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Citrinin inhibits the function of Leydig cells in male rats in prepuberty
Xueyun Li1, Lili Tian2, Xinyi Oiao1
1Department of Anesthesiology, Wenzhou Medical University, 109 Xueyuan West Road, Wenzhou, Zhejiang 325027, China; Department of Pathology, the Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, 109 Xueyuan West Road, Wenzhou, Zhejiang 325027, China.
Abstract:
Citrinin, a mycotoxin existing in fruits, has nephrotoxicity, hepatotoxicity and embryotoxicity. The effects of citrinin on Leydig cell development in prepuberty remains unclear. Male Sprague-Dawley rats were gavaged with 0, 1, 2.5, and 5 mg/kg citrinin from postnatal days 21-28. Citrinin at 5 mg/kg significantly decreased serum testosterone levels, while increasing serum LH and FSH levels. Citrinin at 1-5 mg/kg markedly downregulated Hsd17b3 and HSD17B3 expression, while upregulating Srd5a1 (SRD5A1) and Akr1c14 (AKR1C14) expression at 2.5 and/or 5 mg/kg. Citrinin at 5 mg/kg also significantly increased PCNA-labeling index in Leydig cells. Citrinin at 5 mg/kg significantly raised testicular MDA amount, whiling at 2.5 and 5 mg/kg downregulating SOD1 and SOD2 expression. Citrinin at 5 mg/kg markedly decreased the ratio of Bcl2 to Bax, in consistent with the increased apoptosis in Leydig cells judged by TUNEL assay. Enzymatic assay revealed that citrinin inhibited rat testicular HSD3B1 activity at 100 µM and HSD17B3 activity at 10-100 μM. Citrinin at 50 μM and higher also induced reactive oxygen species (ROS) and apoptosis of R2C cell line. In conclusion, citrinin inhibits Leydig cell development at multiple levels via different mechanisms and oxidative stress partially plays a role.
Insights
Citrinin mycotoxin exposure in young rats disrupts Leydig cell development and function. This toxin impairs testosterone production and induces oxidative stress, impacting reproductive health.
Area of Science:
- Toxicology
- Endocrinology
- Reproductive Biology
Background:
- Citrinin is a mycotoxin found in fruits with known toxic effects.
- Its impact on prepubertal Leydig cell development is not well understood.
- Leydig cells are crucial for testosterone production in males.
Purpose of the Study:
- To investigate the effects of citrinin exposure on Leydig cell development in prepubertal rats.
- To elucidate the mechanisms underlying citrinin's toxicity on Leydig cells.
Main Methods:
- Male Sprague-Dawley rats were administered varying doses of citrinin (0-5 mg/kg) daily from postnatal days 21-28.
- Serum hormone levels (testosterone, LH, FSH), gene expression (Hsd17b3, SRD5A1, AKR1C14, SOD1, SOD2), and testicular oxidative stress markers (MDA) were analyzed.
- Leydig cell proliferation (PCNA), apoptosis (TUNEL assay), and enzymatic activity (HSD3B1, HSD17B3) were assessed. R2C cells were used to study ROS and apoptosis.
Main Results:
- Citrinin (5 mg/kg) significantly reduced testosterone levels while increasing LH and FSH.
- It altered gene expression related to steroidogenesis and increased oxidative stress markers (MDA, decreased SOD1/SOD2).
- Citrinin induced Leydig cell apoptosis, inhibited key steroidogenic enzymes, and increased ROS production in R2C cells.
Conclusions:
- Citrinin inhibits prepubertal Leydig cell development through multiple mechanisms, including hormonal imbalance and oxidative stress.
- The mycotoxin disrupts steroidogenesis and promotes Leydig cell apoptosis.
- Oxidative stress is a significant contributing factor to citrinin-induced testicular toxicity.
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