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Hypoxia Enhances Oxidative Stress in Neutrophils from ZZ Alpha-1 Antitrypsin Deficiency Patients. | LitMetric

AI Article Synopsis

  • Alpha-1 antitrypsin deficiency (AATD) is linked to inflammation, hypoxia, and increased oxidative stress, which can lead to tissue damage.
  • Research shows that neutrophils from AATD patients (ZZ genotype) produce more reactive oxygen/nitrogen species (ROS/RNS) and have lower levels of key antioxidant enzymes compared to healthy controls (MM genotype).
  • The findings suggest that ZZ-AATD neutrophils are more affected by hypoxic conditions, indicating potential for antioxidant therapies to alleviate the oxidative damage associated with the disorder.

Article Abstract

Alpha-1 antitrypsin deficiency (AATD) is a neutrophilic inflammatory disorder that may result in local hypoxia, reactive oxygen and nitrogen species (ROS/RNS) production, and increased damage in adjacent tissues. This study aims to determine the impact of hypoxia on neutrophil oxidative stress profile in AATD patients. Neutrophils were isolated from AATD patients and control volunteers and exposed to hypoxia (1% O for 4 h), ROS/RNS, mitochondrial parameters, and non-enzymatic antioxidant defenses measured by flow cytometry. The expression of enzymatic antioxidant defenses was determined by qRT-PCR. Our results indicate that ZZ-AATD neutrophils produce higher amounts of hydrogen peroxide, peroxynitrite, and nitric oxide and decreased levels of the antioxidant enzymes catalase, superoxide dismutase, and glutathione reductase. Likewise, our results show a decrease in mitochondrial membrane potential, indicating that this organelle could be involved in the production of the reactive species observed. No decrease in glutathione and thiol levels were observed. The accumulation of substances with high oxidative capacity would explain the greater oxidative damage observed in proteins and lipids. In conclusion, our results indicate that, compared to MM control individuals, ZZ-AATD neutrophils show increased ROS/RNS production under hypoxic conditions opening a new rationale for using antioxidant therapies to treat the disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10135227PMC
http://dx.doi.org/10.3390/antiox12040872DOI Listing

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