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Updated: Sep 3, 2025

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Hesperidin partly ameliorates the decabromodiphenyl ether-induced reproductive toxicity in pubertal mice
Shiqi Li1, Siyan Che1, Sunni Chen1
1State Key Laboratory of Food Science and Technology, Institute of Nutrition and School of Food Science, Nanchang University, Nanchang, 330047, China.
Abstract:
Many materials use polybrominated diphenyl ethers (PBDEs) as flame retardants. As one of the most common congeners of PBDEs, decabromodiphenyl ether (PBDE-209) is reported to harm reproductive health. However, little is known research on attenuating the reproductive toxicity induced by PBDE-209. The present study aimed to investigate the effects of hesperidin against PBDE-209-induced reproductive toxicity in male mice. Pubertal male C57BL/6 J mice were exposed to PBDE-209 groups (20, 100, 500 mg/kg·bw) and hesperidin groups (100 mg/kg·bw PBDE-209 + 100 mg/kg·bw hesperidin) for 8 weeks. The results showed that PBDE-209 increased the amount of abnormal morphological sperms and decreased the sex hormone levels. PBDE-209 induced the histopathological lesions of seminiferous tubules and blood-testis barrier in mice testis. Expressions of apoptosis-associated proteins and mRNA (Bax, Bcl-2, etc.) were altered by the PBDE-209 treatment. PBDE-209 prominently increased the malondialdehyde (MDA) levels, the biomarker of oxidative stress. Hesperidin treatment partly alleviated PBDE-209-induced histopathological lesions and apoptosis in mice testis. These findings suggested that hesperidin partly protects against PBDE-induced reproductive toxicity in pubertal mice. We conclude that more work needs to be done to explore the appropriate dosage of hesperidin or find other drugs to protect against the reproductive toxicity of PBDEs.

