Influence of ATP-dependent K+-channel opener on K+-cycle and oxygen consumption in rat liver mitochondria

2010 ◽  
Vol 75 (9) ◽  
pp. 1139-1147 ◽  
Author(s):  
O. V. Akopova ◽  
V. I. Nosar ◽  
V. A. Bouryi ◽  
I. N. Mankovskaya ◽  
V. F. Sagach
Amino Acids ◽  
2006 ◽  
Vol 31 (3) ◽  
pp. 299-302 ◽  
Author(s):  
C. F. Reyes-Toso ◽  
I. R. Rebagliati ◽  
C. R. Ricci ◽  
L. M. Linares ◽  
L. E. Albornoz ◽  
...  

1966 ◽  
Vol 101 (3) ◽  
pp. 707-710 ◽  
Author(s):  
JG Wit ◽  
H Van Genderen

1. Both monophenolic metabolites of 2,6-dichlorobenzonitrile (2,6-dichloro-3-hydroxybenzonitrile and its 4-hydroxy analogue) added to starved yeast cells incubated with a limited quantity of glucose cause a significant rise in oxygen consumption of the cells. 2. The same compounds induce adenosine-triphosphatase activity in isolated intact rat-liver mitochondria. 3. The possible role of the hydroxylation of 2,6-dichlorobenzonitrile in mammals in relation to hepatic injury is discussed.


Author(s):  
E. A. Elfont ◽  
R. B. Tobin ◽  
D. G. Colton ◽  
M. A. Mehlman

Summary5,-5'-diphenyl-2-thiohydantoin (DPTH) is an effective inhibitor of thyroxine (T4) stimulation of α-glycerophosphate dehydrogenase in rat liver mitochondria. Because this finding indicated a possible tool for future study of the mode of action of thyroxine, the ultrastructural and biochemical effects of DPTH and/or thyroxine on rat liver mere investigated.Rats were fed either standard or DPTH (0.06%) diet for 30 days before T4 (250 ug/kg/day) was injected. Injection of T4 occurred daily for 10 days prior to sacrifice. After removal of the liver and kidneys, part of the tissue was frozen at -50°C for later biocheailcal analyses, while the rest was prefixed in buffered 3.5X glutaraldehyde (390 mOs) and post-fixed in buffered 1Z OsO4 (376 mOs). Tissues were embedded in Araldlte 502 and the sections examined in a Zeiss EM 9S.Hepatocytes from hyperthyroid rats (Fig. 2) demonstrated enlarged and more numerous mitochondria than those of controls (Fig. 1). Glycogen was almost totally absent from the cytoplasm of the T4-treated rats.


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