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Ca(2+)-mediated damage to rabbit gastric mucosal cells: modulation by nitric oxide
1Department of Physiology, Faculty of Medicine, University of Western Ontario, London, Canada.
European Journal of Pharmacology
|October 6, 1995
Summary
Inhibiting nitric oxide (NO) synthase in gastric cells worsens calcium-induced damage. This increased cell injury from NG-monomethyl-L-arginine is linked to altered calcium flux, not oxidative stress.
Area of Science:
- Cell Biology
- Gastroenterology
- Biochemistry
Background:
- Cellular calcium (Ca2+) homeostasis is crucial for cell function.
- Nitric oxide (NO) is known to scavenge reactive oxygen species.
- Disruptions in Ca2+ can lead to oxidative stress and cell damage.
Purpose of the Study:
- To investigate the effects of inhibiting nitric oxide (NO) synthase on Ca2+-mediated damage in rabbit gastric mucosal cells.
- To determine the role of oxidative stress and Ca2+ flux in this process.
Main Methods:
- Rabbit gastric mucosal cells were treated with the Ca2+ ionophore A23187.
- Nitric oxide synthase activity was inhibited using NG-monomethyl-L-arginine (NMA).
- Cell damage was assessed by trypan blue uptake and metabolic activity; Ca2+ levels and oxidative stress were measured using fluorescence indicators.
Main Results:
- A23187 induced concentration-dependent cell damage, which was worsened by NMA.
- NO donors ameliorated the damaging effects of A23187 and NMA.
- NMA exacerbated A23187-induced increases in cytosolic Ca2+ and oxidative stress, but the combined cytotoxic effect was not reduced by oxygen radical scavengers.
Conclusions:
- NO synthase inhibition exacerbates Ca2+ ionophore-induced damage in gastric mucosal cells.
- The increased cell damage from NMA is not primarily mediated by oxidative stress but may involve altered cellular Ca2+ flux.