l-Arginine Inhibits Ischemia–Reperfusion Lung Injury in Rabbits

Yoshida, Kazuo; Yoshimura, Kazuhiko; Haniuda, Masayuki

doi:10.1006/jsre.1999.5579

Cited by 10 publications

(2 citation statements)

References 24 publications

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“…Despite optimal lung preservation techniques, the lung remains extremely vulnerable to ischemia-reperfusion (IR) injury (6). IR injury occurs in the context of lung transplantation when blood supply is reintroduced to the ischemic graft at the completion of the implantation procedure (26). The alveolar oxygen represents a cofactor for the generation of reactive oxygen species (ROS), and continuous oxygen supply might thus enhance IR injury (21).…”

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confidence: 99%

“…IR lung injury plays a significant role in clinical situations, including lung transplantation as well as pulmonary thromboendarterectomy, reexpansion of collapsed lungs, and fibrinolysis after lung embolism (21). The pathophysiology of IR injury in the lung involves alveolarcapillary barrier leakage, neutrophil migration, interstitial and alveolar edema, tissue inflammation, and cell injury and death, alteration of nitric oxide synthase (NOS) activity, ROS production, lipid peroxidation, and proinflammation cytokine release (tumor necrosis factor-␣, interferon-␥, and interleukin-1) (26).…”

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Fullerene derivatives protect against oxidative stress in RAW 264.7 cells and ischemia-reperfused lungs

Chen¹,

Hwang²,

Yen³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

109

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. Fullerene derivatives protect against oxidative stress in RAW 264.7 cells and ischemia-reperfused lungs. Am J Physiol Regul Integr Comp Physiol 287: R21-R26, 2004; 10.1152/ajpregu.00310. 2003.-Fullerene derivatives have often been used as effective scavengers for reactive oxygen species (ROS). This study was designed to test whether polyhydroxylated fullerene derivatives [C60(OH)7Ϯ2] protect against oxidative stress in cultured RAW 264.7 cells and ischemia-reperfused (IR) lungs. In RAW 264.7 cells, sodium nitroprusside (SNP, 1 mM) and H 2O2 (400 M) caused a marked (90%) decrease in cell viability, and this decrease was dose dependently reversed by pretreatment with C 60(OH)7Ϯ2 (10-50 M). The increase in ROS production induced by SNP and H 2O2 was significantly suppressed by C 60(OH)7Ϯ2. Also, the decrease in mitochondrial membrane potential induced by SNP and H 2O2 was significantly reversed by C 60(OH)7Ϯ2. However, high concentration of C 60(OH)7Ϯ2 (1 and 1.5 mM) lead to cell death (apoptosis or necrosis). In the isolated rat lung, the increases in pulmonary artery pressure and capillary filtration pressure induced by SNP during IR were reversed significantly by C 60(OH)7Ϯ2 (10 mg/kg). These results indicate that polyhydroxylated fullerene derivatives C 60(OH)7Ϯ2 at low concentrations protect against oxidative stress in RAW 264.7 cells and IR lungs.antioxidants; nitric oxide; reactive oxygen species LUNG TRANSPLANTATION has become an accepted and effective treatment for a variety of end-stage pulmonary diseases (10). Despite optimal lung preservation techniques, the lung remains extremely vulnerable to ischemia-reperfusion (IR) injury (6). IR injury occurs in the context of lung transplantation when blood supply is reintroduced to the ischemic graft at the completion of the implantation procedure (26). The alveolar oxygen represents a cofactor for the generation of reactive oxygen species (ROS), and continuous oxygen supply might thus enhance IR injury (21). IR lung injury plays a significant role in clinical situations, including lung transplantation as well as pulmonary thromboendarterectomy, reexpansion of collapsed lungs, and fibrinolysis after lung embolism (21). The pathophysiology of IR injury in the lung involves alveolarcapillary barrier leakage, neutrophil migration, interstitial and alveolar edema, tissue inflammation, and cell injury and death, alteration of nitric oxide synthase (NOS) activity, ROS production, lipid peroxidation, and proinflammation cytokine release (tumor necrosis factor-␣, interferon-␥, and interleukin-1) (26).Recently, many studies pointed out that IR injury could be attenuated by antioxidant therapy. In 1985, a novel allotrope was reported in which 60 carbon atoms (C 60 ) were arranged as a truncated icosahedron, with 60 vertices and 32 faces, 12 of which were pentagonal and 20 hexagonal (2, 12). Fullerene is a condensed aromatic ring with extended systems (11). Because the inventors commemorated the builder of American Rice University, Buckminister Fuller, C 60 was termed B...

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confidence: 99%

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confidence: 99%

Fullerene derivatives protect against oxidative stress in RAW 264.7 cells and ischemia-reperfused lungs

Chen¹,

Hwang²,

Yen³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

109

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L-Arginine and Ischemia-Reperfusion Injury

Yang

Cai²

2010

Principles of Pulmonary Protection in Heart Surgery

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Epithelial Dysfunction in Lung Diseases: Effects of Amino Acids and Potential Mechanisms

Chen

Jin

Yang

et al. 2020

Advances in Experimental Medicine and Biology

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Lung diseases affect millions of individuals all over the world. Various environmental factors, such as toxins, chemical pollutants, detergents, viruses, bacteria, microbial dysbiosis, and allergens, contribute to the development of respiratory disorders. Exposure to these factors activates stress responses in host cells and disrupt lung homeostasis, therefore leading to dysfunctional epithelial barriers. Despite significant advances in therapeutic treatments for lung diseases in the last two decades, novel interventional targets are imperative, considering the side effects and limited efficacy in patients treated with currently available drugs. Nutrients, such as amino acids (e.g., arginine, glutamine, glycine, proline, taurine, and tryptophan), peptides, and bioactive molecules, have attracted more and more attention due to their abilities to reduce oxidative stress, inhibit apoptosis, and regulate immune responses, thereby improving epithelial barriers. In this review, we summarize recent advances in amino acid metabolism in the lungs, as well as multifaceted functions of amino acids in attenuating inflammatory lung diseases based on data from studies with both human patients and animal models. The underlying mechanisms for the effects of physiological amino acids are likely complex and involve cell signaling, gene expression, and anti-oxidative reactions. The beneficial effects of amino acids are expected to improve the respiratory health and well-being of humans and other animals. Because viruses (e.g., coronavirus) and environmental pollutants (e.g., PM2.5 particles) induce severe damage to the lungs, it is important to determine whether dietary supplementation or intravenous administration of individual functional amino acids (e.g., arginine-HCl, citrulline, N-acetylcysteine, glutamine, glycine, proline and tryptophan) or their combinations to affected subjects may alleviate injury and dysfunction in this vital organ.

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l-Arginine Inhibits Ischemia–Reperfusion Lung Injury in Rabbits

Cited by 10 publications

References 24 publications

Fullerene derivatives protect against oxidative stress in RAW 264.7 cells and ischemia-reperfused lungs

Fullerene derivatives protect against oxidative stress in RAW 264.7 cells and ischemia-reperfused lungs

L-Arginine and Ischemia-Reperfusion Injury

Epithelial Dysfunction in Lung Diseases: Effects of Amino Acids and Potential Mechanisms

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