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Related Concept Videos

Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.
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Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
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Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
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Updated: Jun 11, 2026

A Protocol for Detecting and Scavenging Gas-phase Free Radicals in Mainstream Cigarette Smoke
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Published on: January 2, 2012

Cigarette smoke and human plasma lycopene depletion.

D L Graham1, M Carail, C Caris-Veyrat

  • 1School of Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Byrom Street, Liverpool L3 3AF, UK.

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|July 13, 2010
PubMed
Summary
This summary is machine-generated.

Smokers have lower plasma carotenoid levels. Cigarette smoke exposure directly reduces lycopene and beta-carotene concentrations in plasma and LDL, suggesting smoke inhalation causes these deficiencies.

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Published on: February 21, 2011

Area of Science:

  • Biochemistry
  • Toxicology
  • Nutritional Science

Background:

  • Smokers exhibit lower plasma carotenoid concentrations compared to non-smokers.
  • This reduction may stem from dietary changes or direct effects of cigarette smoke on plasma carotenoids.
  • Reactive nitrogen species from cigarette smoke may enter plasma and modify low-density lipoprotein (LDL), decreasing carotenoid levels.

Purpose of the Study:

  • To investigate the direct impact of cigarette smoke on plasma carotenoid concentrations.
  • To determine the susceptibility of different carotenoids (lycopene isomers and beta-carotene) to cigarette smoke exposure in plasma and LDL.

Main Methods:

  • Treatment of lycopene solutions, human plasma, and isolated LDL with cigarette smoke.
  • Monitoring the depletion of all-(E)-lycopene, 5(Z)-lycopene, and beta-carotene.
  • Comparison of effects with Sin-1 reactions to identify common mechanisms.

Main Results:

  • In plasma, all-(E)-lycopene showed greater depletion (15.0%) than 5(Z)-lycopene (10.4%) or beta-carotene (12.4%).
  • In LDL, both all-(E)-lycopene (20.8%) and 5(Z)-lycopene (15.4%) were more susceptible to depletion than beta-carotene (11.5%).
  • Isomerization of all-(E)-lycopene was observed in both smoke and Sin-1 treatments.

Conclusions:

  • Low plasma lycopene concentrations in smokers may be a direct consequence of smoke inhalation.
  • Cigarette smoke exposure directly degrades carotenoids, particularly lycopene, in plasma and LDL.
  • Reactive nitrogen species in cigarette smoke likely contribute to carotenoid modification and depletion.