Abstract

Pathologic findings, lectin histochemistry, and nuclear estrogen receptors were studied in the reproductive organs of gilts treated with clenbuterol. A ration containing 1 ppm of clenbuterol was fed for 40 days to four Landrace x Large white, 9-month-old gilts, weighing 134 to 172 kg at slaughter (gilt Nos. 5-8). Four gilts (Nos. 1-4) served as controls. Treated animals had macroscopic lesions characterized by microcystic ovaries and uterine atrophy. Histopathologic lesions included atretic degeneration of many ovarian follicles, complete absence of functional corpora lutea, a reduction in the number of endometrial glands, and a decrease in cytoplasmic volume of endometrial and glandular epithelial cells. In ovaries, uterus, and vagina lectin histochemistry, performed with thirteen different biotinylated lectins, revealed a different staining distribution between control and treated gilts. The binding pattern of Ricinus communis agglutinin-I (RCA-I) and -II (RCA-II) in the ovaries of control gilts, displayed labeling of cytoplasm in theca interna cells of Graafian follicles. There was no labeling of the same cells in treated gilts. Labeling patterns with Griffonia simplicifolia agglutinin-I (GS-I), Phaseolus vulgaris agglutinin (PHA), RCA-I and RCA-II documented a difference in the vascularity of the theca interna between Graafian follicles of control and treated gilts. The GS-I and Ulex europaeus agglutinin-I (UEA-I) binding patterns in uterus and vagina of treated gilts when compared to control gilts suggested that there was a block of the cycling activity in the proliferative stage. Immunohistochemical staining for estrogen receptors in the endometrium was positive in all but one treated gilts, and negative to weakly positive in control gilts. Serum progesterone concentrations were decreased in treated animals when compared to control; estradiol concentrations were similar in both group of gilts. Cystic ovaries, uterine atrophy, and reduction in progesterone concentrations suggested that clenbuterol changed ovarian hormonal activity in treated animals.

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