| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
* To whom correspondence should be addressed. E-mail: lluo{at}jhsph.edu.
Previous studies have shown that testosterone production by the Leydig cells of aged Brown Norway rats is reduced from the relatively high levels produced by Leydig cells of young rats, and that this reduction is not secondary to decreased serum luteinizing hormone (LH) concentration. The free radical theory of aging proposes that imbalance between pro-oxidants and the antioxidant defense system ultimately results in oxidative damage to cellular processes. With this in mind, we hypothesized herein that age-related reductions in steroidogenesis by Brown Norway rat Leydig cells may be associated with the impairment of the antioxidant defense system of these cells. To begin to test this hypothesis, we compared the activities and steady-state mRNA and protein levels of the antioxidant enzymes CuZn superoxide dismutaste (CuZnSOD, SOD1), Mn superoxide dismutase (MnSOD, SOD2) and glutathione peroxidase (GPx), and the levels of reduced (GSH) and oxidized (GSSG) glutathione in Leydig cells isolated from the testes of young (4 month-old) and aged rats (20 month-old) Brown Norway rats. For some studies, Leydig cells were isolated separately from aged testes that either had regressed because of age-related losses of germ cells, or were non-regressed. SOD (total) and GPx activities were found to decrease significantly with age whether or not the testes were regressed. CuZnSOD and MnSOD mRNA levels decreased with aging, though the magnitude of the decreases were considerably less than the respective decreases in enzyme activities. GPx mRNA levels also decreased, consistent with the decreases seen in enzyme activity. MnSOD protein expression declined with age, and to a lesser extent CuZnSOD did as well. Reduced and oxidized glutathione also exhibited age-related reductions in cells from both normal and regressed aged testes. The age-related decreases in Leydig cell antioxidant enzyme activities, gene expression and protein levels, and in glutathione, were consistent with the hypothesis that the loss of steroidogenic function that accompanies Leydig cell aging may result in part from a decrease in the fidelity of the cellular antioxidant defense system.
This article has been cited by other articles:
 |
|
 |
|
  H. Chen, A. S. Pechenino, J. Liu, M. C. Beattie, T. R. Brown, and B. R. Zirkin Effect of Glutathione Depletion on Leydig Cell Steroidogenesis in Young and Old Brown Norway Rats Endocrinology, May 1, 2008; 149(5): 2612 - 2619. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Y. Takahashi, P. Votruba, M. Abu-Rub, K. Mielke, and J. D. Veldhuis Age Attenuates Testosterone Secretion Driven by Amplitude-Varying Pulses of Recombinant Human Luteinizing Hormone during Acute Gonadotrope Inhibition in Healthy Men J. Clin. Endocrinol. Metab., September 1, 2007; 92(9): 3626 - 3632. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. P. Weir and B. Robaire Spermatozoa Have Decreased Antioxidant Enzymatic Capacity and Increased Reactive Oxygen Species Production During Aging in the Brown Norway Rat J Androl, March 1, 2007; 28(2): 229 - 240. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. L. Carrington and F. L. Bellino Developing a Research Agenda in Biogerontology: Physiological Systems Sci. Aging Knowl. Environ., June 28, 2006; 2006(10): pe17 - pe17. [Abstract] [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
