Buerger's disease in young men who started smoking in teen age!
In few countries Buerger's disease affecting the small blood vessels in the leg disappeared, but in the other countries it is still a problem. This disease is more often noted in the rural population or societies where childhood or teenage smoking is a problem. It gives us the suspicion that the endothelium may be responding in different ways depending on the age, but that fact was not tested and published till now. Here is one paper trying the test that hypothesis in rats.
Cigarette smoke causes oxidative stress in the lung
resulting in injury and disease. The purpose of this study was to determine if
there were age-related differences in cigarette smoke extract (CSE)-induced
production of reactive species in single and co-cultures of alveolar epithelial
type I (AT I) cells and microvascular endothelial cells harvested from the
lungs (MVECLs) of neonatal, young and old male Fischer 344 rats.
Cultures of AT I cells and MVECLs grown separately (single
culture) and together (co-culture) were exposed to CSE (1, 10, 50, 100%).
Cultures were assayed for the production of intracellular reactive oxygen
species (ROS), hydroxyl radical (OH), peroxynitrite (ONOO(-)), nitric oxide
(NO) and extracellular hydrogen peroxide (H(2)O(2)). Single and co-cultures of
AT I cells and MVECLs from all three ages produced minimal intracellular ROS in
response to CSE. All ages of MVECLs produced H(2)O(2) in response to CSE, but
young MVECLs produced significantly less H(2)O(2) compared to neonatal and old
MVECLs. Interestingly, when grown as a co-culture with age-matched AT I cells,
neonatal and old MVECLs demonstrated ~50% reduction in H(2)O(2) production in response
to CSE. However, H(2)O(2) production in young MVECLs grown as a co-culture with
young AT I cells did not change with CSE exposure.
To begin investigating for a
potential mechanism to explain the reduction in H(2)O(2) production in the
co-cultures, we evaluated single and co-cultures for extracellular total
antioxidant capacity. We also performed gene expression profiling specific to
oxidant and anti-oxidant pathways. The total antioxidant capacity of the AT I
cell supernatant was ~5 times greater than that of the MVECLs, and when grown
as a co-culture and exposed to CSE (≥ 10%), the total antioxidant capacity of
the supernatant was reduced by ~50%. There were no age-related differences in
total antioxidant capacity of the cell supernatants. Gene expression profiling
found eight genes to be significantly up-regulated or down-regulated. This is
the first study to describe age-related differences in MVECLs exposed to CSE.
Microvasc Res. 2011 Nov;82(3):311-7. Epub
2011 Oct 6.
