Mammal Cells Double Their Total RNAs against Diabetes, Ischemia Reperfusion and Malaria-Induced Oxidative Stress

Zhang, Zhongwei; Cheng, Jian; Xu, Fengming; Yuan, Ming; Du, Junbo; Shang, Jing; Wang, Yong; Du, Lei; Li, Zi-Lin; Yuan, Shu

doi:10.2119/molmed.2010.00155

Cited by 3 publications

(3 citation statements)

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“…Reperfusion of ischemic tissues is usually accompanied with microvascular damage, which increases capillary and arteriole permeability and leads to fluid filtration and diffusion. These damaged endothelial cells generate more ROS but less nitric oxide after reperfusion, and the disequilibrium induces subsequently inflammatory responses [ 3 , 12 , 13 ]. At the same time, leukocytes, circulated with the newly returning blood, release interleukins, free radicals, and other inflammatory factors, which damage the tissue further [ 3 , 12 , 13 ].…”

Section: Ros-burst-mediated Acute Diseasesmentioning

confidence: 99%

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Mitochondrion‐Permeable Antioxidants to Treat ROS‐Burst‐Mediated Acute Diseases

Zhang

Liu

et al. 2015

Oxidative Medicine and Cellular Longevity

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Reactive oxygen species (ROS) play a crucial role in the inflammatory response and cytokine outbreak, such as during virus infections, diabetes, cancer, cardiovascular diseases, and neurodegenerative diseases. Therefore, antioxidant is an important medicine to ROS-related diseases. For example, ascorbic acid (vitamin C, VC) was suggested as the candidate antioxidant to treat multiple diseases. However, long-term use of high-dose VC causes many side effects. In this review, we compare and analyze all kinds of mitochondrion-permeable antioxidants, including edaravone, idebenone, α-Lipoic acid, carotenoids, vitamin E, and coenzyme Q10, and mitochondria-targeted antioxidants MitoQ and SkQ and propose astaxanthin (a special carotenoid) to be the best antioxidant for ROS-burst-mediated acute diseases, like avian influenza infection and ischemia-reperfusion. Nevertheless, astaxanthins are so unstable that most of them are inactivated after oral administration. Therefore, astaxanthin injection is suggested hypothetically. The drawbacks of the antioxidants are also reviewed, which limit the use of antioxidants as coadjuvants in the treatment of ROS-associated disorders.

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Section: Ros-burst-mediated Acute Diseasesmentioning

confidence: 99%

“…Then ROS may also trigger redox signalling indirectly and the subsequent cell death or apoptosis. Leukocytes may also bind to the small capillary endothelium, causing more ischemia [ 3 , 12 , 13 ].…”

Section: Ros-burst-mediated Acute Diseasesmentioning

confidence: 99%

Mitochondrion‐Permeable Antioxidants to Treat ROS‐Burst‐Mediated Acute Diseases

Zhang

Liu

et al. 2015

Oxidative Medicine and Cellular Longevity

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“… 12 Mitochondria have a critical role in mediating calcium overload and oxidative damage (e.g., hydrogen peroxide)-induced cell death, such as ischemia reperfusion (IR) injury. 18 , 19 , 20 The mitochondrial permeability transition (mPT) after this injury leads to mitochondrial swelling, outer membrane rupture and the release of apoptotic mediators (such as cytochrome c ). 18 The mPT pore is thought to consist of the adenine nucleotide translocator, a voltage-dependent anion channel and cyclophilin D. Cyclosporin A (CsA) can effectively inhibit cyclophilin D and, therefore, it protects myocardial cells form IR injury (such as myocardial infarction).…”

Section: Protectant Of Mitochondrial Membrane Permeabilitymentioning

confidence: 99%

Drugs to cure avian influenza infection – multiple ways to prevent cell death

Yuan

2013

Cell Death Dis

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New treatments and new drugs for avian influenza virus (AIV) infection are developed continually, but there are still high mortality rates. The main reason may be that not all cell death pathways induced by AIV were blocked by the current therapies. In this review, drugs for AIV and associated acute respiratory distress syndrome (ARDS) are summarized. The roles of antioxidant (vitamin C) and multiple immunomodulators (such as Celecoxib, Mesalazine and Eritoran) are discussed. The clinical care of ARDS may result in ischemia reperfusion injury to poorly ventilated alveolar cells. Cyclosporin A should effectively inhibit this kind of damages and, therefore, may be the key drug for the survival of patients with virus-induced ARDS. Treatment with protease inhibitor Ulinastatin could also protect lysosome integrity after the infection. Through these analyses, a large drug combination is proposed, which may hypothetically greatly reduce the mortality rate.

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Cystine rather than cysteine is the preferred substrate for β-elimination by cystathionine γ-lyase: implications for dietary methionine restriction

et al. 2023

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Dietary methionine restriction (MR) increases longevity by improving health. In experimental models, MR is accompanied by decreased cystathionine β-synthase activity and increased cystathionine γ-lyase activity. These enzymes are parts of the transsulfuration pathway which produces cysteine and 2-oxobutanoate. Thus, the decrease in cystathionine β-synthase activity is likely to account for the loss of tissue cysteine observed in MR animals. Despite this decrease in cysteine levels, these tissues exhibit increased H2S production which is thought to be generated by β-elimination of the thiol moiety of cysteine, as catalyzed by cystathionine β-synthase or cystathionine γ-lyase. Another possibility for this H2S production is the cystathionine γ-lyase-catalyzed β-elimination of cysteine persulfide from cystine, which upon reduction yields H2S and cysteine. Here, we demonstrate that MR increases cystathionine γ-lyase production and activities in the liver and kidneys, and that cystine is a superior substrate for cystathionine γ-lyase catalyzed β-elimination as compared to cysteine. Moreover, cystine and cystathionine exhibit comparable Kcat/Km values (6000 M−1 s−1) as substrates for cystathionine γ-lyase-catalyzed β-elimination. By contrast, cysteine inhibits cystathionine γ-lyase in a non-competitive manner (Ki ~ 0.5 mM), which limits its ability to function as a substrate for β-elimination by this enzyme. Cysteine inhibits the enzyme by reacting with its pyridoxal 5′-phosphate cofactor to form a thiazolidine and in so doing prevents further catalysis. These enzymological observations are consistent with the notion that during MR cystathionine γ-lyase is repurposed to catabolize cystine and thereby form cysteine persulfide, which upon reduction produces cysteine.

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Mammal Cells Double Their Total RNAs against Diabetes, Ischemia Reperfusion and Malaria-Induced Oxidative Stress

Cited by 3 publications

References 50 publications

Mitochondrion‐Permeable Antioxidants to Treat ROS‐Burst‐Mediated Acute Diseases

Mitochondrion‐Permeable Antioxidants to Treat ROS‐Burst‐Mediated Acute Diseases

Drugs to cure avian influenza infection – multiple ways to prevent cell death

Cystine rather than cysteine is the preferred substrate for β-elimination by cystathionine γ-lyase: implications for dietary methionine restriction

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