The mechanism of microcystin leucine-arginine (MC-LR)-induced injury of Sertoli cell immune response and biological behavior.
- Author:
Kaili ZHU
1
;
Changcheng ZHANG
2
;
Xiaoping WU
1
;
Shangyu LIU
1
;
Xueyi ZHAO
1
;
Ding YUAN
1
;
Haixia ZHAO
3
Author Information
1. Third-grade Pharmacological Laboratory on Traditional Chinese Medicine, State Administration of Traditional Chinese Medicine, China Three Gorges University, Yichang 443002, China.
2. Third-grade Pharmacological Laboratory on Traditional Chinese Medicine, State Administration of Traditional Chinese Medicine, College of Basic Medical Sciences, College of Medicine and Health Sciences, China Three Gorges University, Yichang 443002, China.
3. Third-grade Pharmacological Laboratory on Traditional Chinese Medicine, State Administration of Traditional Chinese Medicine, College of Basic Medical Sciences, China Three Gorges University, Yichang 443002, China. *Corresponding author, E-mail: zhaohaixia.mm@163.com.
- Publication Type:Journal Article
- MeSH:
Male;
Humans;
Sertoli Cells;
Leucine/pharmacology*;
Arginine/pharmacology*;
Microcystins/metabolism*;
Immunity
- From:
Chinese Journal of Cellular and Molecular Immunology
2023;39(8):753-758
- CountryChina
- Language:Chinese
-
Abstract:
Microcystin-leucine arginine (MC-LR), a potentially carcinogenic toxin, is produced by Cyanobacteria such as Microcystis and Ananabacteria during water bloom. Increasing evidence demonstrated that MC-LR induces male reproductive toxicity, mainly by inducing germ cell apoptosis, destroying cell cytoskeleton, interfering with DNA damage repair pathway, and damaging blood-testicular barrier (BTB), which eventually lead to male sterility. Testicular Sertoli cells are the somatic cells that directly contact with spermatogenic cells in seminiferous tubules. They not only regulate immune response to maintain testicular immune homeostasis by secreting a variety of cytokines and immunosuppressive factors, but also provide the protective effects of spermatogenic cells by forming BTB. MC-LR induces inflammation and apoptosis of Sertoli cells, and destroys the integrity of the BTB, and then causes spermatogenesis dysfunction.
