Β-glucuronidase Activity Is Elevated in the Rat Harderian Gland after Bromocriptine but Decreased after Cyproterone Acetate Treatment or Castration. Postcastrational Effects on the Ultrastructure of the Gland

Objective. To investigate the effect of castration, bromocriptine and cyproterone acetate treatment on lysosomal hydrolytic enzymes and ultrastructure of the rat Harderian gland. Methods. Groups of rats were subjected to the treatment by bromocriptine, cyproterone acetate and castration. Harderian glands were dissected from each experimental animal, cut into small pieces and immediately stored in liquid nitrogen. Only those from castrated animals were fixed in Karnovsky fluid and processed for electron microscopy. The activity of acid phosphatase and βglucuronidase were estimated by kits from Sigma (St. Louis, Mo, USA). Semi-thin sections were stained with 1% toluidine blue and ultra-thin sections with uranyl acetate and counter-stained with lead citrate. The examination was performed by Joel JEM-1200 EX II electron microscope.. Results. The treatment of male rats with the prolactin release inhibitor bromocriptine induced a significant increase in β-glucuronidase activity. On the contrary, such activity was significantly decreased after treatment with the testosterone receptor antagonist cyproterone acetate as well as after castration. However, these treatments did not alter the activity of lysosomal acid phosphatase. Castration induced dramatic changes mostly in type A cells such as the appearance of lipid vacuoles with irregular forms and the predomination of smooth endoplasmic reticulum (SER) throughout the cytoplasm. The most dramatic postcastrational change was the degeneration of the mitochondria. These changes in type A cells might be due to the uneven distribution of the testosterone receptors in the rat Harderian gland which are more numerous in type A cells. Conclusions. the gland physiology is responsive to alteration in circulating prolactin and testosterone levels.