Zarros, A. , Theocharis, S., Skandali, N. and Tsakiris, S. (2008) Effects of fulminant hepatic encephalopathy on the adult rat brain antioxidant status and the activities of acetylcholinesterase, (Na(+),K (+))- and Mg (2+)-ATPase: comparison of the enzymes' response to in vitro treatment with ammonia. Metabolic Brain Disease, 23(3), pp. 255-264. (doi: 10.1007/s11011-008-9091-8) (PMID:18665440)
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Abstract
Hepatic encephalopathy can be a life-threatening complication of fulminant hepatic failure. By understanding the pathophysiology involved in the induction of this neuropsychiatric disorder, future therapeutic and/or preventive attempts could be considered. In this study, an attempt has been made in order to shed more light on the mechanisms involved in the effects of thioacetamide (TAA)-induced fulminant hepatic encephalopathy on: (a) the adult rat brain total antioxidant status (TAS) and (b) the activities of acetylcholinesterase (AChE), (Na(+),K(+))-ATPase and Mg(2+)-ATPase. Moreover, in vitro experiments were conducted in order to evaluate the possible role of ammonia (incubated as NH(4)Cl, in a toxic concentration of 3mM) in the observed effects of TAA-induced fulminant hepatic encephalopathy on the examined adult rat brain enzyme activities. Fulminant hepatic encephalopathy caused a significant decrease in TAS (-22%, p < 0.001) and the activity of Na(+),K(+)-ATPase (-26%, p < 0.001), but had non-significant effects on the whole brain AChE and Mg(2+)-ATPase activities. The in vitro experiments (conducted through a 3h incubation with ammonia), showed no significant alterations in any of the examined parameters. Our in vitro and in vivo findings suggest that alterations in AChE and Mg(2+)-ATPase activities are not involved in the pathophysiology of the adult-onset fulminant hepatic encephalopathy, while the observed Na(+),K(+)-ATPase inhibition could be a result of the oxidative stress, neurotransmission deregulation, and/or of the presence of other toxic substances (that appear to act as direct or indirect inhibitors of the enzyme) and not due to the excess accumulation of ammonia in the brain.
| Item Type: | Articles |
|---|---|
| Status: | Published |
| Refereed: | Yes |
| Glasgow Author(s) Enlighten ID: | Zarros, Dr Apostolos |
| Authors: | Zarros, A., Theocharis, S., Skandali, N., and Tsakiris, S. |
| Subjects: | R Medicine > RB Pathology R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry R Medicine > RM Therapeutics. Pharmacology |
| College/School: | College of Medical Veterinary and Life Sciences > School of Cancer Sciences |
| Journal Name: | Metabolic Brain Disease |
| Publisher: | Springer |
| ISSN: | 0885-7490 |
| ISSN (Online): | 1573-7365 |
| Published Online: | 30 July 2008 |
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