The effect of Co Q10 on rat liver mitochondria succinoxidase activity in carbon tetrachloride liver injury

1963 ◽  
Vol 19 (2) ◽  
pp. 88-89 ◽  
Author(s):  
Anna Casu
Micron (1969) ◽  
1979 ◽  
Vol 10 (3) ◽  
pp. 167-168
Author(s):  
Michael J. Brabec ◽  
Roberta K. Brabec ◽  
Robert H. Gray

1987 ◽  
Vol 246 (2) ◽  
pp. 313-317 ◽  
Author(s):  
A Tomasi ◽  
E Albano ◽  
S Banni ◽  
B Botti ◽  
F Corongiu ◽  
...  

Alterations in liver mitochondria as consequence of rat poisoning with carbon tetrachloride (CCl4) have been reported over many years, but the mechanisms responsible for causing such damage are still largely unknown. Isolated rat liver mitochondria incubated under hypoxic conditions with succinate and ADP were found able to activate CCl4 to a free-radical species identified as trichloromethyl free radical (CCl3) by e.s.r. spectroscopy coupled with the spin-trapping technique. The incubation of mitochondria in air decreased free-radical production, indicating that a reductive reaction was involved in the activation of CCl4. However, in contrast with liver microsomes (microsomal fractions), mitochondria did not require the presence of NADPH, and the process was not significantly influenced by inhibitors of cytochrome P-450. The addition of inhibitors of the respiratory chain such as antimycin A and KCN decreased free-radical formation by only 30%, whereas rotenone displayed a greater effect (approx. 84% inhibition), but only when preincubated for 15 min with mitochondria not supplemented with succinate. These findings suggest that the mitochondrial electron-transport chain is responsible for the activation of CCl4. A conjugated-diene band was observed in the lipids extracted from mitochondria incubated with CCl4 under anaerobic conditions, indicating that stimulation of lipid peroxidation was occurring as a result of the formation of free-radical species.


1983 ◽  
Vol 18 ◽  
pp. 42 ◽  
Author(s):  
de Castro C.R. ◽  
G. Fernandez ◽  
M.C. Villarruel ◽  
A. Berkiacchi ◽  
J.A. Castro

Author(s):  
Y. Z. Maksimchik ◽  
I. K. Dremza ◽  
E. A. Lapshina ◽  
V. T. Cheshchevik ◽  
E. Ju. Sudnikovich ◽  
...  

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.


Author(s):  
Olga A. Gonchar ◽  
Valentina I. Nosar ◽  
Larisa. V. Bratus ◽  
I. N. Tymchenko ◽  
N. N. Steshenko ◽  
...  

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