Effects of ethanol on neurotrophic factors, apoptosis-related proteins, endogenous antioxidants, and reactive oxygen species in neonatal striatum: relationship to periods of vulnerability

Ischemia/reperfusion (I/R) injury is the central cause of global death in cardiovascular diseases, which is characterized by disorders such as angina, stroke, and peripheral vascular disease, finally causing severe debilitating diseases and death. The increased rates of morbidity and mortality caused by I/R are parallel with aging. Aging-associated cardiac physiological structural and functional deterioration were found to contribute to abnormal reactive oxygen species (ROS) production during I/R stress. Disturbed redox homeostasis could further trigger the related signaling pathways that lead to cardiac irreversible damages with mitochondria dysfunction and cell death. It is notable that sirtuin proteins are impaired in aged hearts and are critical to maintaining redox homeostasis via regulating substrate metabolism and inflammation and thus preserving cardiac function under stress. This review discussed the cellular and functional alterations upon I/R especially in aging hearts. We propose that mitochondria are the primary source of reactive oxygen species (ROS) that contribute to I/R injury in aged hearts. Then, we highlight the cardiomyocyte protection of the age-related proteins Sirtuin1 (SIRT1) and Sirtuin1 (SIRT3) in response to I/R injury, and we discuss their modulation of cardiac metabolism and the inflammatory reaction that is involved in ROS formation.

Download Full-text

Divergent Effects of Sulforaphane on Basal and Glucose-Stimulated Insulin Secretion in β-Cells: Role of Reactive Oxygen Species and Induction of Endogenous Antioxidants

Pharmaceutical Research ◽

10.1007/s11095-013-1013-8 ◽

2013 ◽

Vol 30 (9) ◽

pp. 2248-2259 ◽

Cited By ~ 20

Author(s):

Jingqi Fu ◽

Qiang Zhang ◽

Courtney G. Woods ◽

Hongzhi Zheng ◽

Bei Yang ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Insulin Secretion ◽

Reactive Oxygen ◽

Oxygen Species ◽

Β Cells ◽

Endogenous Antioxidants ◽

Glucose Stimulated Insulin Secretion

Download Full-text

Reactive oxygen species, dietary restriction and neurotrophic factors in age-related loss of myenteric neurons

Aging Cell ◽

10.1111/j.1474-9726.2006.00214.x ◽

2006 ◽

Vol 5 (3) ◽

pp. 247-257 ◽

Cited By ~ 76

Author(s):

C. Thrasivoulou ◽

V. Soubeyre ◽

H. Ridha ◽

D. Giuliani ◽

C. Giaroni ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Dietary Restriction ◽

Neurotrophic Factors ◽

Reactive Oxygen ◽

Oxygen Species ◽

Myenteric Neurons ◽

Age Related

Download Full-text

Proteomic analysis of reactive oxygen species (ROS)-related proteins in rice roots

Plant Cell Reports ◽

10.1007/s00299-007-0441-5 ◽

2007 ◽

Vol 27 (2) ◽

pp. 363-375 ◽

Cited By ~ 29

Author(s):

Sang Gon Kim ◽

Sun Tae Kim ◽

Sun Young Kang ◽

Yiming Wang ◽

Wook Kim ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Proteomic Analysis ◽

Reactive Oxygen ◽

Oxygen Species ◽

Rice Roots ◽

Related Proteins

Download Full-text

Pardaxin Activates Excessive Mitophagy and Mitochondria-Mediated Apoptosis in Human Ovarian Cancer by Inducing Reactive Oxygen Species

Antioxidants ◽

10.3390/antiox10121883 ◽

2021 ◽

Vol 10 (12) ◽

pp. 1883

Author(s):

Yen-Po Chen ◽

Po-Chang Shih ◽

Chien-Wei Feng ◽

Chang-Cheng Wu ◽

Kuan-Hao Tsui ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Ovarian Cancer ◽

