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Published on: July 3, 2015
Effects of subchronic samarium exposure on the histopathological structure and apoptosis regulation in mouse testis
De-Yong Zhang1, Xiu-Ying Shen2, Qin Ruan3
1College of Biology and Environmental Engineering, Zhejiang Shuren University, Hangzhou 310015, China.
Abstract:
To evaluate the reproductive toxicity of samarium, a widely used rare earth element, male ICR mice were orally exposed to samarium nitrate for 90 days for lesion evaluation in the testis. Decreased organ coefficients, disorganized seminiferous tubules, and decreased spermatogenic cells and sperm of the testis were observed extensively in the treated groups, indicating that the testis is a target organ of samarium. Electron microscopy confirmed that the lesions inside the spermatogenic cells and sperm mainly included mitochondrial swelling, mitochondrial vacuolization, fuzzy nuclear membranes, and marginated chromatin. Increased spermatogenic cell apoptosis rate in the testis was confirmed with a TUNEL assay. And expression up-regulation of p53 and Bax, and down-regulation of Bcl-2 were observed (p<0.05), indicating the apoptosis is related to p53 mediated pathway.
Insights
Samarium exposure harms male mouse testes, causing cell damage and apoptosis. This rare earth element impacts reproductive health by disrupting sperm production and testicular function.
Area of Science:
- Toxicology
- Reproductive Toxicology
- Environmental Health
Background:
- Samarium (Sm) is a rare earth element with increasing industrial applications.
- Potential health risks, particularly reproductive toxicity, require thorough investigation.
- Understanding samarium's impact on male reproductive organs is crucial.
Purpose of the Study:
- To assess the reproductive toxicity of samarium nitrate in male ICR mice.
- To identify target organs and cellular mechanisms of samarium-induced toxicity.
- To investigate the role of apoptosis in samarium-related testicular damage.
Main Methods:
- Male ICR mice were orally administered samarium nitrate for 90 days.
- Testicular histopathology and organ coefficients were evaluated.
- Electron microscopy, TUNEL assay, and Western blotting were employed.
Main Results:
- Samarium exposure led to decreased testicular organ coefficients and disorganized seminiferous tubules.
- Significant reductions in spermatogenic cells and sperm were observed.
- Mitochondrial damage, nuclear membrane abnormalities, and increased apoptosis in spermatogenic cells were confirmed.
- Apoptosis was linked to the p53-mediated pathway, with altered p53, Bax, and Bcl-2 expression.
Conclusions:
- The testis is a primary target organ for samarium toxicity.
- Samarium induces reproductive toxicity through cellular damage and apoptosis in spermatogenic cells.
- The p53 signaling pathway plays a key role in samarium-induced testicular apoptosis.
