Abstract
Exposure to fluoride results in low reproductive capacity; however, the mechanism underlying the impact of fluoride on male [re]productive system still remains obscure. To assess the potential toxicity in testis of mice administrated with fluoride, global genome microarray and real-time PCR were performed to detect and identify the altered transcriptions. The results revealed that 763 differentially expressed genes were identified, including 330 up-regulated and 433 down-regulated genes, which were involved in spermatogenesis, apoptosis, DNA damage, DNA replication, and cell differentiation. Twelve differential expressed genes were selected to confirm the microarray results using real-time PCR, and the result kept the same tendency with that of microarray. Furthermore, compared with the control group, more apoptotic spermatogenic cells were observed in the fluoride group, and the spermatogonium were markedly increased in S phase and decreased in G2/M phase by fluoride. Our findings suggested global genome microarray provides an insight into the reproductive toxicity induced by fluoride, and several important biological clues for further investigations.
© 2016 Wiley Periodicals, Inc. Environ Toxicol, 2016.
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Vitamin E and Lycopene Reduce Coal Burning Fluorosis-induced Spermatogenic Cell Apoptosis via Oxidative Stress-mediated JNK and ERK Signaling Pathways.
Although fluoride has been widely used in toothpaste, mouthwash, and drinking water to prevent dental caries, the excessive intake of fluoride can cause fluorosis which is associated with dental, skeletal, and soft tissue fluorosis. Recent evidences have drawn the attention to its adverse effects on male reproductive system that include
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Toxic effects of sodium fluoride on reproductive function in male mice
To investigate the effects and possible mechanisms of the action of fluoride on testis cell cycle and cell apoptosis in male mice, sexually mature male Kunming mice were exposed to 50, 100, 200, and 300 mg NaF/L in their drinking water for 8 weeks. At the end of the exposure
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Interleukin 17A deficiency alleviates fluoride-induced testicular injury by inhibiting the immune response and apoptosis.
Highlights Exposure to high-levels of fluoride causes reproductive toxicity in humans. Increased testes toxicity and inflammation were seen in a mouse model of fluorosis. The NaF-mediated testes toxicity and inflammation were absent in IL-17A -/- mice. In Leydig cells IL-17A and/or NaF increased apoptosis and decreased testosterone. Il-17A appears
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Positive PCNA and Ki-67 Expression in the Testis Correlates with Spermatogenesis Dysfunction in Fluoride-Treated Rats.
The present study aimed to evaluate the effect of fluoride (F) on spermatogenesis in male rats. F- at 50 and 100 mg/L was administered for 70 days, after which the testicular and epididymis tissues were collected to observe the histopathological structure under a light microscope. The ultrastructure of the testis and sperm
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Fluoride-Induced Sperm Damage and HuR-Mediated Excessive Apoptosis and Autophagy in Spermatocytes.
It is critical to determine the mechanism underlying fluoride (F)-induced damage of the testes to develop appropriate strategies for monitoring and intervention. In the present study, exposure to 50 mg/L sodium fluoride (NaF) for 90 days damaged the normal structure of the testes and quality of the sperm, particularly the spermatocytes, and
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Fluoride's Effect on Male Reproductive System - Human Studies
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Fluoride's Effect on the Male Reproductive System -- In Vitro Studies
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