PMID- 1446622 OWN - NLM STAT- MEDLINE DCOM- 19921230 LR - 20181130 IS - 0013-7227 (Print) IS - 0013-7227 (Linking) VI - 131 IP - 6 DP - 1992 Dec TI - Leydig cell peroxisomes and sterol carrier protein-2 in luteinizing hormone-deprived rats. PG - 2839-45 AB - We investigated the effects of 8 days of LH withdrawal on rat Leydig cell peroxisomal volume, total and intraperoxisomal catalase and sterol carrier protein-2 (SCP2) contents, and LH-stimulated testosterone secretion in vitro. Three groups of adult male Sprague-Dawley rats, i.e. control, TE-implanted (testosterone-17 beta-estradiol-filled Silastic implants to suppress LH), and TELH-implanted (TE-implanted and LH replacement via Alzet mini osmotic pumps), were used. After 8 days, Leydig cell organelle volumes (stereology), intraperoxisomal catalase and SCP2 contents (immunocytochemistry), LH-stimulated testosterone secretion by isolated Leydig cells in vitro (determined by RIA), and total catalase and SCP2 contents in equal numbers of Leydig cells (immunoblot analyses) were determined. Results showed that the TELH-implanted rats were identical to controls in every parameter tested. Testis volume and Leydig cell number per testis in control and TE-implanted rats were not significantly different; however, reductions (P < 0.05) were observed in the average volume of a Leydig cell (one third of controls) and the volume of Leydig cells per testis. All Leydig cell organelle volumes tested were significantly lower in TE-implanted rats than in the controls; however, the volumes of smooth endoplasmic reticulum (SER) and peroxisomes were the most reduced (lowered to one sixth of control values). LH-stimulated testosterone secretion per Leydig cell in vitro correlated well with these changes in the volumes of Leydig cell SER and peroxisomes. Intraperoxisomal catalase in Leydig cells was unchanged in TE-implanted rats, although immunoblotting demonstrated a loss of total catalase content (which reflected the reduction in the volume of peroxisomes). SCP2 in Leydig cells of TE-implanted rats was undetectable with immunoblot analysis (explained by the reductions in Leydig cell peroxisome volume and intraperoxisomal SCP2). These results demonstrate that the organelles SER and peroxisomes and the protein SCP2 in Leydig cells are more LH dependent than the other organelles (e.g. mitochondria, lysosomes) and protein catalase, respectively. Moreover, the findings of this study are consistent with the hypothesis that Leydig cell peroxisomes play a significant role in testosterone production. FAU - Mendis-Handagama, S M AU - Mendis-Handagama SM AD - Department of Population Dynamics, Johns Hopkins School of Hygiene and Public Health, Kennedy Institute, Baltimore, Maryland 21205. FAU - Watkins, P A AU - Watkins PA FAU - Gelber, S J AU - Gelber SJ FAU - Scallen, T J AU - Scallen TJ LA - eng GR - F32-DK-08312-02/DK/NIDDK NIH HHS/United States GR - HD-07204/HD/NICHD NIH HHS/United States PT - Journal Article PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Endocrinology JT - Endocrinology JID - 0375040 RN - 0 (Carrier Proteins) RN - 0 (Plant Proteins) RN - 0 (Sterols) RN - 0 (sterol carrier proteins) RN - 3XMK78S47O (Testosterone) RN - 4TI98Z838E (Estradiol) RN - 9002-67-9 (Luteinizing Hormone) RN - EC 1.11.1.6 (Catalase) SB - IM MH - Animals MH - Carrier Proteins/*metabolism MH - Catalase/metabolism MH - Estradiol/pharmacology MH - Immunoblotting MH - Leydig Cells/drug effects/*metabolism/*ultrastructure MH - Luteinizing Hormone/*administration & dosage/pharmacology MH - Male MH - Microbodies/enzymology/*ultrastructure MH - Organelles/drug effects/ultrastructure MH - *Plant Proteins MH - Rats MH - Rats, Sprague-Dawley MH - Sterols/*metabolism MH - Testis/anatomy & histology/drug effects MH - Testosterone/metabolism/pharmacology EDAT- 1992/12/01 00:00 MHDA- 1992/12/01 00:01 CRDT- 1992/12/01 00:00 PHST- 1992/12/01 00:00 [pubmed] PHST- 1992/12/01 00:01 [medline] PHST- 1992/12/01 00:00 [entrez] AID - 10.1210/endo.131.6.1446622 [doi] PST - ppublish SO - Endocrinology. 1992 Dec;131(6):2839-45. doi: 10.1210/endo.131.6.1446622.