In Vitro Effect of Lead on Na+, K+-ATPase Activity in Different Regions of Adult Rat Brain

2003 ◽  
Vol 26 (2) ◽  
pp. 117-124 ◽  
Author(s):  
Prabhakara Rao Yallapragada ◽  
Jennifer Butler ◽  
Bokara Kiran Kumar ◽  
Bettaiya Rajanna
1985 ◽  
Vol 19 (4) ◽  
pp. 335A-335A ◽  
Author(s):  
Benjamin S Brann ◽  
William J Cashore ◽  
Robert Patrick ◽  
William Oh

1997 ◽  
Vol 20 (1-2) ◽  
pp. 21-29 ◽  
Author(s):  
Bettaiya Rajanna ◽  
Sharada Rajanna ◽  
Elizabeth Hall ◽  
Prabhakara R. Yallapragada

2001 ◽  
Vol 56 (9-10) ◽  
pp. 912-914 ◽  
Author(s):  
Stylianos Tsakiris ◽  
Christos Koromilas ◽  
Kleopatra H. Schulpis

Abstract The effects of different a-D-Glucose (Glu) concentrations (0 -16 mᴍ) on Na+, K+-ATPase and Mg2+-ATPase activities were investigated in homogenates of adult male rat whole brain at 37 °C. The enzyme activities were determined after 1h preincubation with Glu. Brain Na+, K+-ATPase was not affected by Glu different concentrations. On the contrary, Mg2+-ATPase activity was considerably reduced with Glu concentrations lower than 4 mᴍ. The enzyme was inhibited 40%, 50% or 80% with 3, 2 or 1 mᴍ of Glu, respectively. The above results suggest: a) The various concentrations of Glu have no effect on brain Na+, K+-ATPase activity, b) The inhibited brain Mg2+-ATPase in hypoglycemia produces low intracellular Mg2+, which could modulate the activity of Mg2+ -dependent enzymes and the rates of protein syn­thesis and growth of the cell.


1985 ◽  
Vol 101 (6) ◽  
pp. 2411-2415 ◽  
Author(s):  
D Giulian ◽  
T J Baker

Peptides that stimulate astroglial proliferation are produced in traumatized adult rat brain by 10 d after injury. These same peptides are released by ameboid microglia activated in vitro. Our findings suggest that astroglial scarring is regulated in part by the release of factors from ameboid microglia near the site of brain injury.


2010 ◽  
Vol 3 (4) ◽  
pp. 122-126 ◽  
Author(s):  
Zdenka Gáspárová ◽  
Oľga Ondrejičková ◽  
Alena Gajdošíková ◽  
Andrej Gajdošík ◽  
Vladimír Šnirc ◽  
...  

Oxidative stress induced by the Fe2+/ascorbic acid system or model ischemiain vitro: effect of carvedilol and pyridoindole antioxidant SMe1EC2 in young and adult rat brain tissueNew effective strategies and new highly effective neuroprotective agents are being searched for the therapy of human stroke and cerebral ischemia. The compound SMe1EC2 is a new derivative of stobadine, with enhanced antioxidant properties compared to the maternal drug. Carvedilol, a non-selective beta-blocker, possesses besides its cardioprotective and vasculoprotective properties also an antioxidant effect. We compared the effect of carvedilol and SMe1EC2, antioxidants with a similar chemical structure, in two experimental models of oxidative stress in young and adult rat brain tissue. SMe1EC2 was found to improve the resistance of hippocampal neurons to ischemiain vitroin young and even in 18-month-old rats and inhibited formation of protein carbonyl groups induced by the Fe2+/ascorbic acid pro-oxidative system in brain cortex homogenates of young rats. Carvedilol exerted a protective effect only in the hippocampus of 2-month-old rats and that at the concentration 10-times higher than did SMe1EC2. The inhibitory effect of carvedilol on protein carbonyl formation induced by the pro-oxidative system was not proved in the cortex of either young or adult rats. An increased baseline level of the content of protein carbonyl groups in the adult versus young rat brain cortex confirmed age-related changes in neuronal tissue and may be due to increased production of reactive oxygen species and low antioxidant defense mechanisms in the adult rat brain. The results revealed the new pyridoindole SMe1EC2 to be more effective than carvedilol in neuroprotection of rat brain tissue in both experimental models involving oxidative stress.


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