2015
DOI: 10.1096/fj.15-271825
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Abstract: Point mutations and deletions of mitochondrial DNA (mtDNA) accumulate in tissues during aging in animals and humans and are the basis for mitochondrial diseases. Testosterone synthesis occurs in the mitochondria of Leydig cells. Mitochondrial dysfunction (as induced here experimentally in mtDNA mutator mice that carry a proofreading‐deficient form of mtDNA polymerase γ, leading to mitochondrial dysfunction in all cells types so far studied) would therefore be expected to lead to low testosterone levels. Althou… Show more

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Cited by 16 publications
(16 citation statements)
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“…This could potentially limit the capacity for increased steroidogenic flux to maintain normal testosterone levels in the face of reduced LC number. For example, in other rodent models, with up to a 75% reduction in LC number, testosterone levels are maintained because of functional compensation by the remaining LC population (35, 41, 95). Indeed, reduced circulating testosterone in constitutive CISD2-KO animals was not entirely explained by correction for the reduction in LC number, confirming a primary LC dysfunction in this model.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…This could potentially limit the capacity for increased steroidogenic flux to maintain normal testosterone levels in the face of reduced LC number. For example, in other rodent models, with up to a 75% reduction in LC number, testosterone levels are maintained because of functional compensation by the remaining LC population (35, 41, 95). Indeed, reduced circulating testosterone in constitutive CISD2-KO animals was not entirely explained by correction for the reduction in LC number, confirming a primary LC dysfunction in this model.…”
Section: Discussionmentioning
confidence: 99%
“…Studies by Wiley et al (30) demonstrated that CISD2-loss results in a pro-oxidative intracellular environment, which may explain the reduction in testosterone observed in CISD2-KO mice. However, in prematurely aging mitochondrial DNA mutator mice, despite a 7-fold increase in LC superoxide production, testosterone biosynthesis was unaffected; therefore, increased ROS may not be directly toxic to LCs (95). As such, maintenance of LC function in our LC-KO mice supports the hypothesis of Chen et al (26), stating that alterations in factors extrinsic to LCs may be responsible for impaired steroidogenic function of the aged testis.…”
Section: Discussionmentioning
confidence: 99%
“…MMP was determined using a cationic fluorescent dye tetramethylrhodamine methyl ester (TMRM), as previously described [ 30 ]. The fluorescence intensity of this dye is proportional to the magnitude of MMP.…”
Section: Methodsmentioning
confidence: 99%
“…These results indicate that NRF1 may get involved in the regulation of steroidogenesis in goat LGCs. It has been reported that mitochondrial dysfunction leads to low levels of testosterone synthesis in Leydig cells (Shabalina et al 2015). Blocked mitochondrial fusion by mitofusin 2 (Mfn2) knockdown has a negative impact on steroid synthesis (Duarte et al 2012).…”
Section: Discussionmentioning
confidence: 99%