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Types of adrenocorticoids and their effect on organophosphorus-induced delayed neuropathy in chickens
M Ehrich1, B S Jortner, W B Gross
1Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg 24061.
Abstract:
The present study examined the effects of a glucocorticoid and a mineralocorticoid on organophosphorus-induced delayed neuropathy (OPIDN) as previous investigations have indicated that an endogenous steroid with both properties could alter this syndrome in chickens. The glucocorticoid triamcinolone and the mineralocorticoid deoxycorticosterone were provided in the diet beginning 1 day before and continuing 10 days after triortho-tolyl phosphate (TOTP, 360 mg/kg po), phenyl saligenin phosphate (PSP, 2.5 mg/kg im), and diisopropyl phosphorofluoridate (DFP, 1 mg/kg sc). In a manner similar to that seen with corticosterone, a low concentration (0.1 ppm) of triamcinolone reduced and a high concentration (10 ppm) exacerbated clinical signs. Concentrations of deoxycorticosterone under 80 ppm also partially delayed or ameliorated ataxia induced by TOTP, PSP, and DFP, but a combination of 0.1 ppm triamcinolone and 80 ppm deoxycorticosterone was not more effective than triamcinolone alone. Peripheral nerve damage was noted in all chickens given organophosphorus compounds, whether or not they had been given corticoids. Both steroids induced hydroxylase activity, but effects on most other enzyme systems examined were unremarkable. High concentrations of triamcinolone (10 ppm) could, however, also reduce liver cytochrome P450 levels and liver cholinesterase activity. Exacerbation of OPIDN was most notable in chickens under highest stress, as indicated by elevated heterophil-to-lymphocyte ratios. The clinical, pathological, biochemical, and hematological indices of exposure to adrenocorticoids and agents inducing OPIDN in chickens were, therefore, similar for both a synthetic glucocorticoid and the endogenous steroid corticosterone.
Insights
Synthetic glucocorticoids and mineralocorticoids affect organophosphorus-induced delayed neuropathy (OPIDN) in chickens. Low doses of triamcinolone reduced OPIDN signs, while high doses exacerbated them, similar to corticosterone effects.
Area of Science:
- Veterinary Toxicology
- Neuropharmacology
- Endocrinology
Background:
- Organophosphorus-induced delayed neuropathy (OPIDN) is a neurotoxic syndrome.
- Endogenous steroids with glucocorticoid and mineralocorticoid properties may influence OPIDN.
- Previous studies suggest corticosterone alters OPIDN in chickens.
Purpose of the Study:
- To investigate the effects of a synthetic glucocorticoid (triamcinolone) and a mineralocorticoid (deoxycorticosterone) on OPIDN in chickens.
- To compare the effects of synthetic steroids with endogenous corticosterone on OPIDN.
- To assess the impact of these steroids on clinical, pathological, biochemical, and hematological parameters related to OPIDN.
Main Methods:
- Chickens were administered organophosphorus compounds: triortho-tolyl phosphate (TOTP), phenyl saligenin phosphate (PSP), and diisopropyl phosphorofluoridate (DFP).
- Triamcinolone and deoxycorticosterone were administered orally or via diet before and after organophosphorus exposure.
- Clinical signs, peripheral nerve damage, enzyme activities (hydroxylase, cytochrome P450, cholinesterase), and heterophil-to-lymphocyte ratios were evaluated.
Main Results:
- Low-dose triamcinolone (0.1 ppm) reduced OPIDN clinical signs; high-dose (10 ppm) exacerbated them.
- Deoxycorticosterone concentrations below 80 ppm partially ameliorated OPIDN.
- Peripheral nerve damage occurred in all organophosphorus-treated chickens, regardless of steroid administration.
- High-dose triamcinolone reduced liver cytochrome P450 and cholinesterase activity.
- Elevated heterophil-to-lymphocyte ratios indicated increased stress, correlating with OPIDN exacerbation.
Conclusions:
- Synthetic glucocorticoids and mineralocorticoids modulate OPIDN in chickens, mirroring effects of endogenous corticosterone.
- Steroid dosage is critical, with low doses potentially protective and high doses detrimental.
- Stress, indicated by hematological changes, influences the severity of OPIDN exacerbation by steroids.