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[Effects of As2O3 on apoptosis and Bcl-2/Bax expression of rat spermatogenic cells]
Wei Chen1, Xiao-lin Shu, Xiang Lu
1Department of Histology and Embryology, Zunyi Medical College, Zunyi 563003, China. jcbzupei@163.com
Objective:
To investigate the occurrence of germ cell apoptosis and the expression of Bcl-2/Bax after aniso-doses arsenic (As2O3) administration in the testes of the adult male rats.
Method:
Forty healthy male Sprague-Dawley rats were divided randomly into four groups and were administered respectively with 0 (control group), 0.375, 0.75, 1.5 mg x kg(-1) of As2O3 by intragastric administration consecutively for 16 weeks. The numbers of testicular sperm head were counted and the coefficient of testicular viscera and daily sperm production (DSP) were calculated in every group. The apoptosis of germ cell were assessed by in situ terminal deoxynucleotityl transferase mediated dTUP nick end labeling (TUNEL) technique. The expression of Bel-2/Bax in spermatogenic cells of different grades were located and quantitated by the method of immunohistochemistry.
Result:
(1) In the testes of As2O3-treated rats, the coefficient of testicular viscera, the number of testicular sperm head and DSP in the middle and high dose groups decreased significantly, compared with those in the control group (P < 0.01); however the apoptosis index of germ cell (AI) significantly increased compared with that in the control group (P < 0.01). Bcl-2 expression of middle dose group and high dose group decreased significantly compared with that in the control group (P < 0.01). Bax expression of middle dose group and high dose group increased significantly compared with that in the control group (P < 0.01); (2)The dependability analysis between DSP and AI showed a negative correlation (r = -0. 563, P <0. 01). (3) The negative correlation was significant between AI and Bcl-2 expression of spermatogenic cells (r = -0.825, P < 0.01); The positive correlation was significant between AI and Bax expression of spermatogenic cells (r = 0.710, P < 0.01).
Conclusion:
One of the mechanisms of male reproduction toxicity of As2O3 might be that Bcl-2 expression is inhibited and Bax expression is encouraged which induces the decrease of quantity of sperm cells.
Insights
Arsenic trioxide (As2O3) exposure in male rats significantly reduces sperm production and testicular health. This toxicity is linked to increased germ cell apoptosis and altered Bcl-2/Bax protein expression, impacting male reproductive function.
Area of Science:
- Toxicology
- Reproductive Biology
- Cellular Biology
Background:
- Arsenic trioxide (As2O3) is a known toxicant with potential adverse effects on male reproductive health.
- Understanding the mechanisms of As2O3-induced reproductive toxicity is crucial for risk assessment and mitigation.
Purpose of the Study:
- To investigate the impact of varying doses of As2O3 on germ cell apoptosis and the expression of Bcl-2 and Bax proteins in adult male rat testes.
- To elucidate the relationship between As2O3 exposure, germ cell apoptosis, sperm production, and the expression of apoptosis-related proteins.
Main Methods:
- Adult male Sprague-Dawley rats were administered different doses of As2O3 (0, 0.375, 0.75, 1.5 mg/kg) for 16 weeks.
- Evaluated testicular parameters including organ coefficient, sperm head count, and daily sperm production (DSP).
- Assessed germ cell apoptosis using the TUNEL technique and quantified Bcl-2/Bax expression via immunohistochemistry.
Main Results:
- As2O3 exposure significantly decreased testicular organ coefficient, sperm head count, and DSP in a dose-dependent manner.
- Germ cell apoptosis index (AI) significantly increased with As2O3 administration.
- Bcl-2 expression decreased, while Bax expression increased significantly in As2O3-treated groups.
- Negative correlations were observed between DSP and AI, AI and Bcl-2, and a positive correlation between AI and Bax.
Conclusions:
- As2O3 induces male reproductive toxicity by promoting germ cell apoptosis.
- The mechanism involves the inhibition of Bcl-2 expression and the encouragement of Bax expression, leading to reduced sperm count.
