Leukotriene C4 is the major trigger of stress-induced oxidative DNA damage

Dvash, Efrat; Har-Tal, Michal; Barak, Sara; Meir, Ofir; Rubinstein, Menachem

doi:10.1038/ncomms10112

Cited by 92 publications

(88 citation statements)

References 67 publications

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“…Other examples, which are connected to H 2 O 2 transit across the ER membrane, are granulocyte colonystimulating factor receptor signaling [29], oxidative DNA damage in response to cellular stresses [30][31][32], activation of survival pathways upon H 2 O 2 generation in the ER [33,34], and the regulatory roles of ER-luminal peroxidases in various settings of cytosolic signal transduction [29,[35][36][37][38]. These findings clearly indicate the permeability of the ER membrane for H 2 O 2 .…”

Section: H 2 O 2 Can Readily Permeate Through the Endoplasmic Reticulmentioning

confidence: 97%

Transit of H2O2 across the endoplasmic reticulum membrane is not sluggish

Appenzeller-Herzog¹,

Bánhegyi

Bogeski

et al. 2016

Free Radical Biology and Medicine

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Section: H 2 O 2 Can Readily Permeate Through the Endoplasmic Reticulmentioning

confidence: 97%

Transit of H2O2 across the endoplasmic reticulum membrane is not sluggish

Appenzeller-Herzog¹,

Bánhegyi

Bogeski

et al. 2016

Free Radical Biology and Medicine

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“…However, the level of NOX4 under extensive ER stress is greatly reduced using LTC 4 antagonists. LTC 4 receptor antagonists also attenuated cell death and mouse morbidity (32). Now, LTC 4 inhibitors are widely used in the clinical treatment of asthma.…”

Section: -Lipoxygenase (5-lo) 5-lo Activating Protein (Flap) Andmentioning

confidence: 99%

“…Leukotriene C4 (LTC 4 ) can elicit nuclear translocation of NADPH oxidase 4 (NOX4), ROS accumulation and oxidative DNA damage. LTC 4 inhibitors, which are used clinically for asthma, were associated with endoplasmic reticulum (ER) stress activated NOX4 (32). It is interesting that NADPH oxidase 2 (Nox2) deficiency results in induced experimental asthma, which is caused by aggravate Th2 effector function in a T cell intrinsic manner; however, the underlying mechanism must be studied further (32).…”

Section: Endogenous Oxidants and Allergic Asthmamentioning

confidence: 99%

Recent developments in the role of reactive oxygen species in allergic asthma

Zhong

et al. 2017

J. Thorac. Dis.

131

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Allergic asthma has a global prevalence, morbidity, and mortality. Many environmental factors, such as pollutants and allergens, are highly relevant to allergic asthma. The most important pathological symptom of allergic asthma is airway inflammation. Accordingly, the unique role of reactive oxygen species It is well known that reactive oxygen species (ROS), endogenous nitric oxide (NO) and NO derived reactive nitrogen species (RNS) have been reported to mediate oxidative stress and airway inflammation and pathogenesis. However, ROS are more common in allergic asthma development (6,7). Hence, in our review, we mainly focus on the relationship between ROS and allergic asthma. ROS, such as hydrogen peroxide, may be directly or indirectly involved in epithelial cell apoptosis and inactivation of antioxidant enzymes and contribute to allergic asthma (8-11). ROS are derived from endogenous or exogenous oxidants. Endogenous ROS are composed of mitochondria, NADPH, and the xanthine/xanthine oxidase (XO) system. Exogenous sources of ROS production have been linked to strong oxidizing gases, such as ozone (O 3 ), sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ) and particulate matter (PM), which are a major component of air pollution (12,13). The oxygen stress level in asthma is increased because of inflammatory cells in vivo, and cigarette smoke (CS) or PM produces ROS in vitro. For example, compared with normal subjects, the level of H 2 O 2 and superoxide that are produced by eosinophils and neutrophils are significantly increased in asthma patients (14). Increased levels of ROS can cause harmful pathophysiological disorders of allergic asthma. Studies have reported that excessive ROS can damage DNA, carbohydrates, proteins, and lipids, ultimately leading to an increased inflammatory response in allergic asthma (15,16). In this review, we will discuss the updated pathophysiological and mechanisms of oxidative stress relating to allergic asthma. Exogenous oxidants and allergic asthmaPatients' exposure to the environmental atmosphere is the main way that exogenous oxidative stress is induced (17). CS is a complex mixture including more than 4,000 different compounds. It has been demonstrated that inhaled CS can increase ROS levels. Most of these compounds have ability to generate ROS during their metabolism. The mechanism of CS induced inflammation is incorporated with oxidative stress leading to cell death and oxidative DNA damage via apoptosis and/or necrosis (7). It was reported that antioxidants have the ability to protect cells from cigarette smoke extract (CSE) induced apoptosis (18). Isolated human airway smooth muscle (hASM) cells were used to determine Ca 2+ responses and hASM proliferation, as well as ROS level and cytokine generation, by incubating these cells in the presence or absence of CSE. The results revealed that Ca 2+ regulatory proteins alter airway remolding and function in smoking-related airway disease, especially allergic asthma (19). CSE can damage bronchial epithelial cells from asthm...

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“…However, most chemotherapeutic drugs kill the tumor cells and those proliferating cells non-selectively [3,4], so it often leads to serious injury to normal tissues [5][6][7][8][9]. For example, chemotherapy generates a large amount of excess reactive oxygen species (ROS) in the bone marrow that would result in a random damage to the hematopoietic tissues [10,11], leading to serious myelosuppression [12][13][14] as well as severe injury of some normal organs [15,16].…”

Section: Introductionmentioning

confidence: 99%

A novel bone marrow targeted gadofullerene agent protect against oxidative injury in chemotherapy

et al. 2017

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Chemotherapy as an effective cancer treatment technique has been widely used in tumor therapy. However, it is still a challenge to overcome the serious side effects of chemotherapy, especially for its myelotoxicity. Here we report a novel strategy using the water soluble gadofullerene nanocrystals (GFNCs) to protect against chemotherapy injury in hepatocarcinoma bearing mice, which was induced by the commonly chemotherapeutic agent cyclophosphamide (CTX). The GFNCs were revealed to specifically accumulate in the bone marrow after intravenously injecting to mice and they exhibited excellent radical scavenging function, resulting in a prominent increase of mice blood cells and pathological improvements of the primary organs in the GFNCs (15 mg kg ) therapy. Moreover, the GFNCs maintained and even strengthened the antineoplastic activity of the CTX agent. Therefore, the GFNCs would be the promising chemoprotective agents in chemotherapy based on their high efficiency, low toxicity and metabolizable property.

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Leukotriene C4 is the major trigger of stress-induced oxidative DNA damage

Cited by 92 publications

References 67 publications

Transit of H2O2 across the endoplasmic reticulum membrane is not sluggish

Transit of H2O2 across the endoplasmic reticulum membrane is not sluggish

Recent developments in the role of reactive oxygen species in allergic asthma

A novel bone marrow targeted gadofullerene agent protect against oxidative injury in chemotherapy

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