Age-related histopathological and biochemical testicular damages were ameliorated by vitamin C administration

Heidari, Fatemeh; Kian, Naghmeh; Azad, Nahid; Chiti, Hossein; Freidouni, Mohammadjavad; Fakheri, Farzaneh; Aliaghaei, Abbas; Abdi, Shabnam; Salimi, Maryam; Raoofi, Amir; Abdollahifar, Mohammad‐Amin; Ebrahimi, Vahid

doi:10.1016/j.androl.2021.10.001

Cited by 1 publication

(1 citation statement)

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“…Antioxidants, or compounds that enhance endogenous antioxidant activity, such as the co-factor nicotinamide, have also been shown to enhance testosterone production in ageing rats and preserve the structural integrity of the testes ( Hacioglu et al , 2021 ; Al-Shaikh, 2022 ). Other putative antioxidants such as Korean red ginseng ( Kopalli et al , 2017 ), Cordycepin ( Kopalli et al , 2019 ), Gigantol ( Basque et al , 2021 ), and vitamin C ( Heidari et al , 2023 ) have similar effects. The source of oxidative stress in ageing Leydig cells is thought to be mitochondrial ( Chen et al , 2001 ; Miquel, 2002 ; El Kattawy et al , 2022 ), while the target is thought to be the hormone-sensitive mitochondrial cholesterol transfer step of steroidogenesis ( Diemer et al , 2003 ).…”

Section: Paternal Ageing Testosterone and Oxidative Stressmentioning

confidence: 99%

Male reproductive ageing: a radical road to ruin

Aitken

2023

Human Reproduction

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In modern post-transition societies, we are reproducing later and living longer. While the impact of age on female reproductive function has been well studied, much less is known about the intersection of age and male reproduction. Our current understanding is that advancing age brings forth a progressive decline in male fertility accompanied by a reduction in circulating testosterone levels and the appearance of age-dependent reproductive pathologies including benign prostatic hypertrophy and erectile dysfunction. Paternal ageing is also associated with a profound increase in sperm DNA damage, the appearance of multiple epigenetic changes in the germ line and an elevated mutational load in the offspring. The net result of such changes is an increase in the disease burden carried by the progeny of ageing males, including dominant genetic diseases such as Apert syndrome and achondroplasia, as well as neuropsychiatric conditions including autism and spontaneous schizophrenia. The genetic basis of these age-related effects appears to involve two fundamental mechanisms. The first is a positive selection mechanism whereby stem cells containing mutations in a mitogen-activated protein kinase pathway gain a selective advantage over their non-mutant counterparts and exhibit significant clonal expansion with the passage of time. The second is dependent on an age-dependent increase in oxidative stress which impairs the steroidogenic capacity of the Leydig cells, disrupts the ability of Sertoli cells to support the normal differentiation of germ cells, and disrupts the functional and genetic integrity of spermatozoa. Given the central importance of oxidative stress in defining the impact of chronological age on male reproduction, there may be a role for antioxidants in the clinical management of this process. While animal studies are supportive of this strategy, carefully designed clinical trials are now needed if we are to realize the therapeutic potential of this approach in a clinical context.

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