Protective effects of vitamin E against bisphenol A-induced reproductive toxicity in male Kunming mice

2019 ◽  
Vol 101 (1-2) ◽  
pp. 117-128
Author(s):  
Yu Wang ◽  
Jiayi Li ◽  
Rui Zhou ◽  
Lincai Yang ◽  
Peisheng He ◽  
...  
2017 ◽  
Vol 27 (7) ◽  
pp. 551-559 ◽  
Author(s):  
Yangcai Wang ◽  
Bailin Chen ◽  
Tao Lin ◽  
Shengde Wu ◽  
Guanghui Wei

2007 ◽  
Vol 26 (4) ◽  
pp. 297-306 ◽  
Author(s):  
Recep Kutlubay ◽  
Emin Oğuzhan Oğuz ◽  
Belgin Can ◽  
M. Cengiz Güven ◽  
Zafer Sinik ◽  
...  

Different forms of Aluminium (Al) are environmental xenobiotics that induce free radical–mediated cytotoxicity and reproductive toxicity. Vitamin E ( α-tocopherol) is an antioxidative agent that has been reported to be important for detoxification pathways. This study was thus aimed at elucidating the protective effects of vitamin E towards aluminium toxicity on the histology of the rat testis. Al (5 mg/kg body weight) was administered intraperitoneally in 2 ml saline, either alone or immediately before vitamin E (500 mg/kg body weight), at a different point of abdomen, and the alterations in the testis tissue were analyaed histologically. Seven treated animals were sacrificed for each group, with the testes removed and examined histologically. In the Al-treated group, the germinal epithelium of the seminiferous tubules was thinner in places and spermatids were almost absent; sperm numbers were low and there were no sperm in the lumen. In the Al plus vitamin E rats, there were large numbers of spermatids and sperm in the seminiferous tubule lumen. In the vitamin E alone group, a normal histology was seen. Electron microscopically, in the Al-treated group there were irregularities in the nuclear membrane, some damaged mitochondria, a decrease in the number of ribosomes, and an increase in the number of lysosomes in the sertoli cell cytoplasm. In the primary spermatocyte cytoplasm, there was an increase in the rough endoplasmic reticulum. In the Al plus vitamin E group, the spermatogeneic cells and the sertoli cell cytoplasm showed an almost normal appearance. The ultrastructure of the testis in the vitamin E alone group showed a normal appearance. In conclusion, vitamin E antagonizes the toxic effects of Al at the histological level, thus potentially contributing to an amelioration of the testis histology in the Al-treated rats. The associated biochemical parameters merit further investigation.


Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 634
Author(s):  
Anca Ungurianu ◽  
Anca Zanfirescu ◽  
Georgiana Nițulescu ◽  
Denisa Margină

Vitamin E, comprising tocopherols and tocotrienols, is mainly known as an antioxidant. The aim of this review is to summarize the molecular mechanisms and signaling pathways linked to inflammation and malignancy modulated by its vitamers. Preclinical reports highlighted a myriad of cellular effects like modulating the synthesis of pro-inflammatory molecules and oxidative stress response, inhibiting the NF-κB pathway, regulating cell cycle, and apoptosis. Furthermore, animal-based models have shown that these molecules affect the activity of various enzymes and signaling pathways, such as MAPK, PI3K/Akt/mTOR, JAK/STAT, and NF-κB, acting as the underlying mechanisms of their reported anti-inflammatory, neuroprotective, and anti-cancer effects. In clinical settings, not all of these were proven, with reports varying considerably. Nonetheless, vitamin E was shown to improve redox and inflammatory status in healthy, diabetic, and metabolic syndrome subjects. The anti-cancer effects were inconsistent, with both pro- and anti-malignant being reported. Regarding its neuroprotective properties, several studies have shown protective effects suggesting vitamin E as a potential prevention and therapeutic (as adjuvant) tool. However, source and dosage greatly influence the observed effects, with bioavailability seemingly a key factor in obtaining the preferred outcome. We conclude that this group of molecules presents exciting potential for the prevention and treatment of diseases with an inflammatory, redox, or malignant component.


2016 ◽  
Vol 173 (2) ◽  
pp. 433-442 ◽  
Author(s):  
Xia Li ◽  
Yunlong Zhang ◽  
Yuan Yuan ◽  
Yong Sun ◽  
Yan Qin ◽  
...  

2019 ◽  
Vol 7 (2) ◽  
pp. 087-094
Author(s):  
Mai Mohsen El Maghraby ◽  
Nada Mosaad El Maghraby ◽  
Ameera Ahmed Salama ◽  
Azza Shawky Abdlmonem ◽  
Eman Abdellatefe Authman ◽  
...  

2012 ◽  
Vol 5 ◽  
pp. CMENT.S10711 ◽  
Author(s):  
Min Xiong ◽  
Huangwen Lai ◽  
Chuanhong Yang ◽  
Weiyi Huang ◽  
Jian Wang ◽  
...  

Objective Oxidative damage is a critical role which involves hearing loss induced by impulse noise. That exogenous antioxidant agents reduce noise induced hearing loss (NIHL) has been well demonstrated in both animal studies and clinical practices. Choosing a stronger and more effective antioxidant is very important for treatment of NIHL. Vitamin E, α-lipoic acid, and radix astragali are the most commonly used anti-oxidants for cochlear oxidative damage from acoustic trauma. In this study, the protective effects of radix astragali, α-lipoic acid, and vitamin E on acute acoustic trauma are investigated. Methods Guinea pigs in the experimental groups were intragastrically administered vitamin E, α-lipoic acid, and radix astragali. Auditory thresholds were assessed by sound-evoked auditory brainstem response (ABR) at click and tone bursts of 8, 16 and 32 kHz, 24 hours before and 72 hours after exposure to impulse noise. Cochlear malondialdehyde (MDA) concentrations were detected. Hair cell damage was analyzed by scanning electron microscopy. Results Vitamin E, α-lipoic acid, and radix astragali significantly reduced ABR deficits, reduced hair cell damage, and decreased the concentrations of MDA. α-lipoic acid and radix astragali were better than vitamin E, and there were no significant differences between α-lipoic acid and radix astragali. Conclusions α-lipoic acid or radix astragali are recommended for treatment of NIHL.


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