Serum testosterone and corticosterone levels in acute experimental autoimmune encephalomyelitis (EAE) in male Wistar rats.
OBJECTIVES: Experimental autoimmune encephalomyelitis (EAE) was induced to investigate the levels of circulating total testosterone (TT) and the possible association of corticosterone with the steroid-producing capacity of the testes.
SETTING AND DESIGN: We determined gonad weights, serum TT and corticosterone levels during the development of EAE in male rats.
METHODS: Active EAE was induced in young male Wistar rats by injection of whole myelin in complete Freund's adjuvant. All the rats were weighted and monitored daily for clinical signs and blooded during different phases of the disease. Serum TT was measured by radioimmunoassay and circulating corticosterone was determined using a competitive enzyme immunoassay. Also testes and seminal vesicles were removed to determine their weights.
RESULTS: Seminal vesicle weights and serum TT levels diminished during the acute stage of the disease in all EAE rats and then they began gradually to increase, reaching the normal values at the post-recovery phase. Concomitantly a significant increase in serum corticosterone levels was observed during the acute EAE and the post-recovery phase was accompanied by a decline in corticosterone levels.
MAIN FINDING: Our results indicated an inverse correlation between serum TT and corticosterone levels during the acute EAE. Moreover, the diminution of TT was not a consequence of an alteration of the testes induced by anti-myelin antibodies neither contributed by apoptosis of testis cells by exposure to corticosterone.
CONCLUSIONS: The negative correlation between corticosterone and TT levels associated to EAE may be relevant in understanding the association of the endocrine system and the development of autoimmune demyelinating diseases....
Citation
Macció D, Calfa G, Volosín M, Roth G. Serum testosterone and corticosterone levels in acute experimental autoimmune encephalomyelitis (EAE) in male Wistar rats. Neuro Endocrinol Lett. 2004 Jun; 25(3): 196-200