Altered mitochondrial function and overgeneration of reactive oxygen species precede the induction of apoptosis by 1‐O‐octadecyl‐2‐methyl‐rαc‐grycero‐3‐phosphocholine in p53‐defective hepatocytes

2001 ◽  
Vol 15 (10) ◽  
pp. 1739-1744 ◽  
Author(s):  
ANGELICA S. VRABLIC ◽  
CRAIG D. ALBRIGHT ◽  
CORNELIU N. CRACIUNESCU ◽  
RUDOLF I. SALGANIK ◽  
STEVEN H. ZEISEL
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Function ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Induction Of Apoptosis

Role of reactive oxygen species in the induction of apoptosis by ?-tocopheryl succinate

2004 ◽  
Vol 112 (3) ◽  
pp. 385-392 ◽  
Author(s):  
Young-Hwa Kang ◽  
Eunmyong Lee ◽  
Moon-Kyung Choi ◽  
Ja-Lok Ku ◽  
So Hee Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tocopheryl Succinate ◽  
Induction Of Apoptosis

scholarly journals Intraperitoneal Triamcinolone Reduces Postoperative Adhesions, Possibly through Alteration of Mitochondrial Function

2022 ◽  
Vol 11 (2) ◽  
pp. 301
Author(s):  
Neeraja Purandare ◽  
Katherine J. Kramer ◽  
Paige Minchella ◽  
Sarah Ottum ◽  
Christopher Walker ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Function ◽  
Molecular Mechanisms ◽  
Human Fibroblasts ◽  
Reactive Oxygen ◽  
Retrospective Chart Review ◽  
Oxygen Species ◽  
Abdominal Myomectomy ◽  
Hypoxic Conditions

Adhesions frequently occur postoperatively, causing morbidity. In this noninterventional observational cohort study, we enrolled patients who presented for repeat abdominal surgery, after a history of previous abdominal myomectomy, from March 1998 to June 20210 at St. Vincent’s Catholic Medical Centers. The primary outcome of this pilot study was to compare adhesion rates, extent, and severity in patients who were treated with intraperitoneal triamcinolone acetonide during the initial abdominal myomectomy (n = 31) with those who did not receive any antiadhesion interventions (n = 21), as documented on retrospective chart review. Adhesions were blindly scored using a standard scoring system. About 32% of patients were found to have adhesions in the triamcinolone group compared to 71% in the untreated group (p < 0.01). Compared to controls, adhesions were significantly less in number (0.71 vs. 2.09, p < 0.005), severity (0.54 vs. 1.38, p < 0.004), and extent (0.45 vs. 1.28, p < 0.003). To understand the molecular mechanisms, human fibroblasts were incubated in hypoxic conditions and treated with triamcinolone or vehicle. In vitro studies showed that triamcinolone directly prevents the surge of reactive oxygen species triggered by 2% hypoxia and prevents the increase in TGF-β1 that leads to the irreversible conversion of fibroblasts to an adhesion phenotype. Triamcinolone prevents the increase in reactive oxygen species through alterations in mitochondrial function that are HIF-1α-independent. Controlling mitochondrial function may thus allow for adhesion-free surgery and reduced postoperative complications.

scholarly journals Prohibitin-1 maintains the angiogenic capacity of endothelial cells by regulating mitochondrial function and senescence

2008 ◽  
Vol 180 (1) ◽  
pp. 101-112 ◽  
Author(s):  
Michael Schleicher ◽  
Benjamin R. Shepherd ◽  
Yajaira Suarez ◽  
Carlos Fernandez-Hernando ◽  
Jun Yu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Mitochondrial Function ◽  
Vascular System ◽  
Reactive Oxygen ◽  
Direct Consequence ◽  
Oxygen Species ◽  
Inner Mitochondrial Membrane ◽  
Prohibitin 1

Prohibitin 1 (PHB1) is a highly conserved protein that is mainly localized to the inner mitochondrial membrane and has been implicated in regulating mitochondrial function in yeast. Because mitochondria are emerging as an important regulator of vascular homeostasis, we examined PHB1 function in endothelial cells. PHB1 is highly expressed in the vascular system and knockdown of PHB1 in endothelial cells increases mitochondrial production of reactive oxygen species via inhibition of complex I, which results in cellular senescence. As a direct consequence, both Akt and Rac1 are hyperactivated, leading to cytoskeletal rearrangements and decreased endothelial cell motility, e.g., migration and tube formation. This is also reflected in an in vivo angiogenesis assay, where silencing of PHB1 blocks the formation of functional blood vessels. Collectively, our results provide evidence that PHB1 is important for mitochondrial function and prevents reactive oxygen species–induced senescence and thereby maintains the angiogenic capacity of endothelial cells.

scholarly journals Overproduction of reactive oxygen species – obligatory or not for induction of apoptosis by anticancer drugs

2016 ◽  
Vol 28 (4) ◽  
pp. 383-396 ◽  
Author(s):  
Donika Ivanova ◽  
◽  
Zhivko Zhelev ◽  
Ichio Aoki ◽  
Rumiana Bakalova ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Anticancer Drugs ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Induction Of Apoptosis

scholarly journals Reduced Mitochondrial Content, Elevated Reactive Oxygen Species, and Modulation by Denervation in Skeletal Muscle of Prefrail or Frail Elderly Women