Reactive Oxygen ◽

New Drugs ◽

Oxygen Species ◽

Preclinical Development ◽

Skov3 Cells ◽

Ic50 Values ◽

Induced Apoptosis ◽

Related Proteins

Most ovarian cancer (OC) patients are diagnosed with stage III or higher disease, resulting in a poor prognosis. Currently, paclitaxel combined with carboplatin shows the best treatment outcome for OC. However, no effective drug is available for patients that do not respond to treatment; thus, new drugs for OC are needed. We evaluated the antimicrobial peptide, pardaxin, in PA-1 and SKOV3 cells. Pardaxin induced apoptosis as determined by MTT and TUNEL assays, as well as activation of caspases-9/3, Bid, t-Bid, and Bax, whereas Bcl-2 was downregulated. The IC50 values for pardaxin were 4.6–3.0 μM at 24 and 48 h. Mitochondrial and intracellular reactive oxygen species (ROS) were overproduced and associated with disrupted mitochondrial membrane potential and respiratory capacity. Additionally, the mitochondrial network was fragmented with downregulated fusogenic proteins, MFN1/2 and L-/S-OPA1, and upregulated fission-related proteins, DRP1 and FIS1. Autophagy was also activated as evidenced by increased expression of autophagosome formation-related proteins, Beclin, p62, and LC3. Enhanced mitochondrial fragmentation and autophagy indicate that mitophagy was activated. ROS-induced cytotoxicity was reversed by the addition of N-acetylcysteine, confirming ROS overproduction as a contributor. Taken together, pardaxin demonstrated promising anticancer activity in OC cells, which warrants further preclinical development of this compound.

Download Full-text

Mitochondrial Fission and Mitophagy Reciprocally Orchestrate Cardiac Fibroblasts Activation

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2020.629397 ◽

2021 ◽

Vol 8 ◽

Author(s):

Qing-Yuan Gao ◽

Hai-Feng Zhang ◽

Jun Tao ◽

Zhi-Teng Chen ◽

Chi-Yu Liu ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Transforming Growth Factor ◽

Cardiac Fibroblasts ◽

Mitochondrial Fission ◽

Reactive Oxygen ◽

Oxygen Species ◽

Mitochondrial Impairment ◽

Related Proteins ◽

Tgf Β1

Although mitochondrial fission has been reported to increase proliferative capacity and collagen production, it can also contribute to mitochondrial impairment, which is detrimental to cell survival. The aim of the present study was to investigate the role of mitochondrial fission in cardiac fibroblasts (CF) activation and explore the mechanisms involved in the maintenance of mitochondrial health under this condition. For this, changes in the levels of mitochondrial fission/fusion-related proteins were assessed in transforming growth factor beta 1 (TGF-β1)-activated CF, whereas the role of mitochondrial fission during this process was also elucidated, as were the underlying mechanisms. The interaction between mitochondrial fission and mitophagy, the main defense mechanism against mitochondrial impairment, was also explored. The results showed that the mitochondria in TGF-β1-treated CF were noticeably more fragmented than those of controls. The expression of several mitochondrial fission-related proteins was markedly upregulated, and the levels of fusion-related proteins were also altered, but to a lesser extent. Inhibiting mitochondrial fission resulted in a marked attenuation of TGF-β1-induced CF activation. The TGF-β1-induced increase in glycolysis was greatly suppressed in the presence of a mitochondrial inhibitor, whereas a glycolysis-specific antagonist exerted little additional antifibrotic effects. TGF-β1 treatment increased cellular levels of reactive oxygen species (ROS) and triggered mitophagy, but this effect was reversed following the application of ROS scavengers. For the signals mediating mitophagy, the expression of Pink1, but not Bnip3l/Nix or Fundc1, exhibited the most significant changes, which could be counteracted by treatment with a mitochondrial fission inhibitor. Pink1 knockdown suppressed CF activation and mitochondrial fission, which was accompanied by increased CF apoptosis. In conclusion, mitochondrial fission resulted in increased glycolysis and played a crucial role in CF activation. Moreover, mitochondrial fission promoted reactive oxygen species (ROS) production, leading to mitophagy and the consequent degradation of the impaired mitochondria, thus promoting CF survival and maintaining their activation.

Download Full-text