scholarly journals Effects of simvastatin and fenofibrate on butyrylcholinesterase activity in the brain, plasma, and liver of normolipidemic and hyperlipidemic rats

2019 ◽  
Vol 70 (1) ◽  
pp. 30-35
Author(s):  
Antonija Vukšić ◽  
Jasna Lovrić ◽  
Paško Konjevoda ◽  
Nina Blažević ◽  
Marinko Bilušić ◽  
...  

AbstractThe study objective was to test the hypothesis that simvastatin and fenofibrate should cause an increase in butyrylcholinesterase (BuChE) activity not only in the plasma and liver but also in the brain of normolipidemic and hyperlipidemic rats. Catalytic enzyme activity was measured using acetylthiocholine (ATCh) and butyrylthiocholine (BTCh) as substrates. Normolipidemic and hyperlipidemic rats were divided in four groups receiving 50 mg/kg of simvastatin a day or 30 mg/kg of fenofibrate a day for three weeks and three control groups receiving saline. Simvastatin and fenofibrate caused an increase in brain BuChE activity in both normo- and hyperlipidemic rats regardless of the substrate. The increase with BTCh as substrate was significant and practically the same in normolipidemic and hyperlipidemic rats after simvastatin treatment (14–17% vs controls). Simvastatin and fenofibrate also increased liver and plasma BuChE activity in both normolipidemic and hyperlipidemic rats regardless of the substrate. In most cases the increase was significant. Considering the important role of BuChE in cholinergic transmission as well as its pharmacological function, it is necessary to continue investigations of the effects of lipid-lowering drugs on BuChE activity.

2013 ◽  
Vol 41 (6) ◽  
pp. 1551-1556 ◽  
Author(s):  
Silvia Sacchi

Over the years, accumulating evidence has indicated that D-serine represents the main endogenous ligand of NMDA (N-methyl-D-aspartate) receptors. In the brain, the concentration of D-serine stored in cells is defined by the activity of two enzymes: serine racemase (responsible for both the synthesis and degradation) and D-amino acid oxidase (which catalyses D-serine degradation). The present review is focused on human D-amino acid oxidase, discussing the mechanisms involved in modulating enzyme activity and stability, with the aim to substantiate the pivotal role of D-amino acid oxidase in brain D-serine metabolism.


2005 ◽  
Vol 78 (5) ◽  
pp. 551-558 ◽  
Author(s):  
M FIEGENBAUM ◽  
F DASILVEIRA ◽  
C VANDERSAND ◽  
L VANDERSAND ◽  
M FERREIRA ◽  
...  

Diagnostics ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 2310
Author(s):  
Achmad Adhipatria Perayabangsa Kartamihardja ◽  
Winda Ariyani ◽  
Hirofumi Hanaoka ◽  
Ayako Taketomi-Takahashi ◽  
Noriyuki Koibuchi ◽  
...  

Gadolinium deposition in the brain has been observed in areas rich in iron, such as the dentate nucleus of the cerebellum. We investigated the role of Fe2+ in the effect of gadolinium-based contrast agents (GBCA) on thyroid hormone-mediated Purkinje cell dendritogenesis in a cerebellar primary culture. The study comprises the control group, Fe2+ group, GBCA groups (gadopentetate group or gadobutrol group), and GBCA+Fe2+ groups. Immunocytochemistry was performed with an anti-calbindin-28K (anti-CaBP28k) antibody, and the nucleus was stained with 4′,6-diamidino-2-phenylindole (DAPI). The number of Purkinje cells and their arborization were evaluated with an analysis of variance with a post-hoc test. The number of Purkinje cells was similar to the control groups among all treated groups. There were no significant differences in dendrite arborization between the Fe2+ group and the control groups. The dendrite arborization was augmented in the gadopentetate and the gadobutrol groups when compared to the control group (p < 0.01, respectively). Fe2+ significantly increased the effect of gadopentetate on dendrite arborization (p < 0.01) but did not increase the effect of gadobutrol. These findings suggested that the chelate thermodynamic stability and Fe2+ may play important roles in attenuating the effect of GBCAs on the thyroid hormone-mediated dendritogenesis of Purkinje cells in in vitro settings.


