Inconsistent responses of liver mitochondria metabolism and standard metabolism in Silurus meridionalis when exposed to waterborne cadmium

Author(s):  
Jian Li ◽  
Xiaojun Xie
2011 ◽  
Vol 57 (1) ◽  
pp. 109-115 ◽  
Author(s):  
Yulian Yan ◽  
Xiaojun Xie

Abstract To examine whether metabolic compensation during seasonal acclimatization at the liver mitochondrial level is consistent with that at the whole-animal level, respiration rates of liver mitochondria and resting metabolic rates in winter- and summer-acclimatized southern catfish (Silurus meridionalis Chen) were measured. At 12.5, 17.5, 22.5, 27.5 and 32.5°C, the mean values of state 3 respiration rates were 12.21, 13.84, 18.96, 24.78 and 32.01 nmol O2 min-1 mg-1 mitochondrial protein in the winter group, and 8.56, 9.20, 17.32, 22.74 and 26.32 nmol O2 min-1 mg-1 in the summer group, respectively. At the five assay temperatures the resting metabolic rates were 24.86, 42.68, 61.59, 84.10 and 125.65 mg O2 h-1 kg-1 body mass in the winter group, and 22.89, 40.59, 52.94, 75.13 and 109.35 mg O2 h-1 kg-1 in the summer group, respectively. Total mitochondrial respiration rates in the liver organ were estimated based on state 3 respiration rates, mitochondrial protein content and organ mass, and the mean values were 72.96, 71.87, 112.47, 167.35 and 183.27 nmol O2 min-1 in the winter group, and were 47.89, 47.39, 105.67, 138.18 and 132.29 nmol O2 min-1 in the summer group, respectively. Metabolic compensation caused by seasonal acclimatization occurred at the liver mitochondrial level and compensation at the liver organ level was found to be more efficient because of an increase in metabolic capacity of mitochondria and a boost in organ mass. Metabolic compensation at the whole-animal level was not detected. During seasonal acclimatization, the effect of metabolic compensation at liver mitochondrial level is inconsistent with that at the whole-animal level in the southern catfish. This may be due to different degrees of regulation of metabolic mechanisms among various tissues and organs in an acclimatized organism.


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):  
F. G. Zaki

Choline-deficiency was induced in Holtzman young rats of both sexes by feeding them a high fat - low protein diet.Preliminary studies of the ultrastructural changes in the myocardium of these animals have been recently reported from this laboratory. Myocardial lesions first appeared in the form of intraventricular mural thrombi, loss of cross striation of muscle fibers and focal necrosis of muscle cells associated with interstitial myocarditis. Prolonged choline-deficiency induced cardiomegaly associated with pericardial edema.During the early phase of this nutritional disorder, heart mitochondria - despite of not showing any swelling similar to that usually encountered in liver mitochondria of the same animal - ware the most ubiquitous site of marked structural abnormalities. Early changes in mitochondria appeared as vacuolation, disorganization, disruption and loss of cristae. Degenerating mitochondria were often seen quite enlarged and their matrix was replaced by whorls of myelin figures resembling lysosomal structures especially where muscle fibers were undergoing necrosis. In some areas, mitochondria appeared to be unusually clumped together where some contained membranelined vacuoles and others enclosed dense bodies and granular inclusions.


2019 ◽  
Vol 476 (24) ◽  
pp. 3687-3704 ◽  
Author(s):  
Aphrodite T. Choumessi ◽  
Manuel Johanns ◽  
Claire Beaufay ◽  
Marie-France Herent ◽  
Vincent Stroobant ◽  
...  

Root extracts of a Cameroon medicinal plant, Dorstenia psilurus, were purified by screening for AMP-activated protein kinase (AMPK) activation in incubated mouse embryo fibroblasts (MEFs). Two isoprenylated flavones that activated AMPK were isolated. Compound 1 was identified as artelasticin by high-resolution electrospray ionization mass spectrometry and 2D-NMR while its structural isomer, compound 2, was isolated for the first time and differed only by the position of one double bond on one isoprenyl substituent. Treatment of MEFs with purified compound 1 or compound 2 led to rapid and robust AMPK activation at low micromolar concentrations and increased the intracellular AMP:ATP ratio. In oxygen consumption experiments on isolated rat liver mitochondria, compound 1 and compound 2 inhibited complex II of the electron transport chain and in freeze–thawed mitochondria succinate dehydrogenase was inhibited. In incubated rat skeletal muscles, both compounds activated AMPK and stimulated glucose uptake. Moreover, these effects were lost in muscles pre-incubated with AMPK inhibitor SBI-0206965, suggesting AMPK dependency. Incubation of mouse hepatocytes with compound 1 or compound 2 led to AMPK activation, but glucose production was decreased in hepatocytes from both wild-type and AMPKβ1−/− mice, suggesting that this effect was not AMPK-dependent. However, when administered intraperitoneally to high-fat diet-induced insulin-resistant mice, compound 1 and compound 2 had blood glucose-lowering effects. In addition, compound 1 and compound 2 reduced the viability of several human cancer cells in culture. The flavonoids we have identified could be a starting point for the development of new drugs to treat type 2 diabetes.


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

2012 ◽  
Vol 36 (8) ◽  
pp. 1263 ◽  
Author(s):  
Ling-qing ZENG ◽  
Feng-jie LI ◽  
Xiu-ming LI ◽  
FU Jia-qing HUANG ◽  
Shi-jian FU ◽  
...  

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