Age-related increase in mitochondrial superoxide generation in the testosterone-producing cells of Brown Norway rat testes: relationship to reduced steroidogenic function?

@article{Chen2001AgerelatedII,
  title={Age-related increase in mitochondrial superoxide generation in the testosterone-producing cells of Brown Norway rat testes: relationship to reduced steroidogenic function?},
  author={Haolin Chen and D L Cangello and Scott C. Benson and Janet S Folmer and Hong Zhu and Michael A. Trush and Barry R. Zirkin},
  journal={Experimental Gerontology},
  year={2001},
  volume={36},
  pages={1361-1373}
}
Effect of glutathione depletion on Leydig cell steroidogenesis in young and old brown Norway rats.
TLDR
The hypothesis that alteration in the oxidant/antioxidant environment may play a significant, causative role in the age-related reduced ability of Leydig cells to produce testosterone is supported.
Aging and the brown Norway rat leydig cell antioxidant defense system.
TLDR
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 Leydigs cell aging may result in part from a decrease in the fidelity of the cellular antioxidant defense system.
Aging-related increase of cGMP disrupts mitochondrial homeostasis in Leydig cells.
TLDR
Long-term PDE5-inhibition prevented age-related NO and cGMP elevation, improved mitochondrial dynamics/function, and testosterone production and pointed on cG MP-signaling in Leydig cells as a target for pharmacological manipulation of aging-associated changes in mitochondrial function and testosteroneProduction.
Dibutyryl cyclic adenosine monophosphate restores the ability of aged Leydig cells to produce testosterone at the high levels characteristic of young cells.
TLDR
It is demonstrated that culturing the aged cells with dibutyryl cAMP, a membrane-permeable cAMP agonist that bypasses the LH receptor-adenlyly cyclase cascade, restores testosterone production to levels comparable to those of young cells and also restores steroidogenic acute regulatory protein and P450scc, the proteins involved in the rate-limiting steps of steroidogenesis.
Reactive oxygen disrupts mitochondria in MA-10 tumor Leydig cells and inhibits steroidogenic acute regulatory (StAR) protein and steroidogenesis.
TLDR
Examination of ROS on steroidogenic acute regulatory (StAR) protein in MA-10 cells and mitochondrial perturbation of the mitochondria and dissipation of Deltapsi(m) results in the inhibition of StAR protein expression and its import, processing, and cholesterol transfer activity.
Age-related changes in the steroid-producing cells of rat testis
TLDR
Results obtained suggest that effects of ageing on steroidogenesis are mainly due to structural and functional alterations in Leydig cells resulting in a decreased testosterone production.
Role of peroxiredoxin 2 in H2O2‑induced oxidative stress of primary Leydig cells.
TLDR
It is indicated that Prdx2 may prevent H2O2 accumulation in Leydig cells, and may be important in oxidative stress‑induced apoptosis and decreased testosterone production.
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References

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TLDR
The results, taken together, suggest that the reduced testosterone production seen in aged rats is related to defects in the steroidogenic pathway beyond the LH receptor-cAMP cascade.
Does age-associated reduced Leydig cell testosterone production in Brown Norway rats result from under-stimulation by luteinizing hormone?
TLDR
The inability of exogenously administered LH to increase testosterone production by testes and Leydig cells of aged rats suggests that Leydigs cell steroidogenic deficits in the aged Brown Norway rat are unlikely to be the result of age-related changes in LH.
Regulation of Leydig Cell Steroidogenic Function During Aging1
TLDR
Long-term suppression of steroidogenesis was found to prevent or delay the reduced steroidogenesis that accompanies Leydig cell aging, and a possible explanation is that long-term suppressed steroidogenesis prevents free radical damage to the cells by suppressing the production of the reactive oxygen species that are a by-product of steroidsogenesis itself.
Are Leydig cell steroidogenic enzymes differentially regulated with aging?
TLDR
It is concluded that age-related loss of steroidogenic function results at least in part from reductions in the levels and activities of each of the steroidogenic enzymes responsible for converting cholesterol to testosterone, and not by differential regulation of these enzymes.
Steroid synthesis-dependent, oxygen-mediated damage of mitochondrial and microsomal cytochrome P-450 enzymes in rat Leydig cell cultures.
TLDR
The results suggest that the enhanced loss of mitochondrial and microsomal cytochrome P-450 activities in cAMP-treated cultures is caused by the increased production of pregnenolone and testosterone, respectively, which generate reactive damaging species derived from reduced dioxygen.
Long-term suppression of Leydig cell steroidogenesis prevents Leydig cell aging.
  • H. Chen, B. Zirkin
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 1999
TLDR
By placing the Leydig cells in a state of steroidogenic "hibernation," the reductions in LeydIG cell testosterone production that invariably accompany aging did not occur.
Depletion and repopulation of Leydig cells in the testes of aging brown Norway rats.
TLDR
Although situated in an aged testis and in the environment of an aged hypothalamic-pituitary axis, the steroidogenic function of the Leydig cells restored to aged rat testes was equivalent to that of young rat LeydIG cells.
The effects of hydrogen peroxide on steroidogenesis in mouse Leydig tumor cells.
TLDR
H2O2 inhibits steroidogenesis in Leydig tumor cells primarily by inhibiting the activity of the 3 beta-hydroxysteroid dehydrogenase, but that other effects of H2 O2 such as inhibition of protein synthesis and the transfer of cholesterol to the cholesterol side-chain cleavage complex may also be involved.
Steroid product-induced, oxygen-mediated damage of microsomal cytochrome P-450 enzymes in Leydig cell cultures. Relationship to desensitization.
TLDR
Data are consistent with the hypothesis that the decline in microsomal P-450 enzymes in desensitized Leydig cells results from product (pseudosubstrate)-induced, oxygen-derived, free-radical damage rather than a steroid receptor-mediated process.
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