Data Availability The datasets generated during and/or analyzed during the current study are not publicly available due to our research continues, such as exploring the mechanism of up regulation of HuR caused by fluorine. Hence, our original data will not be public temporarily. [REASON(S) WHY DATA ARE NOT PUBLIC] but are available from the corresponding author on reasonable request. References Buzalaf MAR (2018) Review of fluoride intake and appropriateness of

Abstract

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 triggered overexpression of human antigen R (Elavl1/HuR) according to western blotting and immunofluorescence. Furthermore, 0.5 mM NaF exposure for 24 h exposure increased the proportion of apoptosis and expression of caspase-3 and caspase-9 in mouse spermatocytes (GC-2spd cell line), whereas inhibition of HuR reduced apoptosis and the expression of caspase-3 and caspase-9. Additionally, inhibition of HuR alleviated F-induced autophagy based on observation of the autophagy bodies, detection of autophagy activity, and analysis of the expression of the LC3II/LC3I and p62 proteins. These results reveal that excessive F can lead to overexpression of HuR, resulting in high levels of apoptosis and autophagy in spermatocytes. These findings improve the understanding of the mechanisms underlying F-induced male reproductive toxicity, and HuR may be explored as a treatment target for certain conditions.

Graphical abstract

Excessive fluoride can induce overexpression of HuR in testis and result in excessive apoptosis and autophagy in spermatocytes as well as male reproductive damage, such as a decreased sperm count, decreased sperm motility, and increased deformity rate.


Excerpt:

Data Availability

The datasets generated during and/or analyzed during the current study are not publicly available due to our research continues, such as exploring the mechanism of up regulation of HuR caused by fluorine. Hence, our original data will not be public temporarily. [REASON(S) WHY DATA ARE NOT PUBLIC] but are available from the corresponding author on reasonable request.

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Acknowledgements

The authors thank Center for Health Aging (Changzhi Medical College) and College Central Laboratory (Changzhi Medical College) for valuable help in our experiment.

Funding

This work is supported by Doctoral research fund of Changzhi Medical College (No. BS202006).

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