Abstract
β-carotene, precursor of vitamin A, is an excellent antioxidant with many beneficial properties. It is a lipid-soluble antioxidant and a very effective quencher of reactive oxygen species (ROS) to reduce the oxidative stress. In contrast to vitamin A, β-carotene is not toxic even consumed in higher amount when it is delivered from natural plant products. Recently, we found that β-carotene acts as a potential antioxidant in the oocyte to improve its quality. Even though many studies have been reported that β-carotene has the beneficial contribution to the ovarian development and steroidogenesis, it is unknown the effects of β-carotene on the spermatogenesis. This investigation aimed to explore the hypothesis that β-carotene could improve spermatogenesis and the underlying mechanism. And we found that β-carotene rescued busulfan disrupted spermatogenesis in mouse with the increase in the sperm concentration and motility. β-carotene improved the expression of genes/proteins important for spermatogenesis, such as VASA, DAZL, SYCP3, PGK2. Moreover, β-carotene elevated the testicular antioxidant capability by the elevation of the antioxidant glutathione and antioxidant enzymes SOD, GPX1, catalase levels. In conclusion, β-carotene may be applied for the infertile couples by the improvement of spermatogenesis, since, worldly many couples are infertile due to the idiopathic failed gametogenesis (spermatogenesis).
Highlights
Infertility is a growing issue worldwide which impacts 10%–15% of all couples with half of the cases being attributed to male factors (Zhou et al, 2016; Wang et al, 2018)
We found that β-carotene rescued busulfan disrupted spermatogenesis in mouse with the increase in the sperm concentration and motility. β-carotene improved the expression of genes/proteins important for spermatogenesis, such as VASA, DAZL, SYCP3, PGK2
We found that β-carotene acts as a potential antioxidant in the oocyte to improve its quality (Yu et al, 2019)
Summary
Infertility is a growing issue worldwide which impacts 10%–15% of all couples with half of the cases being attributed to male factors (Zhou et al, 2016; Wang et al, 2018). Busulfan can cause azoospermia by destroying testicular germ cells and increasing sperm abnormalities (Chi et al, 2013; Jung et al, 2015; Liu et al, 2019). It has been reported that molybdenum (Mo) rescued mouse spermatogenesis by the improvement of male germ cell development s, and maintaining of blood hormone levels (testosterone, estradiol, and luteinizing hormone) (Liu et al, 2019). Genistein has been reported to decrease intra-testicular testosterone (ITT) level and to rescue busulfan disrupted spermatogenesis in rats (Chi et al, 2013). Zhao et al (2020) found that alginate oligosaccharides (AOS) improved busulfan disrupted spermatogenesis at the single cell level
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