Deficit of circulating stem--progenitor cells in opiate addiction: a pilot study
Albert S Reece1, Peter Davidson
1Southcity Family Medical Centre, 39 Gladstone Rd,, Highgate Hill, Brisbane, Queensland, 4101, Australia. sreece@bigpond.net.au
Substance Abuse Treatment, Prevention, and Policy
|July 7, 2007
Summary
Addiction significantly lowers endothelial progenitor cells (EPCs), indicating accelerated aging in opiate-dependent individuals. This finding suggests underestimated toxicity of addiction and its treatments.
Area of Science:
- Addiction research
- Toxicology
- Aging
Background:
- Addictive drugs are known to impede cell growth and promote apoptosis.
- Previous research indicates a link between substance use disorder and accelerated aging.
- The impact of addiction on stem cell populations requires further investigation.
Purpose of the Study:
- To compare hematopoietic stem cells (HSCs) and endothelial progenitor cells (EPCs) in opiate-dependent patients versus non-addicted individuals.
- To investigate the potential role of stem cell depletion in addiction-related aging.
- To assess the implications for understanding addiction toxicology and treatment.
Main Methods:
- Flow cytometry was used to analyze peripheral blood samples.
- CD34(+) CD45(+) cells were quantified as HSCs.
- CD34(+) KDR(+) (VEGFR2(+)) cells were quantified as EPCs in 10 patients with substance use disorder (SUD) and 11 non-SUD controls.
Main Results:
- No significant difference was observed in HSC counts between SUD and non-SUD groups.
- EPC counts were significantly lower in the SUD group compared to the non-SUD group (0.09 vs. 0.26 cells/mcl).
- This reduction in EPCs was observed despite the SUD group being significantly younger than the non-SUD group.
Conclusions:
- Reduced EPCs in opiate-dependent individuals suggest accelerated aging.
- Stem cell pool alterations are implicated in addiction toxicology and aging processes.
- The toxicity of addiction and long-term agonist therapies may be underestimated, necessitating policy review.
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