Oxidative Stress: A Unifying Mechanism for Cell Damage Induced by Noise, (Water-Pipe) Smoking, and Emotional Stress-Therapeutic Strategies Targeting Redox Imbalance

Antioxid Redox Signal. 2018 Mar 20;28(9):741-759. doi: 10.1089/ars.2017.7257. Epub 2018 Jan 12.


Significance: Modern technologies have eased our lives but these conveniences can impact our lifestyles in destructive ways. Noise pollution, mental stresses, and smoking (as a stress-relieving solution) are some environmental hazards that affect our well-being and healthcare budgets. Scrutinizing their pathophysiology could lead to solutions to reduce their harmful effects. Recent Advances: Oxidative stress plays an important role in initiating local and systemic inflammation after noise pollution, mental stress, and smoking. Lipid peroxidation and release of lysolipid by-products, disturbance in activation and function of nuclear factor erythroid 2-related factor 2 (Nrf2), induction of stress hormones and their secondary effects on intracellular kinases, and dysregulation of intracellular Ca2+ can all potentially trigger other vicious cycles. Recent clinical data suggest that boosting the antioxidant system through nonpharmacological measures, for example, lifestyle changes that include exercise have benefits that cannot easily be achieved with pharmacological interventions alone.

Critical issues: Indiscriminate manipulation of the cellular redox network could lead to a new series of ailments. An ideal approach requires meticulous scrutiny of redox balance mechanisms for individual pathologies so as to create new treatment strategies that target key pathways while minimizing side effects.

Future directions: Extrapolating our understanding of redox balance to other debilitating conditions such as diabetes and the metabolic syndrome could potentially lead to devising a unifying therapeutic strategy. Antioxid. Redox Signal. 28, 741-759.

Keywords: antioxidants; exercise; mental stress; noise; oxidative stress; smoking.

Publication types

  • Review

MeSH terms

  • Antioxidants / therapeutic use
  • Humans
  • Inflammation / epidemiology
  • Inflammation / etiology
  • Inflammation / physiopathology*
  • Lipid Peroxidation / genetics
  • NF-E2-Related Factor 2 / genetics
  • Noise / adverse effects*
  • Oxidation-Reduction
  • Oxidative Stress / genetics*
  • Reactive Oxygen Species / metabolism
  • Signal Transduction
  • Smoking / adverse effects
  • Stress, Psychological / epidemiology*
  • Stress, Psychological / pathology


  • Antioxidants
  • NF-E2-Related Factor 2
  • NFE2L2 protein, human
  • Reactive Oxygen Species