The protective effect of chloramphenicol against CCL4 — induced changes in mitochondrial function and phospholipid composition

1983 ◽  
Vol 18 ◽  
pp. 140
Author(s):  
A. Wisner-Gebhart ◽  
M.J. Brabec
2005 ◽  
Vol 280 (50) ◽  
pp. 41387-41394 ◽  
Author(s):  
Yonit Tsatskis ◽  
Jumana Khambati ◽  
Martina Dobson ◽  
Mikhail Bogdanov ◽  
William Dowhan ◽  
...  

2000 ◽  
Vol 279 (1) ◽  
pp. E25-E32 ◽  
Author(s):  
Jane McHowat ◽  
Michael H. Creer ◽  
Kristine K. Hicks ◽  
Janet H. Jones ◽  
Raetreal McCrory ◽  
...  

Diabetes-induced changes in phospholipase A2(PLA2) activity have been measured in several tissues but are undefined in diabetic myocardium. We measured ventricular PLA2 activity in control, streptozotocin-induced diabetic, and insulin-treated diabetic rats and characterized myocardial phospholipids to determine whether diabetes altered myocardial phospholipid metabolism. Increased membrane-associated Ca2+-independent PLA2 (iPLA2) activity was observed in diabetes that was selective for arachidonylated phospholipids. Increased iPLA2 activity was accompanied by an increase in choline lysophospholipids. Diabetes was associated with marked alterations in the phospholipid composition of the myocardium, characterized by decreases in esterified arachidonic and docosahexaenoic acids and increases in linoleic acid. The decrease in polyunsaturated fatty acids was confined to diacylphospholipids, whereas the relative amount of these fatty acids in plasmalogens was increased. Diabetes-induced changes in PLA2 activity, lysophospholipid production, and alterations in phospholipid composition were all reversed by insulin treatment of diabetic animals. Diabetes-induced changes in membrane phospholipid content and phospholipid hydrolysis may contribute to some of the alterations in myocardial function that are observed in diabetic patients.


2019 ◽  
Vol 711 ◽  
pp. 134376
Author(s):  
Rehana Khatoon ◽  
Md. Zeeshan Rasheed ◽  
Mahika Rawat ◽  
M. Mumtaz Alam ◽  
Heena Tabassum ◽  
...  

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Jiahui Zhao ◽  
Shuyun Zhang ◽  
Liesong Chen ◽  
Xiaolong Liu ◽  
Haihong Su ◽  
...  

Abstract The toxic effects of ionizing radiation on the gonads have been widely recognized. Sphingosine 1-phosphate (S1P) has a protective effect on ovarian injury, and although it is known that mitochondria are involved in this process, the specific mechanism is not fully understood. The present study analysed the changes in the serum AMH and ovarian histology in Sprague-Dawley female rats exposed to X-ray radiation only or co-administered with S1P. The mRNA expression profile of ovarian tissue was further analysed via next-generation sequencing and bioinformatics approaches to screen out candidate mitochondria-related genes. Finally, differentially expressed target genes were verified by real-time PCR. The results showed that ionizing radiation could reduce the serum AMH level, destroy ovarian structure and decrease the number of follicles in rats, while S1P administration significantly attenuated the impairment of ovarian function. Gene ontology (GO) and KEGG pathway analysis revealed that a variety of genes related to mitochondrial function were differentially expressed, and the protective effect of S1P on mitochondria was more obvious in the acute phase 24 h after radiation. The differentially expressed mitochondrial function-related genes associated with the protective effect of S1P were UQCRH, MICU2 and GPX4, which were subsequently verified by RT-PCR. Therefore, ionizing radiation has a significant effect on ovarian function, and S1P has a protective effect on radiation-induced ovarian injury, in which mitochondria may play an important role. This study sheds new light on the mechanism of radiation-induced ovarian injury and helps develop a novel potential strategy to control it.


1992 ◽  
Vol 263 (2) ◽  
pp. C405-C411 ◽  
Author(s):  
Y. Park ◽  
T. M. Devlin ◽  
D. P. Jones

The dimer and trimer of 16,16-dimethyl-15-dehydroprostaglandin B1 (16,16-diMePGB1) previously have been shown to have protective effects on mitochondrial function. To examine the potential mechanisms involved in protection against mitochondrial failure, we have studied the effects of the dimer of 16,16-diMe-PGB1 (dicalciphor) on mitochondrial function in hepatocytes exposed to KCN. Addition of micromolar concentrations of dicalciphor provided substantial protection against KCN-induced toxicity in a concentration- and time-dependent manner. Dicalciphor, however, had no effect on total or mitochondrial ATP losses in KCN-treated cells. The dimer prevented the marked loss of mitochondrial membrane potential (delta psi) and delta pH that occurs as a result of KCN treatment and prevented KCN-induced loading of phosphate in mitochondria. Furthermore, the dimer of 16,16-diMePGB1 also prevented KCN-induced mitochondrial and cellular swelling. These results demonstrate that dicalciphor protects against KCN-induced damage and that this protection is associated with regulation of specific mitochondrial ion transport functions.


2002 ◽  
Vol 136 (3) ◽  
pp. 472-480 ◽  
Author(s):  
Takeshi Iwai ◽  
Kouichi Tanonaka ◽  
Sayaka Kasahara ◽  
Rie Inoue ◽  
Satoshi Takeo

Sign in / Sign up

Export Citation Format

Share Document