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Toxic effects of ketamine on reproductive system via disrupting hypothalamic-pituitary-testicular axis.
OBJECTIVE: In this paper, we focused on the toxic effect of ketamine on the reproductive system in male rats and its underlying mechanisms.
MATERIALS AND METHODS: Rats were randomly allocated into four groups (n=10), i.e. a control group and 3 ketamine groups (high-dose, mid-dose, low-dose). Animals in the ketamine groups received an intraperitoneal injection of ketamine (20, 40 or 60 mg/kg) every 3 days for 7 times. Control rats were injected with normal saline instead. To investigate the disruption potential on the hypothalamic-pituitary-testicular (HPG) axis, the relative hormone levels in serum and mRNA expressions for some reproduction-related genes in reproductive organs were evaluated.
RESULTS: Ketamine significantly decreased the serum concentrations of testosterone (T), inhibin B, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Meanwhile, the mRNA expressions of GnRH in the hypothalamus, GnRH receptor, LH-β and FSH-β in the pituitary, and LH receptor and FSH receptor in testes were also significantly inhibited by ketamine compared with the control (p<0.01).
CONCLUSIONS: These results demonstrated that the ketamine had a toxic effect on the reproductive system via breaking the HPG equilibrium.
MATERIALS AND METHODS: Rats were randomly allocated into four groups (n=10), i.e. a control group and 3 ketamine groups (high-dose, mid-dose, low-dose). Animals in the ketamine groups received an intraperitoneal injection of ketamine (20, 40 or 60 mg/kg) every 3 days for 7 times. Control rats were injected with normal saline instead. To investigate the disruption potential on the hypothalamic-pituitary-testicular (HPG) axis, the relative hormone levels in serum and mRNA expressions for some reproduction-related genes in reproductive organs were evaluated.
RESULTS: Ketamine significantly decreased the serum concentrations of testosterone (T), inhibin B, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Meanwhile, the mRNA expressions of GnRH in the hypothalamus, GnRH receptor, LH-β and FSH-β in the pituitary, and LH receptor and FSH receptor in testes were also significantly inhibited by ketamine compared with the control (p<0.01).
CONCLUSIONS: These results demonstrated that the ketamine had a toxic effect on the reproductive system via breaking the HPG equilibrium.
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