Lipid peroxidation as the cause of the ascorbic acid induced decrease of adenosine triphosphatase activities of rat brain microsomes and its inhibition by biogenic amines and psychotropic drugs

1975 ◽  
Vol 24 (19) ◽  
pp. 1781-1786 ◽  
Author(s):  
András Schaefer ◽  
Márta Komlós ◽  
András Seregi
2002 ◽  
Vol 131 (4) ◽  
pp. 565-570 ◽  
Author(s):  
K. Yumino ◽  
I. Kawakami ◽  
M. Tamura ◽  
T. Hayashi ◽  
M. Nakamura

1998 ◽  
Vol 28 (4) ◽  
pp. 411-422 ◽  
Author(s):  
Laurence Barrier ◽  
Gulene Page ◽  
Bernard Fauconneau ◽  
Fabrice Juin ◽  
Claude Tallineau

1966 ◽  
Vol 100 (3) ◽  
pp. 762-767 ◽  
Author(s):  
N Gruener ◽  
Y Avi-Dor

1. The adenosine-triphosphatase activity of rat-brain microsomes was measured between 0 degrees and 37 degrees . The stimulatory effect of Na(+) plus K(+) on the Mg(2+)-dependent adenosine-triphosphatase activity decreased sharply with decreasing temperature and became negligible at 0 degrees . An Arrhenius plot drawn from the experimental data showed two discontinuities: one at about 6 degrees and the other at about 20 degrees . 2. The increment in activity induced by Na(+) plus K(+) was more sensitive to oligomycin at lower than at higher temperatures, but the opposite was observed for ouabain. The action of oligomycin showed a biphasic character, since below a certain concentration it caused slight activation of Na(+)-plus-K(+)-activated adenosine triphosphatase. 3. Where oligomycin increased the activity of the enzyme, it also enhanced the accumulation of an acid-precipitable phosphorylated compound formed through the transfer of the gamma-phosphate group of [(32)P]ATP to the enzyme system. Stimulatory concentrations of oligomycin did not interfere with K(+)-mediated dephosphorylation of the intermediate, though high concentrations of oligomycin counteracted the effect of K(+). 4. The temperature profile of K(+)-stimulated microsomal phosphatase qualitatively resembled that of microsomal adenosine triphosphatase.


1998 ◽  
Vol 17 (1) ◽  
pp. 23-28 ◽  
Author(s):  
Syed Saleem Haider ◽  
A A Abdel-Gayoum ◽  
Mustafa El-Fakhri ◽  
Kilani M Ghwarsha

The protective effect of selenium on the neurotoxicity of vanadium in different brain regions of rats was investigated. The lipid peroxidation was significantly accentuated after intraperitoneal (i.p.) administration of vanadium (1.5 mg kg71 b.wt) for a period of 12 consecutive days to rats. The increase in lipid peroxidation was inhibited by selenium treatment (0.02 mg kg71 b.wt., i.p.) for 12 consecutive days. Vanadium exposure produced a decrease in nonprotein sulfhydryl group. Selenium treatment prevented the depression in nonprotein sulfhydryl group in all the brain regions of the vanadium exposed rats. The concentration of ascorbic acid was decreased after co-administration of selenium and vanadium. These results suggest that selenium protects neuronal cells against neurotoxic effects of vanadium by maintaining the availability of antioxidant nonprotein sulfhydryl groups. The decrease in ascorbic acid levels may have been due to its consumption in forming complexes with vanadium.


2009 ◽  
Vol 97 (01) ◽  
pp. 103-106
Author(s):  
C. D. Dey ◽  
P. C. Das ◽  
K. Das ◽  
P. B. Patra ◽  
S. Dasgupta

Sign in / Sign up

Export Citation Format

Share Document