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Does endogenous zinc protoporphyrin modulate carbon monoxide formation from heme? Implications for long-term
G S Marks1, K Nakatsu, J F Brien
1Department of Pharmacology and Toxicology, Queen's University, Kingston, ON, Canada.
Canadian Journal of Physiology and Pharmacology
|October 1, 1993
Summary
Carbon monoxide (CO) may regulate cell function and communication similarly to nitric oxide. Inhibiting CO formation with zinc protoporphyrin blocks long-term potentiation, suggesting CO
Area of Science:
- Neuroscience
- Biochemistry
- Cellular signaling
Background:
- Carbon monoxide (CO) is an endogenous gas produced from heme breakdown.
- CO shares signaling properties with nitric oxide (NO).
- CO's role in cellular regulation and communication is under investigation.
Purpose of the Study:
- To investigate the potential role of endogenous carbon monoxide in modulating cellular functions.
- To explore the relationship between heme oxygenase activity, CO production, and long-term potentiation (LTP).
Main Methods:
- Utilized zinc protoporphyrin (ZnPP), a heme oxygenase inhibitor.
- Examined the effect of ZnPP on the induction of long-term potentiation.
Main Results:
- Zinc protoporphyrin inhibited the induction of long-term potentiation.
- This suggests that heme oxygenase activity and subsequent CO formation are crucial for LTP.
Conclusions:
- Endogenous carbon monoxide, regulated by heme oxygenase, likely plays a physiological role.
- CO modulates long-term potentiation, potentially impacting memory and cognitive functions.