium overload impairs astroglial homeostatic systems. Previously, we had reported that chronic

The morphology of the intestinal wall and the activity of certain mucosal enzyme systems in the course of neomycin treatment were evaluated. Conventional and, to study the role of the bacterial flora, germ-free rats received 500 mg neomycin daily by stomach tube. Rats were sacrificed after seven

A 53-year-old male patient was admitted to our hospital with abdominal pain in the right upper quadrant. There was no change in laboratory investigations other than a slight increase in serum levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), and gamma glutamyl transferase (GGT).

We present a case of a 75-year-old man with end-stage renal disease caused by immunoglobulin A nephropathy who developed hepatic encephalopathy 15 months after starting continuous ambulatory peritoneal dialysis therapy. Liver test results were normal except for hyperammonemia (ammonia, 317 microg/dL

C/EBPalpha is highly expressed in liver and regulates many genes that are preferentially expressed in liver. Because C/EBPalpha-null mice die soon after birth, it is impossible to analyze the function of C/EBPalpha in the adult with this model. To address the function of C/EBPalpha in adult

OBJECTIVE Valproic acid (VPA)-induced adverse effects, which are sometimes serious in children, can be associated with alterations in VPA metabolism. VPA-evoked toxicity is attributed to both the parent compound and its unsaturated metabolites, primarily formed by the cytochrome P450 (CYP)2C9