Cytophotometric assessment of granulosa cell protein and nucleic acid levels during the estrous cycle in rats treated with T-2 toxin

• Published in: Life sciences (1973) Vol. 43; no. 26; p. 2231
• Main Authors: Miller-Patrick, K, Ballough, G P, Wickersham, E W, Anthony, A
• Format: Journal Article
• Language: English
• Published: Netherlands 1988
• Subjects: Animals; DNA - drug effects; DNA - metabolism; Estrus - drug effects; Female; Granulosa Cells - cytology; Granulosa Cells - drug effects; Granulosa Cells - metabolism; Proteins - metabolism; Rats; Rats, Inbred Strains; Reference Values; RNA - drug effects; RNA - metabolism; Sesquiterpenes - pharmacology; T-2 Toxin - pharmacology
• ISSN: 0024-3205
• DOI: 10.1016/0024-3205(88)90416-X

Female Sprague-Dawley rats (160-180g.) with normal estrous cyclicity established by vaginal smears, were injected intraperitoneally with 0.45 mg/kg (low dose) or 0.68 mg/kg (high dose) of T-2 toxin, a trichothecene with potent protein inhibitory abilities. Control animals were injected with only the 100% ethanol vehicle. All animals were decapitated at 8 hours post-exposure, and their ovaries removed and processed for paraffin sectioning. Coomassie, Feulgen, and azure B/DNase staining procedures were used to show granulosa cell protein levels, F-DNA stainability, and basophilia/RNA levels, respectively. Quantification of these parameters was accomplished using scanning-integrating microdensitometry. T-2 toxin treatment groups had granulosa cell protein levels significantly lower than those of the control animals. However, rats exposed to the lower dose of T-2 toxin generally showed a more marked suppression of protein levels than the high dose group, regardless of the stage of the estrous cycle. In addition, rats that received lower doses of T-2 toxin had impaired translation and template activity in response to injury, when compared with the rats in the high dose group. These results are attributed to the lesser degree of circulatory impairment in the low T-2 toxin dosage group, which allows a higher amount of T-2 toxin to interact with the cells.