Antagonistic effect of vitamin E on di-2-ethylhexyl phthalate-induced reproductive toxicity in male rats.

Chao-yun Wang; Juan-juan Zhang; Peng Duan

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Antagonistic effect of vitamin E on di-2-ethylhexyl phthalate-induced reproductive toxicity in male rats.

Author: Chao-Yun WANG ¹ ; Juan-Juan ZHANG ¹ ; Peng DUAN ²
Author Information

1. Center of Reproductive Medicine, Taihe Hospital of Shiyan / The Affiliated Hospital of Hubei Medical University, Shiyan, Hubei 442000, China.
2. Family Planning Research Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Publication Type:Journal Article
Keywords: male reproductive toxicity; mitochondrial apoptosis pathway; vitamin E; di-2-ethylhexyl phthalate
MeSH: Animals; Antioxidants; pharmacology; Apoptosis; genetics; Autophagy-Related Protein 5; metabolism; Caspase 3; metabolism; Diethylhexyl Phthalate; antagonists & inhibitors; Epididymis; Follicle Stimulating Hormone; blood; Luteinizing Hormone; blood; Male; Malondialdehyde; metabolism; Mitochondria; drug effects; Oxidative Stress; drug effects; Oxidoreductases; metabolism; Random Allocation; Rats; Rats, Sprague-Dawley; Reproduction; Spermatozoa; drug effects; physiology; Superoxide Dismutase; metabolism; Testis; drug effects; Testosterone; blood; Vitamin E; pharmacology
From:National Journal of Andrology 2018;24(7):589-595
CountryChina
Language:Chinese
Abstract:
ObjectiveTo explore the antagonistic effect of vitamin E (VE) on male reproductive toxicity induced by di-2-ethylhexyl phthalate (DEHP) in pubertal SD rats and its underlying mechanisms.
METHODSThirty 5-week-old male SD rats were randomly divided into five groups of equal number, corn oil control, low-dose (10 mg/kg/d), medium-dose (100 mg/kg/d) and high-dose DEHP exposure (500 mg/kg/d), and VE intervention (high-dose DEHP + VE ［100 mg/kg/d］), and treated respectively for 30 successive days. At 3 days after treatment, the testes of the animals were harvested for determination of the oxidative stress index, serum reproductive hormone levels, cauda epididymal sperm parameters, and expressions of cell apoptosis-related genes and proteins.
RESULTSCompared with the control group, the rats of the medium- and high-dose DEHP groups showed significant decreases in the levels of such serum reproductive hormones as follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone (T), sperm parameters as average path velocity (VAP), straight line velocity (VSL), curvilinear velocity (VCL), straightness (STR), linearity (LIN) and wobble (WOB), and the activities of superoxide dismutase (SOD) and glutathione peroxide (GSH-Px), but significant increases were observed in the latter two groups in the content of malondialdehyde (MDA)(［3.32±0.87］ nmol/mg pro vs ［2.13±0.49］ nmol/ mg pro), mRNA expressions of Bad, Bax, Cytochrome C, Caspase-3 and the Bax/Bcl-2 ratio, and protein expressions of Cytochrome C and Caspase-3. In comparison with the high-dose DEHP group, the VE intervention group exhibited remarkably increased serum LH and T levels, sperm VAP, VSL, VCL, STR and WOB, and activities of SOD and GSH-Px, but markedly decreased mRNA expressions of Bad, Bax, Cytochrome C, Caspase-3 and the Bax/Bcl-2 ratio as well as the protein expressions of Cytochrome C and Caspase-3 in the testis tissue (P<0.05).
CONCLUSIONSExposure to DEHP induces androgen secretion disorders, causes oxidative damage to the testicular tissue, activates the mitochondrial apoptosis pathway in the testis, and ultimately reduces the quality of epididymal sperm, while VE can protect the rat testis from DEHP-induced reproductive toxicity.