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Lindane effect upon the vasoactive intestinal peptide receptor/effector system in rat enterocytes
I Carrero1, M D Fernández-Moreno, M A Pérez-Albarsanz
1Departmento de Bioquímica y Biología Molecular, Universidad de Alcalá, Alcalá de Henares-Madrid, Spain.
Biochemical and Biophysical Research Communications
|March 31, 1989
Summary
The insecticide lindane significantly reduces the effectiveness of vasoactive intestinal peptide (VIP) in stimulating cyclic AMP in rat cells. This inhibition is specific to certain lindane isomers and may involve changes in cell membrane fluidity or protein kinase C activation.
Area of Science:
- Toxicology
- Cell Biology
- Neuroendocrinology
Background:
- Vasoactive intestinal peptide (VIP) is a crucial neuropeptide regulating cellular functions, including cyclic AMP (cAMP) accumulation.
- Insecticides, such as lindane, can interfere with normal physiological processes in target organisms.
- Enterocytes play vital roles in nutrient absorption and signaling within the gastrointestinal tract.
Purpose of the Study:
- To investigate the impact of the insecticide lindane on VIP-stimulated cAMP accumulation in isolated rat enterocytes.
- To determine the dose- and time-dependency of lindane's effect.
- To explore the potential mechanisms underlying lindane's inhibitory action.
Main Methods:
- Isolated rat enterocytes were incubated with varying concentrations and durations of lindane.
- The accumulation of cyclic AMP in response to VIP stimulation was measured.
- The binding affinity of VIP to its receptors was assessed.
- The effects of different hexachlorocyclohexane (HCCH) isomers and related compounds were compared.
Main Results:
- Lindane significantly inhibited VIP-induced cAMP accumulation in a time- and dose-dependent manner.
- Optimal inhibition occurred after 5 minutes of incubation with 0.5 mM lindane.
- The inhibitory effect was specific to lindane (gamma-HCCH) and endrin, while alpha-HCCH showed a similar pattern and beta-HCCH and dieldrin were inactive.
- Inhibition was not due to reduced VIP receptor binding.
- Potential mechanisms include altered membrane fluidity or Ca2+-dependent protein kinase C activation.
Conclusions:
- Lindane disrupts VIP signaling in rat enterocytes by inhibiting cAMP accumulation.
- The insecticide's action is isomer-specific and does not involve direct interference with VIP receptor binding.
- Proposed mechanisms involve modulation of membrane properties or activation of intracellular signaling pathways like protein kinase C.