2011 ◽  
Vol 26 (S2) ◽  
pp. 2124-2124
Author(s):  
J. Horacek ◽  
J. Flegr ◽  
D. Holub ◽  
J. Tintera ◽  
T. Novak ◽  
...  

BackgroundThe role of coccidian protozoa Toxoplasma gondii represents one of the most enigmatic and unexplained questions in the field of pathophysiology of schizophrenia. To address the role of latent Toxoplasma gondii (T. gondii) infection in pathophysiology of schizophrenia we studied the influence of latent toxoplasmosis on brain morphology in schizophrenia.MethodsMagnetic resonance imaging was analyzed by an optimized voxel-based-morphometry (VBM) in 44 schizophrenic patients (12 T. gondii positive) and 56 controls (13 T. gondii positive). The full factorial model of analysis of variance with diagnosis and seropositivity for latent toxoplasmosis as factors was used to address the differences in gray and white matter.FindingsVBM analyses showed the grey matter (GM) volume reduction in schizophrenia patients compared with controls bilaterally in the neocortical regions, hippocampus, middle and posterior cingulate and in the caudate. In the subgroup of patients and controls seropositive to T. gondii the reduction of GM was located in the same regions as in the whole sample and consisted of 11660 over-threshold voxels (p£0.05, FWR corrected). The differences between T. gondii negative patients and controls consisted only of 289 voxels in temporal and mediotemporal regions.DiscussionOur study is the first to document that latent toxoplasmosis reduces GM in schizophrenia but not in controls. The higher morphological vulnerability of patients but not controls to T. gondii infection represents an indirect support for the epidemiological evidence of the role of latent toxoplasmosis in schizophrenia.AcknowledgmentsThis work was supported by grants 1M0517.


Author(s):  
J.E. Johnson

Although neuroaxonal dystrophy (NAD) has been examined by light and electron microscopy for years, the nature of the components in the dystrophic axons is not well understood. The present report examines nucleus gracilis and cuneatus (the dorsal column nuclei) in the brain stem of aging mice.Mice (C57BL/6J) were sacrificed by aldehyde perfusion at ages ranging from 3 months to 23 months. Several brain areas and parts of other organs were processed for electron microscopy.At 3 months of age, very little evidence of NAD can be discerned by light microscopy. At the EM level, a few axons are found to contain dystrophic material. By 23 months of age, the entire nucleus gracilis is filled with dystrophic axons. Much less NAD is seen in nucleus cuneatus by comparison. The most recurrent pattern of NAD is an enlarged profile, in the center of which is a mass of reticulated material (reticulated portion; or RP).


1969 ◽  
Vol 21 (02) ◽  
pp. 294-303 ◽  
Author(s):  
H Mihara ◽  
T Fujii ◽  
S Okamoto

SummaryBlood was injected into the brains of dogs to produce artificial haematomas, and paraffin injected to produce intracerebral paraffin masses. Cerebrospinal fluid (CSF) and peripheral blood samples were withdrawn at regular intervals and their fibrinolytic activities estimated by the fibrin plate method. Trans-form aminomethylcyclohexane-carboxylic acid (t-AMCHA) was administered to some individuals. Genera] relationships were found between changes in CSF fibrinolytic activity, area of tissue damage and survival time. t-AMCHA was clearly beneficial to those animals given a programme of administration. Tissue activator was extracted from the brain tissue after death or sacrifice for haematoma examination. The possible role of tissue activator in relation to haematoma development, and clinical implications of the results, are discussed.


2009 ◽  
Vol 150 (46) ◽  
pp. 2101-2109 ◽  
Author(s):  
Péter Csécsei ◽  
Anita Trauninger ◽  
Sámuel Komoly ◽  
Zsolt Illés

The identification of autoantibodies generated against the brain isoform water channel aquaporin4 in the sera of patients, changed the current diagnostic guidelines and concept of neuromyelitis optica (NMO). In a number of cases, clinical manifestation is spatially limited to myelitis or relapsing optic neuritis creating a diverse. NMO spectrum. Since prevention of relapses provides the only possibility to reduce permanent disability, early diagnosis and treatment is mandatory. In the present study, we discuss the potential role of neuroimaging and laboratory tests in differentiating the NMO spectrum from other diseases, as well as the diagnostic procedures and therapeutic options. We also present clinical cases, to provide examples of different clinical settings, diagnostic procedures and therapeutic decisions.


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