Male Sprague-Dawley rats (200 g) were injected intraperitoneally with T-2 toxin, a trichothecene mycotoxin protein synthesis inhibitor, at dosages of 0.75, 1.0, 1.5, and 6.0 mg/kg (1 LD50 = 0.9 mg/kg) before decapitation at 8-hr postexposure. Correlative data were obtained on changes in physicochemical properties of nuclear chromatin, chromatin dispersion, and nuclear volume of cerebrocortical (layer III) and striatal neurons using Feulgen-DNA (F-DNA) cytophotometry and ocular filar micrometry. Decreased lability of neurons to F-DNA acid hydrolysis (reduced F-DNA yield), nuclear shrinkage, and chromatin aggregation (decreased chromophore area) were used as indices of suppression of genomic template activity, i.e., neuronal nuclear functioning. Conversely, increased F-DNA yield, chromophore area, and nuclear volume signify enhanced neuronal activation. At 8 hr following T-2 toxin exposure, cerebrocortical and striatal neurons exhibited a dose-dependent decrease in F-DNA hydrolyzability, i.e., impaired chromatin activity, and increases in both chromatin dispersion and nuclear volume. Microscopic observation revealed no gross evidence of T-2 induced neurotoxicity. These data indicate that T-2 toxin elicits both neurochemical injury and adaptive or compensatory processes simultaneously. The toxicological importance of observed nuclear alterations and the role of impairments in central nervous system metabolism in acute T-2 toxicity remain to be ascertained.
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