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Adrenocortical metabolism and plasma corticosterone in soman intoxicated rabbits
Abstract:
The organophosphate neurotoxin soman produced impairments in adrenocortical RNA and protein metabolism. Fasciculate and reticular cell RNA and protein contents were suppressed with sublethal to acutely lethal dosages (20, 30 and 40 micrograms/kg, s.c.) during the acute excitatory phase of intoxication and at 6-8 h post injection. All three dosages produced ca 90% inactivation of plasma cholinesterase. A transient elevation of plasma corticosterone occurred with 20 micrograms/kg soman whereas there was a protracted increase with 30 micrograms/kg. Corticosterone was not significantly elevated with 40 micrograms/kg, but death occurred at 13 +/- 4 min. Thus, the magnitude and/or nature of soman-induced metabolic impairments does not appear to prevent adrenal activation.
Insights
Organophosphate soman impairs RNA and protein metabolism in the adrenal cortex. Despite these metabolic changes, the adrenal gland can still activate in response to soman exposure.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Organophosphate compounds, such as soman, are potent neurotoxins.
- Soman exposure can lead to significant disruptions in cellular metabolism and physiological functions.
- Understanding the impact of soman on the adrenal cortex is crucial for developing effective countermeasures.
Purpose of the Study:
- To investigate the effects of soman on adrenocortical RNA and protein metabolism.
- To determine the relationship between soman dosage, metabolic changes, and adrenal activation.
- To assess the impact of soman on plasma cholinesterase and corticosterone levels.
Main Methods:
- Administration of sublethal to acutely lethal doses of soman (20, 30, and 40 µg/kg) to subjects.
- Measurement of RNA and protein content in fasciculate and reticular cells of the adrenal cortex.
- Assay of plasma cholinesterase activity and corticosterone levels at various time points post-injection.
Main Results:
- Soman suppressed RNA and protein content in adrenal cells at all tested dosages.
- All dosages caused approximately 90% inactivation of plasma cholinesterase.
- A transient elevation of plasma corticosterone was observed with 20 µg/kg, and a protracted increase with 30 µg/kg soman.
Conclusions:
- Soman significantly impairs adrenocortical RNA and protein metabolism.
- Despite metabolic disruptions, the adrenal gland demonstrates activation, indicated by corticosterone elevation.
- The observed metabolic impairments do not prevent adrenal activation, suggesting complex toxicological pathways.