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Cadmium disrupts spermatogenic cell cycle via piRNA-DQ717867/p53 pathway.

Authors :
Wei J
Dai J
Shi X
Zhao R
Fu G
Li R
Xia C
Zhang L
Zhou T
Wang H
Shi Y
Source :
Reproductive toxicology (Elmsford, N.Y.) [Reprod Toxicol] 2024 Apr; Vol. 125, pp. 108554. Date of Electronic Publication: 2024 Feb 06.
Publication Year :
2024

Abstract

Cadmium (Cd) is a harmful environmental pollutant that disrupts public health, including respiratory, digestive, and reproductive systems. In this study, male rats were exposed to CdCl <subscript>2</subscript> at a dose of 3 mg/kg by oral for 28 days to investigate the impact on spermatogenesis. Testis tissue samples were collected after sacrifice, and piRNA expression levels were measured using piRNA microarray and qPCR. PiRNAs, specialized molecules involved in spermatogenesis, were examined. CdCl <subscript>2</subscript> exposure led to disrupted piRNA expression, particularly in piRNA-DQ759395 in rats. This piRNA was found to have a binding site with p53, and a similar piRNA-DQ717867 was discovered in mice. In GC-2spd cells, CdCl <subscript>2</subscript> exposure increased piRNA-DQ717867 expression, which resulted in cell cycle arrest and abnormal expression of cell cycle-related proteins. The activation of p53-related pathways and disruptions in cell cycle regulation were also observed. Antagomir-717867 transfections and PFT-a pretreatment in GC-2spd cells supported the involvement of piRNA-DQ717867 in regulating cell cycle-related proteins. This study suggests that Cd exposure induces abnormal expression of piRNA-DQ759395 in rat testis and that piRNA-DQ717867 may regulate p53, causing cell cycle abnormalities in GC-2spd cells. These findings help understand the mechanisms of male reproductive toxicity caused by Cd exposure and emphasize the role of piRNAs in cell cycle regulation and male reproductive health.<br />Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.<br /> (Copyright © 2024 Elsevier Inc. All rights reserved.)

Details

Language :
English
ISSN :
1873-1708
Volume :
125
Database :
MEDLINE
Journal :
Reproductive toxicology (Elmsford, N.Y.)
Publication Type :
Academic Journal
Accession number :
38331007
Full Text :
https://doi.org/10.1016/j.reprotox.2024.108554