Protective effect of hydrocortisone on iminodipropionitrile-induced neurotoxicity in rats.
Author: Tariq M, Khan HA, Siddiquei MM, Al Moutaery K, Al Deeb S.
Source:
Basic & clinical pharmacology & toxicology, 100(3), 176-181.
Occupational and environmental exposure of synthetic nitriles is of potential
relevance to human health. Iminodipropionitrile (IDPN), a prototype nitrile
toxin, has been shown to produce dyskinetic syndrome in rodents. This study
reports the effect of concomitant exposure of rats to hydrocortisone and IDPN on
behavioural abnormalities namely excitation, circling and chorea (ECC) syndrome.
Four groups of female Wistar rats were given hydrocortisone (0, 10, 30 and 60
mg/kg, gavage, for 10 days) 30 min. before IDPN (100 mg/kg, intraperitoneally for
8 days). Two additional groups of rats were treated with either saline (control
group) or 60 mg/kg of hydrocortisone (drug alone group). The animals were
observed for neurobehavioural abnormalities including dyskinetic head movement,
circling, tail hanging, air righting reflex and contact inhibition of righting
reflex. After behavioural studies, the animals were killed, and the discrete
brain regions and temporal bones were collected for biochemistry and inner ear
histopathology, respectively. Hydrocortisone significantly and dose dependently
attenuated the incidence and severity of IDPN-induced behavioural syndrome.
Administration of hydrocortisone (60 mg/kg) alone significantly increased
glutathione (GSH) levels in olfactory bulb and striatum, whereas IDPN alone
significantly reduced GSH levels in olfactory bulb, striatum and hippocampus.
Hydrocortisone (60 mg/kg) significantly compensated IDPN-induced depletions of
GSH in different brain regions. Hydrocortisone also protected the animals against
IDPN-induced vestibular hair cell degeneration. The protective effect of
hydrocortisone may be attributed to its anti-inflammatory and antioxidant
properties.