Lower dietary n-6 : n-3 ratio and high-dose vitamin E supplementation improve sperm morphology and oxidative stress in boars

2017 ◽  
Vol 29 (5) ◽  
pp. 940 ◽  
Author(s):  
Qing Liu ◽  
Yuanfei Zhou ◽  
Runjia Duan ◽  
Hongkui Wei ◽  
Siwen Jiang ◽  
...  

A 2 × 2 factorial experiment (10 boars per treatment) was conducted for 16 weeks to evaluate the effects of the dietary n-6 : n-3 ratio (14 : 1 vs 6 : 1) and vitamin E (200 vs 400 mg kg–1) on boar sperm morphology and oxidative stress. Sperm mitochondrial membrane potential (MMP), reactive oxygen species (ROS), DNA damage (8-hydroxydeoxyguanosine; 8-OHdG), seminal lipoperoxidation (malondialdehyde; MDA) and antioxidant capacity in the serum, spermatozoa and seminal plasma were assessed as indicators of oxidative stress. Sperm production was similar among groups but increased (P < 0.05) throughout the 16 weeks of the study. Although sperm α-tocopherol content, ROS and seminal MDA did not differ between the two dietary n-6 : n-3 ratio treatments, enhanced antioxidant enzyme activity and MMP, but decreased 8-OHdG, were found in spermatozoa from boars consuming the 6 : 1 diet. The diet with the 6 : 1 ratio positively affected sperm morphology at Weeks 12 and 16 (P < 0.05). The α-tocopherol content and antioxidant capacity increased in boars with increasing levels of vitamin E supplementation. Compared with low-dose vitamin E, high-dose vitamin E supplementation improved sperm morphology. Overall, the results indicate that an n-6 : n-3 ratio of 6 : 1 and 400 mg/kg vitamin E have beneficial effects on sperm morphology by improving antioxidative stress.

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1810-1810
Author(s):  
Jiaqi Huang ◽  
Stephanie Weinstein ◽  
Wendy Mack ◽  
Howard Hodis ◽  
Demetrius Albanes

Abstract Objectives Vitamin E is an essential micronutrient and critical human antioxidant that has been tested for cancer and cardiovascular preventative effects for decades with conflicting results. For example, prostate cancer incidence was reduced by a low-dose vitamin E supplement in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, but the findings were not replicated by high-dose vitamin E trials such as the Selenium and Vitamin E Cancer Prevention Trial (SELECT). The present investigation examined the serum metabolomic responses to low- and high-dose vitamin E supplementation in order to gain biological insight into the divergent trial outcomes. Methods We examined baseline and on-study serum samples for 154 men randomly assigned to receive 400 IU vitamin E (as alpha-tocopheryl acetate; ATA) or placebo daily in the Vitamin E Atherosclerosis Prevention Study (VEAPS), and 100 men administered 50 IU ATA or placebo daily in the ATBC Study. Over 970 known metabolites were identified using an ultrahigh-performance LC-MS/MS platform. Linear regression models estimated the change in serum metabolites of men supplemented with vitamin E to those assigned to placebo in VEAPS compared with ATBC. Results Serum alpha-carboxyethyl hydrochroman (CEHC) sulfate, alpha-tocopherol, and beta-/gamma-tocopherol were significantly altered by supplementation with ATA in both the VEAPS and ATBC trials (all P-values ≤ 5.1 × 10−5, the Bonferroni multiple-comparisons corrected statistical threshold). Serum C22 lactone sulfate was also significantly decreased in response to the high-dose vitamin E supplement in VEAPS (β = −0.70, P-value = 8.1 × 10−6), but not altered in the low-dose ATBC trial (β = −0.17, P-value = 0.4). Additionally, changes in several androgenic steroid metabolites were strongly related to the vitamin E supplement-associated change in C22 lactone sulfate only in the high-dose VEAPS trial. Conclusions We found evidence of a dose-dependent vitamin E supplementation effect on a novel C22 lactone sulfate compound as well as several androgenic steroids that may have relevance to previous controlled trial findings for prostate cancer. Funding Sources This research was supported by the Intramural Research Program of the National Cancer Institute, National Institutes of Health, U.S. Public Health Service, Department of Health and Human Services.


2019 ◽  
Vol 17 (2) ◽  
pp. 127 ◽  
Author(s):  
Khadijeh Mirzaei Khorramabadi ◽  
Ali Reza Talebi ◽  
Abolghasem Abbasi Sarcheshmeh ◽  
Aghdas Mirjalili

Background: Generation of free radicals and oxidative stress are a major contributorto diabetes. These factors lead to the development of diabetic testicles disorders.Objective: In this study, the protective effect of vitamin E on functional disordersassociated with diabetes induced oxidative stress in male reproductive systems hasbeen investigated.Materials and Methods: Thirty-three adult male Mice were divided into control,diabetic, and untreated diabetic groups. Streptozotocin was used to induce diabetes.In the treated group, vitamin E was given to the Mice intraperitoneally for 30 days.Then, animals were anesthetized and sacrificed. Animal testicles were isolated andhomogenized in phosphate buffer and used for measuring sperm count, motility andsurvival of sperm, MDA concentration and antioxidant capacity (TAC). Apoptosis wasalso performed with the TUNEL test.Results: The results of reduction (12.03±98.11) TAC, MDA concentration (–28.5±2.58),sperm motility (unstable sperma= 86.4±7.48), sperm count (171.51), Sperm morphology(natural morphology= 49.69±31.93) and abnormal morphology (9.77±49.7)with increased oxidative damage. These changes were statistically significant incomparison with the control group for all variables other than MDA (p= 0.05). Treatmentof vitamin E diabetic Mice improved the ability of antioxidants to prevent oxidativedamage in the testicles, restore the sperm movement, and increase the number ofnormal sperm as well as TAC. The level of apoptosis in the treated group has decreasedcompared to the untreated group.Conclusion: Vitamin E protects the reproductive system against diabetes mellitus.Therefore, it was concluded that vitamin E may be a suitable agent for protecting thesperm and testicular parameters against undesirable effects of diabetes.


2019 ◽  
Vol 76 ◽  
pp. 48-49 ◽  
Author(s):  
M.M. Fagan ◽  
A. Adams ◽  
P. Harris ◽  
A. Krotky ◽  
K.J. Duberstein

2002 ◽  
Vol 48 (1) ◽  
pp. 6-9 ◽  
Author(s):  
Takao MORINOBU ◽  
Ryoichi BAN ◽  
Sosuke YOSHIKAWA ◽  
Takuji MURATA ◽  
Hiroshi TAMAI

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