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Consequences of exposure of human Sertoli cells to TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin): evaluation of the aryl hydrocarbon receptor pathway and response to stress

Grant number: 15/06149-1
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): July 01, 2015
Effective date (End): June 30, 2016
Field of knowledge:Biological Sciences - Morphology - Cytology and Cell Biology
Principal Investigator:Wellerson Rodrigo Scarano
Grantee:Carolina Fazio Campos
Host Institution: Instituto de Biociências (IBB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil


Infertility affects 10-15% of couples on reproductive age and male factor may be responsible for 30-50% of cases. Studies suggest that 60-70% male infertility cases are considered idiophatic, once the molecular mechanisms involved in spermatogenesis are still unknown. Male fertility and spermatogenesis process are directly related to the ability of Sertoli cells to produce factors for germ cells development. Male reproductive function gets a lot of attention in recent years due to reports of several reproductive and developmental abnormalities that may be associated with different lifestyles and environmental factors such as toxic agents. An important group of organic compounds with high toxicity are dioxins, having as its main representative 2,3,7,8-tetrachlorodibenzo-p- dioxin (TCDD). TCDD interacts with the aryl hydrocarbon receptor (AhR). This receptor participates in essential physiological processes such as cell growth, differentiation and death, and is also an important regulator of male reproductive processes. AhR is controlled by its AHRR repressor by binding to the nuclear translocator (ARNT), acting as a transcriptional repressor. Experimental models of exposure (mice) showed that TCDD can act changing the male reproductive function, resulting in low sperm count and delayed puberty. Thus, this study aims to evaluate the effect of exposure to TCDD in Sertoli cells with respect to gene and protein expression of AhR, AHRR and its effect on oxidative stress with gene and protein evaluation of SOD2 and NRF2.

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