Natural antioxidants could delay age-related decline in male testosterone production

Increase in the spontaneous pregnancy rates along with improvement in sperm concentration and motility was reported by the studies evaluating the effect of oral use of antioxidants on male infertility. It can be concluded that antioxidant use improves the serum sex hormone levels and increases an individual’s fertility chances. Reduced LH levels cannot sufficiently stimulate the Leydig cells for testosterone production. As a result, the circulating testosterone levels decrease because of the suppression of androgen synthesis and induction of apoptosis in the Leydig cells. This study investigated the effect of antioxidant treatment on reproductive hormones. Several studies have reported that antioxidant treatment may improve sperm DNA damage and other sperm parameters.
In this study, the effect of antioxidants on sperm parameters and serum gonadal hormone levels in men with idiopathic infertility was investigated. However, no clinical study has investigated the effect of antioxidants on male serum gonadal hormone levels. This study aimed at evaluating the effect of antioxidant treatment on serum gonadal hormones and sperm parameters in men with idiopathic infertility. A review of dozens of clinical trials showed that DHEA supplements do increase blood testosterone levels in men and women. A 12-week study published in Obesity Research concluded that daily oral ingestion of forskolin helps boost testosterone levels, https://pads.jeito.nl/s/PirF0pDXyr improve body composition, and increase bone mass in overweight and obese men (6).
The oxidative balance score (OBS) and testosterone levels were derived from interview data and laboratory measurements. The balance between oxidative and antioxidant capacity plays a critical role in testosterone deficiency. Thus, anthocyanidins may promote testosterone production by Leydig cells through their antioxidant properties. Such discrepancy in the effects of catechins on testosterone levels needs further investigation to better define their regulatory mechanisms. Moreover, injections with catechins or its derivatives also increased testosterone plasma concentrations . Rutin (12) also partially reversed cadmium-induced decline in plasma testosterone levels in male rats by increasing Hsd3b and Hsd17b3 enzyme activity 74,75.
Writing—original draft preparation, L.J.M. and M.T.; writing—review and editing, L.J.M. and M.T.; funding acquisition, L.J.M. and M.T. Although numerous polyphenols demonstrate either activation or inhibition effects on androgen biosynthesis, consideration should be taken for combined exposure to naturally occurring flavonoids and isoflavonoids and their potential additive or synergistic effects on steroidogenesis. Considering the entire data reported on the regulation of steroidogenesis by flavonoids and isoflavonoids, a structure-activity relationship may explain the differences in inhibition and activation of androgen production. Cyanidin-3-glucoside (20) was also reported to improve the expression levels of steroidogenic proteins (StAR, Hsd3b, and Cyp11a1) and of the LH receptor within the testes of mice exposed to cadmium, an important neuroendocrine disruptor . In addition, this anthocyanin also upregulated the activities of the MAPK and PKA signalling pathways , promoting steroid production.
Hesperidin (16), a glycosylated form of hesperetin, (Figure 7) was also reported to reverse the decline of testosterone production in diabetic rats . Overall, flavonols such as quercetin (7) are promising in increasing steroidogenic enzymes activities and may prevent age-related decline in testosterone production in men. Taxifolin (13) has been shown to inhibit androgen production in immature rat Leydig cells by inhibiting the activities of Hsd3b and Cyp17a1 enzymes . Icariin (11) has been shown to reverse the adverse effects of di(2-ethylhexyl) phtalate (DEHP) on primary Leydig cell proliferation and testosterone synthesis . Quercetin (7) also contributes to the improvement of testosterone production in rats exposed to either cadmium chloride or the herbicide atrazine, where the enzyme activities of Hsd3b and Hsd17b3 are recovered 68,69.
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