Membrane alterations and fluidity changes in cerebral cortex during acute ammonia intoxication.

Acute ammonia intoxication is known to cause alterations in activities of several membrane bound enzymes like Na+ K+ ATPase, acetylcholine esterase and glutamate uptake in brain. The alteration in these membrane associated activities could be a consequence of altered membrane architecture. To probe this, the effect of pathophysiological concentrations of ammonia on lipid composition and fluidity of membranes isolated from cerebral cortex of rats, were investigated in the present study. Administration of acute doses of ammonium acetate caused depletion of membrane sphingomyelin and cholesterol levels thereby reducing cholesterol: phospholipid (C: PL) ratio. Levels of phosphatidylserine increased while those of phosphatidylcholine and phosphatidylethanolamine remain unaltered. Membrane fluidity estimations using 1,6-diphenyl-1,3,5-hexatriene (DPH), 1-[4-(trimethylammonio)phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH) indicated no changes in core and surface membrane fluidity following ammonium acetate administration. Acute ammonia toxicity induced no alteration in bulk fluidity but a decrease in annular fluidity of membranes, as determined using pyrene fluorescence. Elevated levels of malondialdehyde and declined level of total thiols in cerebral cortex membranes of rats under acute ammonia intoxication indicated the existence of oxidative stress.