Protective Effect of Quercetin on Testis Structure and Apoptosis Against Lead Acetate Toxicity: an Stereological Study
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Protective Effect of Quercetin on Testis Structure and Apoptosis Against Lead Acetate Toxicity: an Stereological Study Zahra Khodabandeh 1 & Parisa Dolati 2 & Mohammad Javad Zamiri 2 & Davood Mehrabani 1,3 & Hossein Bordbar 4,5 & Sanaz Alaee 6 & Iman Jamhiri 1 & Negar Azarpira 7 Received: 20 July 2020 / Accepted: 20 October 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Exposure to environmental pollutants tightly impacts on the male fertility. In the present study, we examined the toxic effects of lead acetate (Pb) on testicular structure and the possible effect of quercetin on mitigating these effects. The apoptotic changes in the testes were also studied by the TUNEL assay and changes in apoptosis-related gene (Bax, Bcl-2, and caspase-3) expression. Twenty-one male mice were randomly divided into 3 groups of control, Pb, and lead acetate + quercetin. Testicular weight, both absolute and relative, was higher in Pb-exposed mice in comparison with the control and Pb-quercetin groups. The increase in size of testis was related to the lumen and connective tissue in this group. Lead acetate induced different patterns in testicular cell number; as spermatogonia, spermatocyte, and Sertoli cells number did not affect in lead acetate exposed group, while total number of round spermatids and long spermatids significantly reduced. In addition, Bcl-2 expression was downregulated, and Bax expression was upregulated in Pb-treated group in comparison with the control and Pb + quercetin groups. The TUNEL assay revealed that the number of apoptotic cells in Pb-treated group were increaed significantley in comparison to other groups. In conclusion, Pb administration adversely impacted on the cellular organization and activation of the apoptotic pathways in the testis; on the other hand, quercetin co-administration with lead partially ameliorated these adverse effects. Keywords Antioxidant . Apoptosis . Gene expression . Heavy metal . Male fertility
* Zahra Khodabandeh [email protected] Parisa Dolati [email protected] Mohammad Javad Zamiri [email protected] Davood Mehrabani [email protected] Hossein Bordbar [email protected] Sanaz Alaee [email protected]
1
Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
2
Department of Animal Science, College of Agriculture, Shiraz University, Shiraz, Iran
3
Li Ka Shing Center for Health Research and Innovation, University of Alberta, Edmonton, AB, Canada
4
Histomorphometry and Stereology Research Center, Shiraz University of Medical Science, Shiraz, Iran
5
Department of Anatomy, Shiraz University of Medical Sciences, Shiraz, Iran
6
Department of Reproductive Biology, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran
7
Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
Iman Jamhiri [email protected] Negar Azarpira [email protected]
Khodabandeh et al.
Introduction Hazardous chemicals pollute the
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