Bisphenol A affects cell viability involved in autophagy and apoptosis in goat testis sertoli cell

Autor: Le Han, Hua Yang, Jing Pang, Feng Wang, Yanli Zhang, Guomin Zhang, Fengzhe Li, Peizhen Li
Rok vydání: 2017
Předmět:
0301 basic medicine
Male
endocrine system
Cell Survival
Health
Toxicology and Mutagenesis
Apoptosis
010501 environmental sciences
Biology
Mitochondrion
Endocrine Disruptors
Toxicology
01 natural sciences
03 medical and health sciences
Bcl-2-associated X protein
Phenols
Testis
medicine
Autophagy
Animals
Viability assay
Benzhydryl Compounds
Cells
Cultured
0105 earth and related environmental sciences
bcl-2-Associated X Protein
Pharmacology
chemistry.chemical_classification
Membrane Potential
Mitochondrial
Reactive oxygen species
Sertoli Cells
Dose-Response Relationship
Drug
urogenital system
Goats
General Medicine
Sertoli cell
Cell biology
Mitochondria
Up-Regulation
030104 developmental biology
medicine.anatomical_structure
chemistry
Gene Expression Regulation
Proto-Oncogene Proteins c-bcl-2
biology.protein
Reactive Oxygen Species
hormones
hormone substitutes
and hormone antagonists
Intracellular
Zdroj: Environmental toxicology and pharmacology. 55
ISSN: 1872-7077
Popis: Bisphenol A (BPA) is shown to be the endocrine disruptor that induces reproductive dysfunction in male animals. In this study, we aim to probe the effects of BPA exposure on induction of autophagy in goat Sertoli Cells (gSCs), as well as the relationship between autophagy and apoptosis. Results indicated that exposure to BPA (100, 200, 300, 400, 500 and 600μM) decreased the cell viability in a concentration-dependent manner. Exposure of gSCs to 500μM BPA for 12h resulted in in vitro triggered loss of mitochondrial membrane potential (ΔΨm) and increased reactive oxygen species (ROS) production. Apoptosis with an increase in Bax:Bcl-2 ratio and higher rates of autophagy, such as autophagosome formation and increased expression of autophagy-related markers were also induced in gSCs exposed to 500μM BPA. Furthermore, treatment with 350nM Rapamycin (Rap, autophagy activator) alleviated a decrease in cell viability, intracellular ROS production, and reduction of ΔΨm, as well as decreasing apoptosis. Collectively, our results indicated that gSCs viability was disrupted after BPA treatment through affecting ROS production, mitochondrial membrane potential and inducing autophagy/apoptosis.
Databáze: OpenAIRE
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