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Nitric oxide synthase induction and intestinal epithelial cell viability in rats
B L Tepperman1, J F Brown, B J Whittle
1Department of Pharmacology, Wellcome Research Laboratories, Beckenham, Kent, United Kingdom.
The American Journal of Physiology
|August 1, 1993
Summary
Nitric oxide (NO) synthase activity in intestinal epithelial cells increases with induction, reducing cell viability. This damage can be mitigated by dexamethasone or NO synthase inhibitors, suggesting NO induction contributes to intestinal injury.
Area of Science:
- Gastroenterology
- Molecular Biology
- Cell Biology
Background:
- Nitric oxide (NO) plays various roles in the gastrointestinal tract.
- The function of NO synthase (NOS) in intestinal epithelial cells requires further elucidation.
Purpose of the Study:
- To determine constitutive and inducible NO synthase activities in rat intestinal epithelial cells.
- To investigate the impact of NO induction on intestinal epithelial cell viability.
Main Methods:
- Isolated rat proximal small intestinal epithelial cells.
- Measurement of NO synthase activity via [14C]arginine conversion.
- Induction of NO synthase using Escherichia coli lipopolysaccharide (LPS).
- Assessment of cell viability using trypan blue exclusion.
Main Results:
- Constitutive NO synthase activity was detected in intestinal epithelial cells.
- LPS administration significantly increased NO synthase activity, particularly in villus cells.
- Increased NO synthase activity correlated with decreased cellular viability.
- Dexamethasone and NO synthase inhibitors reduced LPS-induced cell damage.
Conclusions:
- While constitutive NO may have physiological roles, inducible NO synthase activity in epithelial cells can lead to intestinal damage.
- Targeting NO synthase may offer therapeutic strategies for intestinal injury.