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Published on: February 6, 2018
The role of the transsulfuration pathway in spermatogenesis of vitamin D deficient mice
Narges Jamshidian-Ghalehsefidi1,2, Farzaneh Rabiee3, Marziyeh Tavalaee4,5
1ACECR Institute of Higher Education, Isfahan Branch, Isfahan, Iran.
Abstract:
Vitamin D deficiency is a global health problem and has been linked to defective spermatogenesis and male infertility. In this study, we aimed to investigate the main enzymes involved in the transsulfuration pathway of 1-carbon metabolism, and spermatogenesis function. Therefore, sixteen male C57 mice were addressed to a control (standard diet) or vitamin D deficient (VDD) diet for 14 weeks. The results show that compared to the standard diet, VDD increased final body weight and reduced sperm quality, caused damage to the testicular structure, and decreased the serum levels of testosterone. In addition, serum concentrations of homocysteine, vitamin B12, and sperm oxidative stress markers increased. In testicular tissues, the CBS and CSE protein levels were down-regulated whereas HO-1 was up-regulated at both mRNA and protein expression levels. Within a mice deprivation model, VDD deeply suppressed testosterone and impaired spermatogenesis with oxidative stress-mediated mechanisms. The effects of the deprivation appeared to be at least in part independent of genomic and receptor-mediated vitamin D actions and suggest a specific impairment of the alternative transsulfuration pathway.
Insights
Vitamin D deficiency impairs male fertility by reducing sperm quality and testosterone levels. This study suggests the effect is linked to the transsulfuration pathway, not just vitamin D receptors.
Area of Science:
- Endocrinology
- Reproductive Biology
- Nutritional Science
Background:
- Vitamin D deficiency is a widespread issue linked to male infertility.
- Defective spermatogenesis is a known consequence of vitamin D deficiency.
Purpose of the Study:
- To investigate the impact of vitamin D deficiency on enzymes in the transsulfuration pathway.
- To examine the relationship between vitamin D deficiency, spermatogenesis, and 1-carbon metabolism in mice.
Main Methods:
- Male C57 mice were fed either a standard or vitamin D-deficient (VDD) diet for 14 weeks.
- Key enzymes (CBS, CSE, HO-1) in the transsulfuration pathway were analyzed at mRNA and protein levels.
- Sperm quality, testosterone levels, homocysteine, vitamin B12, and oxidative stress markers were measured.
Main Results:
- Vitamin D deficiency reduced sperm quality, testicular structure, and testosterone levels.
- Homocysteine, vitamin B12, and sperm oxidative stress markers increased in deficient mice.
- CBS and CSE protein levels decreased, while HO-1 increased in testicular tissues.
Conclusions:
- Vitamin D deficiency impairs male reproductive function and spermatogenesis via oxidative stress mechanisms.
- The observed effects appear independent of genomic vitamin D actions, suggesting a role for the transsulfuration pathway.
- This highlights a specific impairment of the alternative transsulfuration pathway in vitamin D deficiency-induced infertility.
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