Oxidative stress stimulation leads to cell-specific oxidant and antioxidant responses in airway resident and inflammatory cells

Bilgic, Hayriye Akel; Kilic, Busra; Kockaya, Berfin Doga; Sarac, Basak Ezgi; Süloğlu, Aysun Kılıç; Kalaycı, Ömer; Karaaslan, Çağatay

doi:10.1016/j.lfs.2022.121358

Cited by 12 publications

(5 citation statements)

References 41 publications

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Section: Methodsmentioning

confidence: 99%

“…All examined oxidative stress markers were determined using a commercially available kits from Cayman (Cayman Chemical Company, Michigan, United States) according to the manufacturer standard procedures. [11][12][13][14] The results were expressed as μM/g of tissue (LPO), μM/g of tissue (GSH levels) and IU/g of tissue (CAT and SOD activity).…”

Section: Assessment Of the Oxidative Stress Markersmentioning

confidence: 99%

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N‐acetylcysteine as a potentially safe adjuvant in the treatment of neurotoxicity due to pirimiphos‐methyl poisoning

Piotr,

Konrad,

Hubert

et al. 2024

Basic Clin Pharma Tox

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Exogenous, well‐established antioxidant N‐acetylcysteine can reduce or prevent the deleterious effects of pesticides. In this study, utilizing a mouse model of daily single dose of N‐acetylcysteine administration, we investigated the impact of this adjuvant on the treatment with atropine and/or obidoxime as well as oxidative stress response in pyrimiphos‐methyl‐induced toxicity. We found that N‐acetylcysteine significantly reduces the oxidative stress generated by pyrimiphos‐methyl. The therapy consisting of atropine and/or obidoxime routinely used in organophosphorous insecticide poisonings, including pyrimiphos‐methyl, had no effect on the antioxidant properties of N‐acetylcysteine. Adjunctive treatment offered by N‐acetylcysteine fills therapeutic gap and may provide the full potential against pyrimiphos‐methyl‐induced toxicity.

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Section: Methodsmentioning

confidence: 99%

Section: Assessment Of the Oxidative Stress Markersmentioning

confidence: 99%

N‐acetylcysteine as a potentially safe adjuvant in the treatment of neurotoxicity due to pirimiphos‐methyl poisoning

Piotr,

Konrad,

Hubert

et al. 2024

Basic Clin Pharma Tox

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“…Airway inflammation and airway altitude sickness (AHR) are the core link in the pathological changes and recurrent attacks of asthma ( 89 ). Asthma is a chronic airway inflammatory disease that is closely associated with inflammatory cell infiltration (lymphocytes, mast cells, eosinophils, neutrophils), type II cytokine secretion (IL-4, IL-13, IL-5), and airway epithelial cell damage ( 90 , 91 ).Oxidative stress response is closely associated with inflammation and AHR ( 92 ). Multiple markers of lipid peroxidation have been identified in patients with asthma, further suggesting that the pathophysiology of asthma is associated with ferroptosis ( 93 ).…”

Section: Ferroptosis In Pulmonary Diseasementioning

confidence: 99%

A deep insight into ferroptosis in lung disease: facts and perspectives

Zhang,

Xiang,

et al. 2024

Front. Oncol.

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In the last decade, ferroptosis has received much attention from the scientific research community. It differs from other modes of cell death at the morphological, biochemical, and genetic levels. Ferroptosis is mainly characterized by non-apoptotic iron-dependent cell death caused by iron-dependent lipid peroxide excess and is accompanied by abnormal iron metabolism and oxidative stress. In recent years, more and more studies have shown that ferroptosis is closely related to the occurrence and development of lung diseases. COPD, asthma, lung injury, lung fibrosis, lung cancer, lung infection and other respiratory diseases have become the third most common chronic diseases worldwide, bringing serious economic and psychological burden to people around the world. However, the exact mechanism by which ferroptosis is involved in the development and progression of lung diseases has not been fully revealed. In this manuscript, we describe the mechanism of ferroptosis, targeting of ferroptosis related signaling pathways and proteins, summarize the relationship between ferroptosis and respiratory diseases, and explore the intervention and targeted therapy of ferroptosis for respiratory diseases.

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“…The plasma glutathione peroxidase activity was measured by means of the Glutathione Peroxidase Assay Kit (Cayman Chemical), which measures the GPx activity via a coupled reaction with glutathione reductase [32]. Briefly, samples (20 µL) were incubated in an assay buffer (100 µL Tris-EDTA) and in a co-substrate mixture, which contained NADPH, glutathione, and glutathione reductase (50 µL).…”

Section: Quantification Of the Glutathione Peroxidase Activity (Gpx) ...mentioning

confidence: 99%

Effects of Acetyl-L-Carnitine on Oxidative Stress in Amyotrophic Lateral Sclerosis Patients: Evaluation on Plasma Markers and Members of the Neurovascular Unit

Grossini,

De Marchi,

Venkatesan

et al. 2023

Antioxidants

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Oxidative stress, the alteration of mitochondrial function, and the neurovascular unit (NVU), play a role in Amyotrophic Lateral Sclerosis (ALS) pathogenesis. We aimed to demonstrate the changes in the plasma redox system and nitric oxide (NO) in 32 new ALS-diagnosed patients in treatment with Acetyl-L-Carnitine (ALCAR) compared to healthy controls. We also evaluated the effects of plasma on human umbilical cord-derived endothelial vascular cells (HUVEC) and astrocytes. The analyses were performed at the baseline (T0), after three months (T1), and after six months (T2). In ALS patients at T0/T1, the plasma markers of lipid peroxidation, thiobarbituric acid reactive substances (TBARS) and 4-hydroxy nonenal (4-HNE) were higher, whereas the antioxidants, glutathione (GSH) and the glutathione peroxidase (GPx) activity were lower than in healthy controls. At T2, plasma TBARS and 4-HNE decreased, whereas plasma GSH and the GPx activity increased in ALS patients. As regards NO, the plasma levels were firmly lower at T0–T2 than those of healthy controls. Cell viability, and mitochondrial membrane potential in HUVEC/astrocytes treated with the plasma of ALS patients at T0–T2 were reduced, while the oxidant release increased. Those results, which confirmed the fundamental role of oxidative stress, mitochondrial function, and of the NVU in ALS pathogenesis, can have a double meaning, acting as disease markers at baseline and potential markers of drug effects in clinical practice and during clinical trials.

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Oxidative stress stimulation leads to cell-specific oxidant and antioxidant responses in airway resident and inflammatory cells

Cited by 12 publications

References 41 publications

N‐acetylcysteine as a potentially safe adjuvant in the treatment of neurotoxicity due to pirimiphos‐methyl poisoning

N‐acetylcysteine as a potentially safe adjuvant in the treatment of neurotoxicity due to pirimiphos‐methyl poisoning

A deep insight into ferroptosis in lung disease: facts and perspectives

Effects of Acetyl-L-Carnitine on Oxidative Stress in Amyotrophic Lateral Sclerosis Patients: Evaluation on Plasma Markers and Members of the Neurovascular Unit

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