Effects of castration and testosterone replacement on peritoneal histamine concentration and lung histamine concentration in pubertal male rats A P Lima, L O Lunardi 1 and A A M Rosa e Silva Department of Physiology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil 1 Department of Morphology, Faculty of Odontology of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil (Requests for offprints should be addressed to A A M Rosa e Silva) Abstract Mast cells, which are the main source of histamine, are significantly affected by sex steroids. The present study was undertaken to determine the effects of bilateral castration and testosterone replacement on peritoneal his- tamine concentration and lung histamine concentration in pubertal male rats (Wistar strain). Three groups of animals were used in this study: (1) untreated castrated animals, (2) castrated animals subjected to androgen replacement by injection of propionate of testosterone, and (3) intact males as a control group. Castration alone produced a dramatic reduction in peritoneal histamine concentration. In addition, androgen replacement was effective in restor- ing the histamine concentration to the normal value detected in the control males (P < 0·05, Kruskal–Wallis test). On the other hand, there was no significant variation in the lung histamine concentration between control males, untreated castrated males and castrated males that received androgen replacement (P < 0·05, Kruskal–Wallis test). These results demonstrate for the first time that castration markedly reduces the peritoneum histamine concentration in pubertal male rats, and testosterone replacement prevents the decrease. Further, these pro- cedures do not affect lung histamine concentration, demonstrating that mast cells from different tissues may respond differently to the same biological factors. Journal of Endocrinology (2000) 167, 71–75 Introduction Mast cells have been studied mainly for their involvement in allergic and inflammatory reactions where they secrete biological mediators in response to immunoglobulin E (IgE) and specific antigens (Ags) (Serafin & Austen 1987). Historically, the classification of rodent mast cell subtypes has been based on phenotypical differences between connective tissue mast cells (CTMC), of which peritoneal mast cells are the most studied example, and mucosal mast cells (MMC), particularly of the intestinal lamina propria and lung (Enerback 1986, Galli 1986, Kitamura et al. 1986). A growing body of evidence suggests that mast cells are regulated by the neuroimmunendocrine system. Many authors have reported that mast cells are significantly affected by sex steroids. In general, it seems that estrogens and androgens exert opposite effects on mast cells in rodents: while estrogens appear to stimulate cell prolifer- ation (Modat et al. 1982, Gaytan et al. 1989, 1990, Jaiswal & Krishna 1996), most studies indicate that testosterone is an inhibitory factor of cell proliferation (Payne et al. 1982, Shirama et al. 1988, Menendez-Pelaez et al. 1992). More- over, sex-associated differences in the number of mast cells have been described in a variety of tissues from rodents, the females having a larger number of mast cells than the males (Payne et al. 1982, Shirama et al. 1988, Menendez- Pelaez et al. 1992). However, the role of androgens and ovarian steroids in the regulation of mast cells is still unclear. Since mast cells are the main source of histamine, the present study was conducted to determine the effects of castration and testosterone replacement on (1) peritoneal histamine concentration and (2) lung histamine concentration in pubertal male rats. Materials and Methods Animals Male rats of the Wistar strain were used in this study. All animals were housed in plastic boxes (40 cm 32 cm17 cm), six animals per cage, in a light- and temperature-controlled room (12 h light:12 h darkness; 22 2 C) with food and water available ad libitum. At the 71 Journal of Endocrinology (2000) 167, 71–75 0022–0795/00/0167–071  2000 Society for Endocrinology Printed in Great Britain Online version via http://www.endocrinology.org