2019 ◽  
Vol 74 (12) ◽  
pp. 1887-1895 ◽  
Author(s):  
Vita Sonjak ◽  
Kathryn J Jacob ◽  
Sally Spendiff ◽  
Madhusudanarao Vuda ◽  
Anna Perez ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Frail Elderly ◽  
Elderly Women ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Respiratory Capacity ◽  
Species Response ◽  
Mitochondrial Impairment

Abstract Denervation and mitochondrial impairment are implicated in age-related skeletal muscle atrophy and may play a role in physical frailty. We recently showed that denervation modulates muscle mitochondrial function in octogenarian men, but this has not been examined in elderly women. On this basis, we tested the hypothesis that denervation plays a modulating role in mitochondrial impairment in skeletal muscle from prefrail or frail elderly (FE) women. Mitochondrial respiratory capacity and reactive oxygen species emission were examined in permeabilized myofibers obtained from vastus lateralis muscle biopsies from FE and young inactive women. Muscle respiratory capacity was reduced in proportion to a reduction in a mitochondrial marker protein in FE, and mitochondrial reactive oxygen species emission was elevated in FE versus young inactive group. Consistent with a significant accumulation of neural cell adhesion molecule-positive muscle fibers in FE (indicative of denervation), a 50% reduction in reactive oxygen species production after pharmacologically inhibiting the denervation-mediated reactive oxygen species response in FE women suggests a significant modulation of mitochondrial function by denervation. In conclusion, our data support the hypothesis that denervation plays a modulating role in skeletal muscle mitochondrial function in FE women, suggesting therapeutic strategies in advanced age should focus on the causes and treatment of denervation.

Ascorbic acid improves mitochondrial function in liver of arsenic-treated rat

2010 ◽  
Vol 26 (5) ◽  
pp. 265-272 ◽  
Author(s):  
Sohini Singh ◽  
Suresh Vir Singh Rana
Keyword(s):  
Reactive Oxygen Species ◽  
Ascorbic Acid ◽  
Mitochondrial Function ◽  
Caspase 3 ◽  
Succinic Dehydrogenase ◽  
Reactive Oxygen ◽  
Ultrastructural Changes ◽  
Arsenic Toxicity ◽  
Oxygen Species

Arsenic is an ubiquitous and well-documented carcinogenic metalloid. The most common source of arsenic is drinking water. The mechanism of arsenic toxicity in a cell has historically been centered around its inhibitory effects on cellular respiration and mitochondrial injury. Ascorbic acid, a low molecular weight, water-soluble antioxidant, improves the reduced glutathione (GSH) status by recycling oxidized glutathione. Ascorbic acid can improve mitochondrial function by improving the thiol status; thereby preventing reactive oxygen species— mediated damage to liver as well as kidney. Ascorbic acid has been shown to protect membrane and other cellular compartments by regenerating vitamin E. Therefore, ascorbic acid seems to be a suitable protective factor against arsenic toxicity. Present reports describe the effect of ascorbic acid on oxidative phosphorylation, adenosine triphosphatase (ATPase), succinic dehydrogenase, caspase-3 and apoptosis in the liver of rats treated with arsenic trioxide (AsIII). Ultrastructural changes in the mitochondria have also been reported. We show that cotreatments with ascorbic acid and AsIII improve mitochondrial structure and function. We attribute these improvements mainly to antioxidative role of ascorbic acid. Apoptosis was restricted due to caspase-3 inhibition. Ascorbic acid could protect DNA from the attack of reactive oxygen species generated by AsIII. Consequently its events led to improved ADP:O ratio, normalized ATPase activity and restored the activity of succinic dehydrogenase. Overall, results support the protective role of ascorbic acid against As III-induced liver injury.

scholarly journals Spermatic mitochondria: role in oxidative homeostasis, sperm function and possible tools for their assessment

Zygote ◽  
2018 ◽  
Vol 26 (4) ◽  
pp. 251-260 ◽  
Author(s):  
João Diego de Agostini Losano ◽  
Daniel de Souza Ramos Angrimani ◽  
Roberta Ferreira Leite ◽  
Bárbara do Carmo Simões da Silva ◽  
Valquíria Hyppolito Barnabe ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Function ◽  
Reactive Oxygen ◽  
Sperm Function ◽  
Oxygen Species ◽  
Functional Dynamics ◽  
Fertilization Capacity ◽  
Oxidative Homeostasis

SummaryDespite sperm mitochondrial relevance to the fertilization capacity, the processes involved in the production of ATP and functional dynamics of sperm mitochondria are not fully understood. One of these processes is the paradox involved between function and formation of reactive oxygen species performed by the organelle. Therefore, this review aimed to provide data on the role of sperm mitochondria in oxidative homeostasis and functionality as well the tools to assess sperm mitochondrial function.

Sign in / Sign up

Export Citation Format

Share Document