Antioxidant effect of Vitamin E on the male rat reproductive system by a high oral dose of Bisphenol-A

Abstract

Among researchers, environmental pollutants and their contribution to male fertility are still being discussed. The use of antioxidants manages to boost the reproductive system with the scavenging of free radicals. This study aimed to investigate the inhibiting function of Vitamin E (VE) on Bisphenol-A (BPA) toxicity in the male rats’ reproductive system. Male rats were divided into 4 groups: control (negative control) group, BPA group treated by 250 mg/kg/day (positive control), VE group treated by 150 mg/kg/day (comparative control) and BPA + VE group that received both doses at the same time (Oral treatment by gavage; 56 days). Sperm parameters, testicular tissue morphometric and biochemical tests were evaluated. Sperm count, motility, viability, normal morphology, sperm tail length, spermatogenesis index and serum testosterone levels significantly decreased in the BPA group compared to the control group. Versus a significant enhancement in the positive-TUNEL germinal cells and serum malondialdehyde (MDA) levels were observed. Moreover, BPA exhibited no effect on sperm maturity and DNA integrity. In the simultaneous treatment group (BPA + EV), VE could improve and regulate all the mentioned parameters within the control group range. As mentioned, there was a significant difference in the results in the positive control group compared to the negative control group. But these data improved significantly in the BPA + VE. It can be concluded that in this group, VE was able to overcome the toxicity caused by positive control in their simultaneous treatment and maintain the data at the negative control group range. Therefore, no significant change was observed in the BPA + VE group compared to the negative control group.

In vivo exposure to bisphenol F induces oxidative testicular toxicity: role of Erβ and p53/Bcl-2 signaling pathway

“…BPF treatment distorted testicular histoarchitecture which was sustained after the recovery period. This agrees with previous findings that reported similar effect following the administration of BPF analogues ( 32 , 33 ). The significant reduction in Johnsen's biopsy score (for spermatogenesis), epithelial height and seminiferous tubular diameter, as well as the increase in seminiferous luminal diameter, infer that BPF exerted a negative impact on the germ cell lines and damaged the mature sperm cells, thus reducing the germ cell layers and the volume of sperm cells in the lumen of the seminiferous tubules.…”

Antioxidant, anti-inflammatory, and anti-reprotoxic effects of kaempferol and vitamin E on lead acetate-induced testicular toxicity in male rats

“…The results of the current study are consistent with ( Oyeyemi et al , 2022 ), who reported that vitamin E could reduce testicular MDA and NO concentrations when co-administered with lead acetate due to suppress phospholipid membrane peroxidation and protect testicular cell membranes via its lipophilic properties ( Malmir et al , 2021 ); in addition, tocopherols-OH can replace their hydrogen atom to a single electron of free radicle and removing it before the free radicle binds with cell membranes, so vitamin E considers as a nonenzymatic defense mechanism in testicular mitochondria ( Ahmed et al , 2020 , Malmir et al , 2021 ) that effects on the testicular NO and MDA levels in Pb cotreated with vitamin E.…”

“…The kaempferol exhibited the antioxidant properties to improve the Leydig cells membranes and facilitate cholesterol transfer into mitochondria ( Alam et al , 2020 ), subsequently improving steroidogenesis as StAR protein levels and CYP11A1, 3β-HSD, and 17β-HSD activities and testosterone concentration were upregulated ( Liu et al , 2022 ) as reported in the current research which illustrated that kaempferol administration caused testicular upregulation 3β-HSD, 17β-HSD, and CTP11A1 enzymes and StAR protein gene expression which positively effect on testosterone levels in rats cotreated with kaempferol. Furthermore, the administration of vitamin E following exposure to lead acetate caused elevation of testicular 13β-and 17β- HSD activities and StAR levels due to the ability of vitamin E to promote gene expression of StAR protein and mRNA steroidogenic enzyme in Leydig cells that can upregulate testosterone concentration ( Malmir et al , 2021 ).…”

“…Vitamin E has antioxidant properties that can protect the hypothalamic and pituitary cells from oxidative stress that promotes GnRH, FSH, and LH biosynthesis via upregulated gene expression of hypophyseal GnRHr , LHβ , and FSHβ and testicular FSHr , LHr , and CYP11A1 that enhance serum FSH and LH concentrations in turn that improving the testosterone levels and spermatogenesis ( Oyeyemi et al , 2022 ). Interestingly, the improvement the steroidogenesis and spermatogenesis in Pb co-administered with kaempferol and vitamin E resulted from the prevention of oxidative stress and chelating activities of kaempferol and vitamin E, which ameliorate lead acetate-induced testicular toxicity, thereby improving the levels of LH and FSH that supported steroidogenesis and spermatogenesis in Pb co-treated with kaempferol and vitamin E ( Akefe et al , 2020 , Malmir et al , 2021 ).…”

Effect of Aqueous Extract of Unripe Musa Paradisiaca Linn on Parameters Affecting Reproduction in Rats

“…MDA induces oxidative stress, which has a negative impact on sperm function by affecting membrane fluidity and permeability, as well as reducing sperm function efficiency. 26 …”