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Updated: Jan 19, 2026
Stress Response and Hypothalamic-Pituitary Axis
T-2 toxin impairs male fertility by disrupting hypothalamic-pituitary-testis axis and declining testicular function
Xu Yang1, Xuliang Zhang1, Qiucheng Yao2
1Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin, 150030, China.
Abstract:
T-2 toxin could impair male reproductive function. But, the toxicity mechanism is still unclear. In this study, male Kunming mice were orally administrated with T-2 toxin at the doses of 0, 0.5, 1 or 2 mg/kg body weight for 28 days. The fertility, body weight, reproductive organs volume, daily sperm production (DSP), and sperm malformation rate were detected. The expressions of testosterone (T) biosynthetic enzymes, luteinizing hormone (LH)-receptor, follicle stimulating hormone (FSH)-receptor and androgen binding protein (ABP) in testis were detected. The serum hormone level of gonadotropin-releasing hormone (GnRH), FSH, LH, T and progesterone (P), and the mRNA expression of GnRH, GnRH-receptor, LH and FSH were measured. These results demonstrated that T-2 toxin decreased body weight, reproductive organs volume and DSP, increased sperm malformation rate. T-2 toxin impaired fertility by decreasing the mating index, fertility index, numbers of implantation sites and viable fetuses, and increasing the number of animal with resorptions. Meantime, T-2 suppressed testicular function by inhibiting T biosynthesis and decreasing FSHR, LHR and ABP expression. Furthermore, the serum reproductive hormone contents and key factors expression of hypothalamic-pituitary-testis (HPT) axis were decreased by T-2 toxin. In summary, T-2 toxin impaired the male fertility by disrupting HPT axis and impairing testicular function.
Insights
T-2 toxin exposure in mice significantly reduced male fertility and sperm production. This mycotoxin disrupts the hypothalamic-pituitary-testis axis and impairs testicular function, highlighting its reproductive toxicity.
Area of Science:
- Toxicology
- Reproductive Biology
- Endocrinology
Background:
- T-2 toxin, a prevalent mycotoxin, is known to cause toxicity.
- The precise mechanisms by which T-2 toxin affects male reproductive function remain largely unelucidated.
- Understanding these mechanisms is crucial for assessing reproductive health risks.
Purpose of the Study:
- To investigate the effects of T-2 toxin on male reproductive function in Kunming mice.
- To elucidate the underlying toxicity mechanisms, focusing on the hypothalamic-pituitary-testis (HPT) axis and testicular function.
- To evaluate dose-dependent effects of T-2 toxin on fertility parameters and reproductive hormone levels.
Main Methods:
- Male Kunming mice were administered varying doses of T-2 toxin (0, 0.5, 1, 2 mg/kg) for 28 days.
- Evaluated fertility parameters including mating index, fertility index, sperm production, and sperm morphology.
- Assessed reproductive organ weights, testicular enzyme expression, and serum hormone levels (GnRH, FSH, LH, T, P).
Main Results:
- T-2 toxin exposure led to decreased body weight, reduced reproductive organ volume, and diminished daily sperm production (DSP).
- Sperm malformation rates increased, and fertility was impaired, evidenced by reduced mating/fertility indices and fewer viable fetuses.
- Testicular function was suppressed, indicated by inhibited testosterone biosynthesis and decreased expression of FSH-receptor (FSHR), LH-receptor (LHR), and androgen binding protein (ABP).
Conclusions:
- T-2 toxin significantly impairs male reproductive function and fertility in mice.
- The toxicity mechanism involves disruption of the hypothalamic-pituitary-testis (HPT) axis and direct impairment of testicular function.
- These findings underscore the reproductive risks associated with T-2 toxin exposure.
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